Acute Kidney Injury (AKI) | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about AC cute kidney injury also known as Aki there's going to be a lot to talk about again this is a part of our clinical medicine section if you guys really are enjoying these videos they help you they make sense please support us you can do that a couple different ways one is you can hit the like button you can comment down in the comment section or subscribe also down the description box below there is a link that goes to our website I'm

telling you this because on our website we have a lot of amazing notes illustrations and quiz Banks where you guys can go there test your knowledge to really understand these topics I urge you guys to do that but without further Ado let's get right into talking about Aki when a patient has an acute kidney injury how do we Define that it's an Abrupt drop in urine output along with an Abrupt increase and what we refer to is their serum creaty that's how I would quickly Define an acute kidney injury now again it is a abrupt

drop off in the urine output in an Abrupt increase in the creatinine often times the urine output is a little bit more difficult and hard to be able to Monitor and calculate as compared to the creatinine that's a little bit easier and something that we can kind of feel off of the labs but when we talk about a q kidney injury we often times break them into these three buckets which I think is a really good way of doing it one known as pre-renal intrarenal and postrenal Aki the reason why I like this is because

it helps us to form a a mind map of the potential pathophysiological Concepts as well as it really helps with understanding the causes and helps us a lot with the Diagnostics so let's get into this prerenal Aki is a problem primarily with the blood flow to the kidney so you see here this is our blood vessels right the renal artery the renal vein but we're going to really focus heavily on the renal artery in patients who have pre-renal Aki their primary pathophysiological problem here is a reduction in renal perfusion so the amount of blood that

is feeding in via the renal artery going into the kidneys which is going to hopefully be filtered into the kidney and eventually that GFR is what we kind of determined will filter out particular plasma molecules and water into the actual tubules and eventually will urinate that out but if a patient has a reduced renal profusion what we start to experience here is that the kidney starts struggling with being able to take that blood flow and hopefully maintain a good GFR so what happens is if we're not profusing the kidney what we'll start to see here

is we will see a drop off and the patient what's called glomular filtration rate the amount of blood flow going into the kidney determines the amount of hydrostatic pressure so if you have a low renal profusion you're going to have a low hydrostatic pressure what happens is is when that GFR drops off and if it drops off abruptly your ability to filter and also to secrete the creatinine kind of goes down but more particularly the filtration and so what we'll start to see is we'll see this rise in the serum creatin within the bloodstream this

is a waste product we're supposed to filter this as well as secrete it into the urine and so how do we truly Define this because I need to look at a lab and say oh that c is definitely it's jacked up it's elevated how do I know that well there's a couple different parameters that we look at one and we look at this off the kigo uh kind of guidelines this is going to say if you have a increase in the creatinine let's say greater than or equal to 0.3 mg per DL there's an increase

in 48 hours so if there is a greater than or equal to 0.3 milligram per DL increase in the Katy in 48 hours we would Define that as an acute kidney injury another way that you can look at this is if it is let's say greater than or equal to 1.5 times whatever the Baseline serum creatinine is in 7 days that would also be another potential reason so whenever it is greater than equal to 1.5 times the Baseline increase in the creatinine within a 7-Day period we could also Define that as an acute kidney injury

and again it's all because the profusion to the kidney sucks we're not filtering off potential things like the creatinine the other way that we can also Define this based upon the kigo is that GFR not only determines our creatinine clearance but but it also determines how much of this filtration is going to start leading to making urine and if your GFR sucks guess what's going to happen to your urine output that's also going to suck you know we how we Define this Technically when that urine output's low we Define this as aligura but aligera is

really more specific it's looking at less than 400 or 500 Ms on a 24-hour period but the kigo definition looks at a little bit more specifically and it says that whenever the urine output drops and we say to less than or equal to 0.5 CC's per kilogram per hour for greater than equal to 6 hours that is how we would define an acute kidney injury all right so again a drop in the urine output could be defined as oliguria and we could look at this in the sense of the amount of urine that they're making

per hour over a six-h hour period but aligor as a general definition is more particularly looking at what it's looking at less than 400 to 500 MLS within a 24-hour period all right so this is again a simple concept with the most overarching theme here that the pre-renal Aki is due to a reduction and renal profusion we'll come and go into this because the reduction of renal profusion is dependent upon a couple different factors and we'll go over that in a second but before we do let's actually talk about intrarenal Aki so with intrarenal Aki

the problem is not necessarily with the blood vessels it's a problem with the structures inside of the kidney and you know these structures inside the kidney you know what they're called the ones that make up most of our kidney they're the structural and functional unit of our kidneys the nephrons so whenever there is nephron injury so there is a let's say a big amount of nephron injury so there is an increase in your nefron injury now then that kind of begs the question you got to go back a little bit to your anatomy and physiology

what in the heck is a nefron a nephron is the glomerulus the TFT of capillaries plus the proximal tubal the loop of Henley and the distal tubal if there is some type of injury to the Glarus or that tubular system you will then start to see a drop off in the patient's ability to filter via the Glarus as well as to reabsorb so the problem with this is the same thing they'll experience a drop off in the GF far because of their nefron injury and that will then lead to a what a abrupt increase in

the serum creatinine as well as if they're having difficulty with filtering again what we also notice we'll notice a decreased ability to make urine and we start to experience a drop off in the urine output and again definition wise how do we Define this greater than or equal to 0.3 Mig per DL in a twood DA window or greater than equal to 1.5 times the Baseline increase in the serum craty over 7 days or you're an output less than 0.5 CC's per kilogram per hour for over or equal to 6 hours again this that kigo

definition so again if it's nefron injury this is how we would Define intrarenal Aki now the last one is postrenal Aki has nothing to do with the renal vasculature has nothing to do with the nephrons there is most likely a urinary tract obstruction and that the issue here is that there is some type of urinary tract obstruction and the problem with this is is when you have a urinary tract obstruction it's obstructing the normal flow of filtrate and urine for example if I have some type of obstruction here in the urer or within the kidney

like the renal pelvis or here somewhere again within like maybe the bladder Outlet this problem here is I could have good renal profusion right so maybe the renal profusion here is normal and then the nephrons are fine and so because my renal profusion is normal I'm going to get a normal GFR but then what happens is as as the blood tries to run its way through I the filtrate tries to run its way out to go to the urine it hits this area here where there is a blockage of flow or maybe it hits it

here where there is a block blockage of flow what's the issue with this the problem with this is when you have a urinary tract obstruction you can't allow for normal urine flow so what ends up happening is is you start to have this issue here where you have this obstruction it starts to cause a backflow right so it causes an increase in the backf flow of urine and what that does is is it increases the pressure at the actual uh nefron level so whenever you have fluid and I'll explain this as the fluid starts kind

of backing up into the tubular system it then makes it harder because the pressure inside of the tubular system becomes too high where blood won't easily filter across the Glarus and so that's what will cause this abrupt drop in the GFR and if we have this abrupt drop in the GFR what will happen is you'll see that rise in the creatinine and you'll see that abrupt drop and the you're an output so again this is again that concept so again I will go over this but again urinary tract obstruction this is the primary reason why

there is a back flow of urine and a drop in the GFR increasing the cring decreasing the urine output all right so if I Define this simply pre-renal is a reduction in renal profusion the blood flow to the kidney intrarenal is a damage to the actual intrinsic structures of the kidney such as the nefron that's being injured in some way and then lastly is postrenal Aki is an obstruction at some some point at the collecting duct all the way down to the actual urethra point so if there's an obstruction at any point there there's going

to be a back flow and all of these things will cause a rapid drop in the GFR which will cause a rapid rise in the creatinine and a drop in the urine output all right cool so now the next component here is really kind of giving a better dive into the under kind of or the overarching theme here which this one's a reduction of Ral profusion that one's nephron injury that one's an obstru uction so I kind of want to just take a quick second here and say okay if I have a reduction of renal

profusion what could be some of the basic concepts behind this and often times the reason why the renal profusion is low could be a couple things one is the amount of volume of blood that is moving through the glomerulus is being reduced and then unfortunately that will lead to that abrupt drop in the GFR all right so what are these reasons why we'll get into this but again what is this call whenever the amount of volume that you're circulating through the bloodstream is reduced this is called the effective arterial blood volume when a patient's effective

arterial blood volume is reduced this is going to lead to less blood that are filling the vessels less blood filling the vessels in the kidney and less filtration so that's the concept here so it's a reduction in effective arterial blood volume there's a couple different reasons why and we'll talk about that the other one is your renal arteries could be massively vasoconstricted so what if I have a patient who has intense renal vessel vasoconstriction if I have massive renal vasil constriction now the problem here is that I won't be able to get blood in now

look I got to try to get blood through that tiny little like aper arterial here and into the Glarus you see how difficult that will be so that's one potential reason here is that whenever you have intense renal vasal constriction that will make it difficult to get blood through that tiny little aperin arterial and that'll reduce the filtration there so that will drop your GFR all right and as we see that drop in the GFR we will see the abrupt rise in the creatinine and the drop in the urine output another mechanism it kind of

goes along with this is if the you have we'll talk about this a little bit later not only the AER aterial but sometimes if the eer material is excessively vasodilated I'll explain that a little bit later but I want you to stick with the mechanisms of reduction and effective arterial blood volume and increased renal vasil constriction but again keep the caveat that I'll talk about later with the eer arterial vasil dilation the last category here is what if something is particularly obstructing so what if I have something that is obstructing the flow of blood in

some particular way and I'm not able to get the blood through here if that's the case I'm not going to be able to establish a good GFR right and these are the three concepts as to what can lead to a a reduction and renal profusion is there some type of renal artery obstruction which is kind of obstructing the blood flow into the glomerulus or the aperin arterial super super constricted or the Eep is very vasodilated that's the caveat or the amount of volume that's rushing through the actual chus is reduced and we'll talk about the

mechanisms in each one of these but these are the three things that I need you to remember as we will die into this again and again all right that covers the prerenal now it is a very important uh kind of thing to remember here that prerenal accounts for about 60 to 70% of most patients Aki so if a patient has an Aki there's a high chance that this is the most likely one that they're experiencing the next most common one is intrarenal AI this could account for maybe 35 to 40% of patients who have an

Aki now again I told you that a problem is with the nefron but I want you to divide that up I want you to think about this in the sense that what if there is injury or damage to the Glarus now the Glarus is the capillaries but you also have this basement membrane which are associated with this and so whenever I talk about this if a patient has a significant glomular injury or damage it's going to cause inflammation and this INF inflammation can cause thickening of this membrane it can cause fibrosis but I'd say the

most concerning feature is that sometimes patients with lots and lots of inflammation they can get this weird type of formation here which is super super scary when you get glomular injury and that is that sometimes they can get this kind of epithelialization and a little bit of fibrosis around their kind of Bowman's capsule glomular area and they can form these crescents and these crescents are the inflammation of the Glam BAS membran thickens it if you thicken this area now you have to have filtrate go through the Glarus through the thickened membrane through the fibrosis of

the crescents and then into the Bowman's capsule space do you see how hard that would be so because of that that glomular injury is going to make it more difficult to filter things across and that my friends is what's going to lead to a drop off in the patient's GFR all right so that's one potential thing to be thinking about is if a patient has glomular injury one of the things that it can do is it can cause a thickening let's say thickening of the glomular basement membrane now sometimes this is what we refer to

as rapidly Progressive glamin nefritis if they get a lot of thickening and they form Crescent due to a lot of kind of epithelialization within the Bowman's capsule and that's the scary scary one so I would be really really terrified if a patient develop what called rapidly Progressive GL nefritis but again we'll get into that with glomular injuries I don't want to give too much away okay got to keep you in suspense somehow the next concept is what if it has nothing to do with the Glarus the Glarus is healthy but the tubular cells are the

ones that are damaged so now here's the thing your tubular cells if they're damaged in some way shape or form and then they die off you know when cells die if they die off what watch this imagine these cells they they get killed and then they die off and then all of a sudden these cells they start clumping up into the tubular Lumen if they Clump up in the tubular Lum and what's going to happen it's going to block the flow cuz here you may have this normal kind of filtration process originally but then what's

going to happen this filtrate is going to run right into this kind of like what we call cast and it's going to block it from moving forward and so there's the issue is right there and so this patient will start to experience a drop off in their GFR because they're just not able to get things past the tubules and then on top of that the tubular is not only supposed to be able to help with uh this process but guess what else they're supposed to do they're supposed to secrete things and so you lose the

secretion capacity of creatinine but again the GFR will drop and the reason why is because you have these tubules that are blocking that flow and So eventually the pressure will build up here and it'll make it harder for blood to go from high pressure to low pressure because the pressure of this capsule will start increasing because these casts are blocking them and that's really really important all right so this is one big thing and again we see this most common ly with a lot of tubular injury all right because they can cause these different types

of cast to form and these cast will really really chalk up and block up and booger up this entire tubular Lumen and that's the big thing to remember here all right so we have the most common the second most so we got we got this renal profusion problem effect of Rial blood volume renal Bas of contriction and then renal artery obstruction within the intrarenal it's nephron injury but I'm going to break it into gular and tubular injury the last one is postrenal Aki it's usually urinary tract obstruction now we can Define the obstructions as being

proximal and distal but we'll do that a little bit when we get into more of the causes I want you to understand here that if I have an obstruction somewhere and let's just pretend it's here if I have an obstruction here as compared to like in the tubular the tubular injury right in entry like I was like right here if there's an struction here what's going to happen is filtrate is supposed to go this way but now what's going to happen is the filtrate is going to get stuck and it's going to start backing up

and as it starts to backf flow what happens is it increases the pressure inside of the capsule and that pressure will make it harder for again to have a good gradient because GFR is dependent upon hydrostatic pressure and then also dependent upon the capsular pressure if the hydrostatic pressure is good but the capsular hydrostatic pressure is really really high it's going to make it hard for the blood to flow across and so that's what really happens here is that the obstruction actually what it does is is it increases the capsular hydrostatic pressure so the pressure

inside of the capsule goes up and then that what that does is that reduces the gradient of blood flowing across the Glarus and so as a result this is going to drop off the patient's GFR so again you're going to see an obstruction it's going to increase the pressure here in this particular area so this is going to start going up and up and up and up and it's going to make it harder for the gradient across the glus and that's what happens potentially in this particular area now that's postrenal all right so it's an

obstruction it's either proximal disable but we'll talk about that the last thing is when a patient develops an Aki so they develop an initial injury so you injur the kidneys whether it be to reduce renal profusion nephrine entry or an obstruction what we start to see is the patient can go through three phases and this is where we see a lot of the disease process the first one is they can go into What's called the aliger phase and this is the phase where their urine output starts to drop their GFR starts to drop right this

is usually you know maybe a a week or two but we start to notice that they have a drop in their GFR and we start to notice a drop in their urine output right this stage right here is when most patients experience their complications such as hyperemia metabolic acidosis hyperemia uremia what happens is over time the epithelium will start to reepithelialize you'll give time for the kidneys to start to heal and then what they'll do is is they'll go into this phase called the polyuric phase the problem with the polyuric phase is is that their

GFR will start to kind of begin to normalize and the urine output will massively massively increase so this is where you see a huge huge increase in the urine output what happens is the problem in this phase is that when a patient develops High urine output they can experience complications like dehydration and hypokalemia but then eventually this may last a couple weeks eventually over months you know sometimes worst case scenario years the kidney will completely go into a recovery phase and that's the design and this is usually the progression of Aki and most of the

patients when we see them they're living in this phase where they just had their initial injury their GFR is dropping their urine output's dropping and we're starting to experience complications that we'll talk about a little bit later all right now that we've done this here's what I want to do I want to take each category of Aki starting with preal and really dissect what's decreasing the effect of arterial blood Vol what's causing renal Bas of constriction and what's obstructing the renal artery and then so on and so forth let's do that all right so let's

move on to the causes of pre-renal Aki so we know now that pre reenal Aki is a reduction of renal profusion that's the primary basis of it but we can further divvy that up in the sense that the volume that you're delivering to the kidney is reduced the renal vessels are super vasal constricted reducing the profusion or you have an obstruction that's the three ways I want you to think about it most of the cases come down to the effect of arterial blood volume being reduced now there is two syndromes that often times will present

as kind of a hypovolemic type of patient uh hyperic type of patient and so what do I mean often times they can present with features of Edema so pedal edema so swelling of the legs um they can also present with pulmonary edema or plural affusion so they can have dnia they can have crackles on oscilation they may even have hypoxia and on top of that they may even have evidence of aites right especially in the patients who have like therosis and so these are features that you want to look for in these patients as it's

important to assess the underlying cause of the patients's Aki and the other thing is that in patients who have preal Aki often times you'll see that the first treatment that we initiate is IV fluids these are the patients that you probably want to avoid that in because you can potentially worsen their scenario all right let's talk about these though cardiorenal syndrome this is the person that you want to look for because the underlying trigger for this is a patient with underlying heart failure now this can happen in uh a heart failure with a reduced ejection

fraction or a heart failure with a preserved ejection fraction so if they have systolic or diastolic dysfunction believe it or not both of them can cause this let me explain why if if a patient has a reduced let's say left ventricular ejection fraction one of the things that we may see is that their cardiac output really really stinks and so if their cardiac output kind of starts to go down because you have again some type of let's say left ventricular dysfunction of sorts then you may have difficulty being able to get blood out of the

left ventricle here and then out into the systemic circulation so this may be impeded in some way shape or form and as a result you get a drop in the cardiac output you know what cardiac output determines your mean arterial pressure your mean arterial pressure is the pressure that peruses organs so if the cardiac output drops guess what happens the amount of effective arterial blood volume drops so that's what we're going to see is that the patient will have this drop per se and their mean arterial pressure and the amount of volume of blood that's

circulating their vessels is dependent upon cardiac output so their effective arterial blood volume will go down and then we will struggle to be able to peruse these poor little kidneys and as a response what will happen we'll see a drop off in there urine output and we'll also see a increase in there creatinine and that's the big things that I want you guys to be able to remember is a drop off in their urine output and an increase in their serum creatinine that's one mechanism the other mechanism is actually quite interesting if a patient has

some degree of right heart involvement maybe that's because left heart failures progress them to right heart failure but if they have issues where they're having difficulty getting getting blood out of their right heart now what starts to happen well that blood will then back up into the right atrium then it can move down via the uh inferior vena and when that happens what's going to happen to their Central Venus pressure it goes up if Central Venus pressure goes up guess what that does it makes it harder for blood to leave the kidney because imagine you're

trying to have blood come out of the kidney but the pressure that it's entering into coming out of the kidney is very high that blood flow is going to be slow and it makes it harder for the blood to go into the kidney the driving pressure across the kidney then drops so again with this thing what it can induce is is it can induce what's called Venus congestion and so this is why it's kind of interesting is this can cause Venus congestion of the kidney sometimes we call it like congestive nephropathy and that in itself

can also reduce the effect of AR tyal blood volume right and so that's the thing to remember is that Venus congestion can also lead to this reduction effect of arterial blood volume going into the kidney so this is the big thing to remember for patients with cardiorenal syndrome but again please don't forget that this patient will have heart failure but they'll also have features of look for assess for features and both of these of hyper volia right and what do I mean look for edema look for AES look for hypertension and so these are really

really important things that you can see in both of these patients here with cardiorenal syndrome and patients with hepatorenal syndrome really really important to look and assess for this because this is one thing that will help you to differentiate the two all right cardiio renal syndrome heart failure driving the kidney failure all right hpat renal syndrome is usually the liver is driving the renal failure we often times see this in a patient Who develops what's called decompensated therosis now you're like oh jeez back to the GI huh yeah this is actually a really really interesting

one so in patients who have decompensated curosis right they have underlying liver disease right so they have underlying liver disease and this is kind of a two-fold thing because it's kind of interesting the mechanism of itself when a patient has liver disease severe curosis what happens to the ability of the ocytes to produce alumin it goes down right that's one factor that we know is that that's kind of a prognostic factor is that as liver failure begins to progress alumin can potentially start going down now as albumin goes down what happens is you decrease the

oncotic pressure in your blood vessels what in the heck is oncotic pressure that's the pressure that's designed to be able to keep fluid inside of the blood vessels so if I drop it now here's my albumin molecules and blue here's my alumin what it's supposed to be doing is keeping and pulling water into the bloodstream so all of this is going to be helping to drive the water into the bloodstream but if I have less albumin I have less oncotic pressure am I going to be able to keep that water and drive it into the

bloodstream no this becomes inhibited the amount of volume that's in filling that vessel is reduced so then I reduce my effective arterial blood volume so that's one way that a patient who has a hepatorenal syndrome can have this issue and I really really think this is important in the same way because when we treat patients with cardiio renal syndrome we actually work on increasing cardiac output and then decongesting them so diuretics and inotropes are after load reducers and patients with decompensated therosis alumin would be a treatment now this is again one potential thing I don't

know why I write alumin this should be effective arterial blood volume I apologize guys effective arterial blood volume meaning as a result I will struggle to peruse the kidneys the cattiny will go up and the urine output will start to drop all right so that's one mechanism but the other theory behind this is actually a little bit more complicated and patients have decompensated therosis if they have evidence of what's called portal hypertension so the pressure so they have uh the portal veins if the portal hypertension is existing what happens is is your liver and endothelial

cells start secreting chemicals like little dilators but the problem is these dilators they're supposed to treat portal hypertension it's supposed to get this vessel to dilate these little chemicals they get into the bloodstream into the systemic circulation and what they do is they cause systemic vasod dilation so in other words I start vasod dilating a bunch of different vessels in my body but the most common one that we see this in is the splank niik vessels now you're like what in the dang what is the splank Nick vessels now splank niic Vasa dilation is actually

going to be one of the most prominent ones and this is when you dilate the vessels that is going to the git so the blood flow to the git would actually as a response end up increasing because I'm trying to get more blood flow to go to that area problem is is when you cause systemic Vasa dilation Prim arily primarily by stimulating this process what you can do is is two things if I have more blood easily going this route of less resistance what's going to happen to the blood that's kind of going unfortunately to

the poor little kidneys that's going to be reduced so that's one way that we can think about this reducing the effect of arterial blood volume but there's another concept you know what uh systemic vas of dilation does to your pressure it drops it and so patients often times will have uh kind of a drop in their blood pressure and so whenever they have a drop in their blood pressure what we do is is we actually amp up the renin Angiotensin aldosterone system our sympathetic nervous system and you know what these things do they then cause

renal Vaso constriction and then they clamp down so another thing that they actually kind of try to do here is they actually try to clamp down on this vessel and that also further reduces the effect of arterial blood volume so again when you vasod dilate a patient's body it amps up the renin otens and ostrin system their sympathetic nervous system and they try to Vaso constrict and on top of that they're not getting as much blood going to their poor little kidneys so you see how this really would cause this and it's really interesting because

guess how we treat these patients with a penal syndrome we give them albumin to improve their oncotic pressure we give them drugs that can cause systemic Vaso constriction so that they stop dropping the pressure and shut down this neurohormonal system and then we give drugs that CA splenic Vaso constriction so that we don't pull blood away from the kidneys and going into the GP instead right that's why it's so cool all right and again look for features of hypervolemia in this patient okay we now come forward so into the next concept here is a patient

is not hypervolemic they're hypovolemic so hypovolemia is often times one of the most regarded causes of prerenal Aki and you can oftentimes remember this via the 3DS so I remember diarrhea diuresis and dehydration but I also would not forget blood loss all right so blood loss is another really big one as well but in patients who have diarrhea diuresis dehydration blood loss is another really really really important one don't forget that one as well what happens is you may have a drop in their blood volume so when you drop a patient's blood volume what you

theoretically do is is if I drop their blood volume I drop their preload so whenever you drop a patient's blood volume you theoretically you drop what's called their indolic volume and so the amount of volume that they have to pump out of their heart is reduced well if they have less volume to pump out of their heart what's that called their stroke volume so then what will happen is their stroke volume will reduce well guess what stroke volume determines cardiac output and so we see a drop in the patient's stroke volume and as a response

we see a drop in the patient's cardiac output guess what that determines the effective arterial blood volume oh baby we good and so that's why it's kind of important to think about this because if that happens then I'm not going to peruse my poor little kidneys and if I don't peruse these Katy will go up urine output will start to fall off and that's the concept here that I need you guys to be able to understand now again don't don't forget diarrhea diuresis dehydration I'm just going to put it here so you guys don't forget

here don't forget blood loss this can definitely be an accute cause as well all right but you're looking for the source of hypovolemia and the other thing is for this patient they will have features of hypovolemia they'll have uh the decreased skin turer they'll have the dry mucus membranes they'll also have potentially hypotension Tac cardia so think about these potential features here but more importantly look for the history that's going to suggest this as compared to these scenarios now here's the thing hypovolemia hepatorenal cardiorenal are very very common causes and an ICU setting or an

emergency room setting this starts to become one of the most common causes of pre-renal Aki that can easily become intrarenal hypotension and I'm talking really a patient who is in Frank shock so what do I mean I'm talking about septic shock so septic shock is a really really big one another one would be cardiogenic shock another one would be hypovolemic so even patients who have hypovolemia without severe hypotension and shock can have Aki so remember hypovolemia you can have hypovolemia without shock and still cause Aki so in this particular scenario most these patients who have

shock their end problem is regardless of what it is is that whether it's due to to a problem with the heart whether the blood vessels are super vasodilated right either way in all of these particular scenarios a patient is suffering from severe hypotension so their blood pressure is really low but the more particular parameter that we like to look at here is that their mean arterial pressure is low that's the pressure that drives blood to the kidneys and so as a response their effective arterial blood volume is going to drop so this is the one

that's actually kind of easy because if you see a patient in a clinical vignette who then has some type of underlying acute kidney injury and just recently they had a massive episodes of hypotension whether it's sepsis whether it's cardiogenic shock whether it's hypovolemic shock of some sort their problem is whether it was due to the heart whether it's due to the vessels being super dilated or not filled enough their imun arterial pressure is dropping and they're experiencing multi-stem organ dysfunction not just the kidneys multi system organ dysfunction and so that's the big thing to remember

for this all of these will cover your reduced effect of arterial blood volume so cardiorenal hepatorenal hypovolemia and lastly any type of shock State all right what about the patient who their effective arterial blood volume isn't really an issue in this particular situation it's the renal vessels are super vasal constricted this is an interesting one I'm going to look at it in two different ways one is that the afferent arterial so the afferent arterial the blood that's going into the Glarus the aperin arterial is super Vaso constricted okay and then we're going to add in

the cavat the other one is when the eerin arterial is undergoing intense vasod dilation you're like okay Zach this is weird you're talking about vasil contriction yes this is a little caveat I promise it'll make sense hold on in patients who have intense afferent arterial Vasa constriction this is what I want you to remember we see this in ineds so we see this with insed use and we also see this in drugs like tacr lius which is it's kind of an immunosuppressant drug that we use in like organ transplants especially renal transplants funny enough um

but these are two big ones the eph and arterial vasodilation now here ACE inhibitors and arbs they can cause this but they're more likely more likely to do this mechanism and have a more profound effect via ACE inhibitors or arbs so your angot tenson receptor blockers so if I have a patient who has increased afferent arterial vas of contriction and increased eer arterial vas dilation it's these drugs that are doing that now the question is how in the heck is this doing it Zach I kind of remember this one that if it's clamped down right

I'm going to have less blood flow coming in here right so if I have less blood flow going through this tiny little aerin arterial yes that makes perfect sense why the GFR will kind of drop and while I'll start to to have the patient experience this as you say increase in the creatinine and the drop off and the patient's urine output and so that that part makes sense that definitely makes sense okay here's the question that you may have how in the heck do ineds do this and how does terer do it terer is not

really as well understood it may affect the calcium influx but ineds we do know what ineds do is ineds actually work to inhibit they inhibit what's called prostaglandin I2 and prostaglandins what these are designed to do is is they're supposed to cause afferent arterial Vaso dilation so they supposed to inhibit these and this will cause afferent arterial Vaso dilation but if I inhibit the pgi2 so now I have decreased levels of the pgi2 will I be able to cause AFA dilation no and so this becomes inhibited and that's where the patient starts to experience the

actual opposite the vasoconstrictive response now this is probably where you may be a little bit confused the eeper material Vaso dilation how does this do it well if the eeper material is super Vaso dilated believe it or not what happens is it actually kind of drops the pressure inside of the Glarus so if you have blood that's kind of flowing through here what's going to happen is the pressure that's present inside the Glarus is actually going to drop and so that's what actually happens here is that in these patients we see a drop a decrease

in their glomular pressure because because imagine this if I had this thing super tight it's going to be hard for blood to drain out of the Glarus if I have it super large it's going to be easy for blood to leave the Glarus the pressure inside the Glarus will drop and as a response that'll drop the patient's GFR and so that's what we'll start to see in these patients is we'll see that drop in the GFR all right so we'll see a drop in the glomular pressure and then as a response we'll see a drop

in the patient's GFR and then you'll see as a result an increase in the crine and a decrease in the patient's urine output all right so again when we talk about renal vasil constriction I'm saying inets tacro they're causing air arterial vasil constriction and then for a Inhibitors or arbs they're causing eir material vasod dilation these are the mechanisms which are resulting in this reduction in G GFR okay these patients look for these in the medication history if they're on these you probably want to discontinue them if they're on these you might want to discontinue

this this it really depends if a patient just had a transplant probably wouldn't discontinue this we don't rejection so this is maybe the one that possibly you have to re-evaluate last one is renal artery obstruction this one's really interesting now we call this is usually due to an obstruction there's two types there's what's called renal artery stenosis and this renal artery stenosis can actually should be kind of two types in the sense that this could be AO sclerosis and this could also be something called fibromuscular dysplasia now either way look at these both of them

are narrowing the blood flow so in this particular situation I'm narrowing the blood flow into the kidney and this one I got all of this like weird kind of torturous formation here I'm reducing the blood flow to the kidney so as a response I'm going to experience a drop in GFR and I will experience in this particular scenario what it's going to be like clockwork here an increase in the creatinine and a drop and the UR an output now the question that kind of comes about here is how do I know this one often times

these patients will usually exhibit hypertension so they'll have very very uncontrolled hypertension the other one is that you're going to want to assess for brewes so brewes is a really really big one because of the reduced renal blood flow now the other thing is atherosclerosis you're going to see this in patients more likely you'll see this more likely in patients who are greater than 50 fibromuscular dysplasia you're going to see this in patients who are often times less than 50 years of age so greater than 50 and then this patient less than 50 years of

age but again assess for this in a patient with very very severe hypertension and brewes here's the other thing and I want you guys to remember this often times renal artery obstruction like these diseases don't truly cause severe Aki unless it is this so in Aki really with this you would have to have bilateral renal artery stenosis plus ACE inhibitor use now you're like what in the heck are you talking about Zach in order for us to really cause an acute kidney injury you have to reduce blood flow to both kidneys because one kidney will

compensate so I got to reduce blood flow to both kidneys and on top of that I need to make it even harder I'm going to add in another kind of mix here I'm going to add in an Ace inhibitor because guess what ACE inhibitors do they cause eer arterial Vasa delation and reduce the GFR so the combination of these is oftentimes a recipe for a patient developing an acute kidney injury so this is the big thing to remember here all right we've talked a lot about pre-renal Aki now that we've done that let's move into

the next one which is intrarenal Aki all right so we move on to intrarenal Aki again this is the second most common now when I talk about intrarenal Aki the most common type of ental Aki is going to be ATN so yes it is worth some degree of time to dedicate to the others but I would focus most of your energy into the reasons that patients develop intrarenal Aki is to be ATN it's like 85 to 90% of the time that's very very common so when we talk about these again we broke it down into

tubular and glomular when we talk about tubular injuries often times it breaks it down into ATN and acute interstitial nefritis now remember the tubular are in tubules were injured they sloth off and they block up the flow of that duct right and so you can't get the normal filtration across the Glarus because the pressure is building up in the capsule so what's causing the death of these cells because this is really the issue right these cells are dying off and that's what's really triggering these patients to develop acute tuul necrosis but you have to ask

why one reason is often times a patient has experienced something called so there's two types of acute necrosis one is so write this like this es schic ATN so es schic acute tub necrosis this is one reason now aeic ATN is usually the primary mechanism is that there's a prolonged reduction in renal profusion so it's a reduction and renal profusion and this is prolonged and I think that's really the big thing to remember here so here's what I want you to think about Zach okay you said that prolong renal profusion when it's reduced wa what

was the oh any pre-renal Aki right Zach yeah so when a patient has a reduction of renal profusion any pre-renal Aki so any pre renal Aki can cause this and that's the really important point to remember here is that if a patient has any prenal Aki especially hypotension or hyp vmia that doesn't go treated eventually it causes enough reduction in blood flow CU again you have to have blood circulating through here and guess what the blood does yes we talked about it playing a role in filtration but also it's supposed to run through the eair

material and through the peritubular capillaries and the VAS arcta and it's supposed to give oxygen to these tissues but if I am not giving oxygen to the tissues so there is a decreased oxygen delivery to these tissues what's the problem as a response they're going to undergo death because again I'm just not getting enough blood flow going to these guys that's the concept there this is a big one all right the other one is nephrotoxic ATN and the reason why I want you to think about it like this is that this is usually due to

some type of drug of sort medications of sort sometimes there can be other things that can trigger this so the way that I like to remember the nephrotoxic ones is I first like to remember medications that can trigger this so there is a lot of different medications that have the capacity to induce this injury one I think that's worth remembering here is going to be vanoy so vanoy is often times utilized as an antibiotic like a broad spectrum antibiotic another one could be aminoglycosides these are I hate these drugs they can cause so so much

injury to the tubular cells another one that we use um is going to be otaris so these are two really big antibiotics amphoterin I also like to remember this is otable OTAs which is utilized um in fungal infections can also do this as well now these are really really big triggers right these are the big ones there is a a bunch of different other medications that could cause this as well but I want you to think about these cuz they're commonly prescribed especially if anom and amino glycosides another one is it could be due to

pigments all right and when I say pigments I'm talking about like you know hee pigment molecules and so there's two types one is if I say that a patient is exposed to what's called lots and lots of myoglobin this could be a really really big one so myoglobin we can see this in patients who experience a disease called rabdo myis so rabdomiolisis is whenever a patient has like severe seizures or Crush injuries and they bust open their skeletal muscle cells and release myoglobin the myoglobin gets into the tubular cells and causes direct injury so again

nephrotoxins are causing direct necrosis the esic ATN is causing indirect necrosis via a reduction and oxygen delivery now that's one another cause is it could be due to an increase in hemoglobin so an increase in hemoglobin hemoglobin is also another pigment as well and this can cause this and this would be due to homolysis so homolysis those are the two big pigments there also can be certain types of uh let's say crystals that can also cause this type of process so in patients have um oh and then there's one more drug I forgot about this

one this is a really really big one otaris do not forget about contrast dye so contrast d is a huge huge trigger often times we can see this causing contrast induced nephropathy so contrast diated contrast especially in patients with underlying CKD or reduced renal blood flow this right here has a increased risk of patients developing Aki so again remember these the last one here is again crystals so crystals that kind of deposit up into these tissue cells can also cause death a big one that I like to remember here is going to be lots of

uric acid so when patients have lots of uric acid this can do this and the only reason that you would really see like tons and tons of uric acid is a disease called tumor Lis syndrome so tumor Lis syndrome whenever you're popping open um Hodgkins lymphoma like a patient who has non hodkin lymphoma or acute myogenous leukemia or Al and they end up getting chemotherapy and those cells bust open they release a ton of uric acid the uric acid can form crystals and gets stuck in the tubular cells and cause injury the last one is

imunoglobulin so immunog globulins I'm going to put IG so amog globulins there's a really important one and this is whenever patients get what a lot of what called increase in bench Jones proteins so you have a lot of what's called bench Jones proteins these are like the light chains of the immunoglobulins and we can see this in a very interesting disease called multiple Myoma so in patients who have hypercalcemia as well as bone pain as well as anemia and on top of that they also have an acute kidney injury think about potentially multiple Myoma where

these proteins are depositing into these actual tubular cells and causing death these are the big things that I would really want you to remember here okay now one other thing here is that whenever these cells die off whenever these cells die off right and then they get in here into this actual tubal what happens is the cells get stuck imagine the cells slopping off and they get stuck when they get stuck they kind of form this interesting cast that you can see on your analysis with microscopy and this cast is a bunch of cells kind

of just like clumped up together and they look kind of brownish and what we do is we call this muddy Brown cast so we say these are called muddy Brown cast and that's often times pathon neonic for what we would say as a patient having acute tubular necrosis all right so if a patient has a qtu necrosis think about have they had a prolonged Pro hypo profusion to the kidney or have they been exposed to nephrotoxic medications think about rabdo homolysis uric acid ele elevation and bench Jones proteins and then lastly look at their medical

history and look for any kind of medications that they may have been exposed to that caused this okay the next one is acute inter ntis acute interal nefritis is less common but here's the thing I want you to remember with this one often times the most common offender here is it's usually medications so this is usually medications as well now you would probably like oh well Zach medications can also cause ATN again what's the most common type of interal Aki it's often times ATN but there is the desire to again remember potentially some of these

other ones so patients who are exposed to ineds betal lacum antibiotics ppis these are potential increased risk so again I would think about things like ineds these can cause this um I would also remember betal lactum antibiotics these are really really big offenders I would say this is the big one that you'll see and then lastly I would also even remember things like proton pump inhibitors now the mechanism behind this isn't completely understood but what we think is is that these drugs per se when they're exposed they're creating like a type four or type one

hyper sensitivity reaction and what that's doing is that's drawing pull in a lot of immune system cells into the interstitium right this may be neutrophils this may be eosinophils this may be lymphocytes but all of these are being drawn into this interstitial area and what it's doing is is it's causing first inflammation of the interstitium but then over time if the inflammation continues and you don't fix that it then starts to progress to the tubular cells and as I start to damage those tubular cells those tubular cells will start to sloth off here's the big

thing though when you cause this increased activity of the immune system this not only leads to the presentation of an Aki often times it'll present with a Triad so there is this classic Triad if you will of Ain and often times we remember this as a patient presenting with a fever a rash an increased amounts of eosinophils in their urine and in their bloodstream so that's what I want you to remember MERS look for fever look for rash and then look for an increase in eosinophils that are present in the urine as well as present

within the bloodstream with that being said here's what's really interesting these white blood cells some of them can start to spill into right so they're trying to come to this area and help kind of with this immune this hyper sensitivity reaction however some of them starts to get into right some of them starts to move into these cells and some of these white blood cells will start to kind of Clump up here and then they get stuck in the tubule and as they get stuck into this tubu what happens is as they kind of conform

to the shape of the tubu they'll make these weird casts and you'll get a lot of these and these are called white blood cell cast so you can see a lot of what's called white blood cell cast but here's the big thing the white blood cells that we see the most of is eosinophils so if more than like 1% of the actual white blood cells that are present in the UR or eosinophils we suspect that this could be acute interstitial nefritis however when we talk about the utility of this test it is very very low

sensitivity and specificity and often times you depend upon the Triad and the exposure and this times we'll get better okay the next one is glarin nefritis so in patients who have underlying glarin nefritis they have inflammation of the glomerulus and there's a lot of different reasons why but often times this can come down to what's called Anka vasculitis is a really really big one and another one is it could be due to what's called anti- uh GBM disease which we see with what's called good pasture syndrome but the other ones is it could be due

to other potential factors like infectious glar netis or immune complexes the big one I like to remember here is what's called lupus nefritis now all of these can cause really profound glar nefritis with an AK I the big thing here is that with ankov vasculitis and anti-gbm disease we often times with these see the combination of some type of like pulmonary renal syndrome and again pulmonary renal syndrome what do I mean in other words these patients will have renal involvement via glarin nefritis with heavy hemu and protein UA as well lung involvement via hemoptisis so

that's a really really big thing to remember now with this one what really helps to tell us about glarin nefritis is that whenever they have injury to their actual Glarus and their basement membrane what starts to really really heavily leak out here is something that can be very diagnostically useful one is red blood cells and these red blood cells can get stuck and clogged up with inside of this tub Lumin but the other one is proteins and so you can also lose a lot of proteins into the urine as well and so that's what really

kind of adds the diagnostic utility here is if a patient has um what we referred to as having this classic Triad so let's say the glamar nrtis Triad this would be having protein UA hematuria and an acute kidney injury so if I have a patient who has heavy amounts of protein in their urine let's say at least at least minimum of greater than two gr but you know as you get into the nephrotic range you can even see sometimes up to greater than 3.5 gr so if I see Heavy protein UA I also see lots

of red blood cell cast and this is the huge term that you can see on the actual urine microscopy lots of red blood cell cast and then the presence of an acute kidney injury I would definitely be potentially thinking about glarin aritis and I would even be concerned more specifically about a rapidly Progressive glome aritis which we can see often times most often with an ankle vasculitis and an anti-gbm disease these are the big ones all right the last one I don't want to talk too much about because it's not that common but I do

want to just quickly discuss it in the sense that sometimes you can get a bunch of clots so thrombotic meaning you get a bunch of clots and these can really Gunk up your glomerulus we see this in a couple different diseases I can see this in sometimes what's called uh what's called diic um you can also see this in what's called hus and you can also see this in TTP now with these they can Gunk up the Glarus and when you Gunk up the Glarus you do as a result reduce the blood flow across the

Glarus into the bloodstream I mean into the actual across the Glarus into the tubular system so we can see that as being a potential problem here but here's the thing as blood is flowing through these actual clotted areas what we notice is as as the blood leaves this area of clots we notice that the patient consumes a lot of their plat and their red blood cells in the clot and so we start to see this classic TMA Triad if you will and this TMA Triad is oftentimes remembered on the concept of a patient having hemolytic

anemia thrombocytopenia and an Aki so if a patient has an acute kidney injury they have a decreased number of red blood cells in a homolysis form and a decreased number of platelets this is often times something that you should think about as a patient having thrombotic microangiopathy all right but again this is going to cover the intrarenal Aki let's now talk about the last one postrenal Aki all right my friends so we're going to move on to post renal Aki you're probably like looking at me like Zack wait a second you changed clothes yes I

did we just got a shipment of some shirts check this out tell me this isn't sick like this little like a little bodybuilding style even though I don't have the body to allow for that support but anyway we'll move on past that topic we're going to talk about postre Aki so with postrenal Aki I told you that there's urinary tract obstruction it's either proximately it's that's the big thing to do here in the sense that when we talk about an obstruction I like to think proximal as though it's involving the renal pelvis and the urer

it's anything really before the bladder right so for example what would be a potential etog here the biggest one that I would want you guys to remember is if you have a stone stuck somewhere within the UR or within the renal pelvis what do we call this nephrolithiasis so if a patient has nephrolithiasis this would be a very common cause if we have a proximal obstruction now here's here's the thing in order for us to truly have nephrolithiasis cause aute kidney injury it really has to be bilateral so you really have to have a bilateral

nephrolithiasis to truly cause a q kidney injury there's one exception what is that one exception if you only have one kidney so if you only have one kidney it's kind of like you have bilateral nephrolithiasis in that kind of same example if you will so there's one exception and that one exception tends to be if you have a solitary kidney okay so Bilal nephrolithiasis would be the big one there could be other potential ethiology if I have some type of cancer for example if I have something that's kind of pressing on the outside of the

urer for example if there's like some type of mass that could also be a potential ethology so you could be thinking about some type of cancer for example if I have ovarian cancer that could be a big one if I have some type of like intraabdominal mass of sorts from like rectal cancer that could be compressing onto this those are things but I would say more likely than not it's bilateral nephrolithiasis and the only exception is that is if you have a salitary kidney now here's the big thing if I have let's say an obstruction

here let's say an obstruction right here within the uror if I have an obstruction here what's going to happen is you're going to start seeing back flow right so urine's not going to be able to flow in the direction that you want it's going to back flow when it does back flow it distends these ers right so now this urer is going to be super distended and on top of that I'm going to start seeing this interesting feature here where the fluid will back up into the kidney and then the kidneys will start to become

distended so I'll see this back flow of urine causing the URS to get bigger and then I'll also see the kidneys starting to get kind of fluid logged and that's called hydrosis so again big thing to remember is if you have these Stones here or something compressing the outside of the urer that fluid will back up into the UR cause them to get expanded and then back up into the renal pelvis and cause parts of the pelvis and kses and things like that to also start expanding and getting a little fluid logged and this is

referred to as hydrosis so if a patient has the presence of hydrosis and the presence of a hydro uror I would be on the lookout for an obstruction but here's where I want to kind of take the next step to help Define this hydro nephrosis and hydro urer is not specific for proximal or distal obstruction what is a little bit more specific is if you can find the presence of the actual cause like a stone or a mass but the other thing is if I take the ultrasound I look over the kidneys I see hydrosis

maybe I see some Hydra uror and then I come down to the bladder and when I look at the bladder it looks normal right so it's not super enlarge so so I do not have there's no let's say enlargement of the bladder so there's no enlarged bladder that means that the problem isn't necessarily arising at the bladder or the bladder Outlet it's something proximal to that that's what would help me think about a proximal obstruction as compared to a distal obstruction at this scenario there's something wrong with the muscles maybe the det trusser muscle is

not Contracting very well and in this particular situation if it's not Contracting it's not able to generate a good enough force of contraction to allow for urine to flow through the bladder outlet and out into the urethra so this is the part that's actually being inhibited this could be du the bladder muscles not Contracting or there being a dis Synergy between the bladder muscle and the internal ureth sphincter so sometimes we call this neurogenic bladder so neurogenic bladder is when there is difficulty for the bladder to contract or it is overly Contracting but the internal

urethal syncor is like super super tight in that potential situation I would think about this if a patient has some type of like spinal cord disease so especially a spinal cord disease of sorts I would also think about this in some type of recent stroke or Parkinson's so definitely having a CVA Parkinson's disease would also be kind of a big one as well now the other one that I really want you to think about is medications anticholinergics can definitely do this as well so anti- cholinergics so there's a lot of different medications that can basically

suppress the bladder from being able to contract and then it doesn't actually allow for the urine to outflow the other one is if a bladder Outlet is obstructing the flow this is most often due to a disease called BPH so the prostate is significantly large sometimes prostate cancer can also do this but I'd say BPH is the most common reason so either way if you have some type of problem here or the bladder isn't Contracting or the prostate is obstructing the outflow of urine either way in both of these scenarios the urine's going to back

up and what it's going to do is is it's going to start compressing on the bladder and it's going to distend the bladder it's also going to back up into the urer and it's going to distend the URS and then it's going to back up into the kidney and it's going to cause distension of the kidney and so what would you notice is potentially a difference between the proximal obstruction and the distal obstruction I may notice that they have hydron nephrosis oh well the proximal had that as well all right maybe I pick up Hydro

uror but here's the big kicker I notice a enlarged distended bladder and even better sometimes if we take a and have the patient try to void or we catheterize them sometimes we either see significant Improvement in their Aki if we catheterize them or if we have them pee and then we check their bladder afterwards they looked at What's called the postvoid residual and it's really really high that also would support this problem so the presence of an enlarged bladder oh son of a gun or an elevated postvoid residual Hydro urer and hydron nephrosis would be

more suggestive of a distal obstruction that's how I would want you guys to think about postrenal Aki okay we've talked about all the different types of Aki the biggest thing is now if a patient has the initial injury and they start to have aligera creatinine starts to rise urine output starts to drop what are the complications let's talk about that all right my friends so we're going to talk about the complications of an Aki so when a patient develops a severe Q kidney injury again they're in that oliguric phase maybe they're not making as much

urine as they stop making as much urine they start to experience very potential complic that could be detrimental to the patient it's really important that you recognize these I would say with the most significant importance being on hyperemia hyperemia and uremia but metabolic acidosis is not something that you should forget so let's talk a little bit about this so the metabolic acidosis again what we see is that these patient is having some type of acute kidney injury they're having an acute drop off in their GFR as you have a drop off in the GFR what

is the big thing you're having less things that are being filtered across the Glarus and into the tubules now the problem here is is that you're supposed to allow for you know our acidbase balance one of the things that you're supposed to be able to secrete what protons into the actual tubular system the other thing is that you're supposed to be able to reabsorb bicarbonate into the bloodstream but in this particular situation when you have some type of metabolic acidosis which you can see I'd say a lot of the times these complications are most prevalent

in intr renal Aki but you can see them in the pre- renals when there is this process here and you have less reabsorption of bicarbonate what you'll see is is you'll see that they'll have a retention of protons and they'll have this decrease in the bicarbonate and as this starts to happen you'll notice that as these patients start to rise their protons and drop their bicarbonate their pH will start to go on the down low right this is when we start to experience acidosis the other thing is is if you're not filtering off specific things

the other thing is that you have the inability to secrete not just protons but also you have an inability to secrete other organic acids and so things like sulfates um and phosphates but particularly their acids can also give off protons and so you can have a lot of these that start to accumulate with inside of the bloodstream what we start to see is that these patients start to develop an increase in their anine Gap and so often times this metabolic acidosis is what we refer to as a anion gap metabolic acidosis and with that being

said their an Gap has to be greater than 12 and we see this in the scenario of severe ureia such as an inst stage renal disease or severe acute kidney injury so that's a really important thing to remember now patients that have this this could just be lab finding you may find that if you're measuring their they um getting an ABG or vbg or you're getting a BMP and you're seeing that their bicarb is consistently continue to drop you'll see that they'll have this acidosis but other ways that that acidosis can present is that when

patients have an acidosis it stimulates you know there's these uh little receptors right you have these little receptors here let's say they're right here these are called your chemo receptors your chemo receptors respond to high levels of protons or are drop in the pH and then what they do is they send that to the your actual central nervous system where the medulla is that will then send down firing to your actual respiratory Center and then out via nerves that go to your frenic nerve and your intercostal nerve so what will happen is this high amounts

of protons will stimulate these nerves stimulate these nerves and then increase the contraction of those respiratory muscles guess what will happen you'll start to increase your rate and depth so if you increase your respiratory rate and in depth you'll start to see these patients develop something called tpia and this is a very common compensatory response to the metabolic acidosis so that's a really really big thing to remember okay the other thing that's really important to remember is that when patients have metabolic acidosis it also can exacerbate hyperemia so if you have acute kidney injury that's

also reducing your ability to secrete potassium but on top of that you have an acidosis you know in acidosis it's a very interesting process so you have lots of protons present here in the actual bloodstream and you have potassium mines that are primarily in the cell what happens is when you have potassium moving out protons will move in to maintain Electro neutrality so if I have lots of protons this will cause this pump to become a little bit more active and I'll pump lots of protons in but I'll also pump lots of pottassium ions out

and this will Pres as hyperkalemia and as we'll talk a little bit later when we get to the hyperemia section this can lead to very specific ECG changes that you want to be aware of all right and we'll talk about that the last thing that I want you to be aware of is that in patients who have severe acidosis what it's been shown to do is it may have an effect on our our conduction system and it may have an effect just on General contracti myocardial cells and so we may see that these patients have

what's called lots of vasod dilation and they may have also a reduction in their cardiac output so if the heart is having a difficult time being able to contract and get blood out that's their reduction in cardiac output and if their vessels are becoming super dilated that's the vasodilatory effect this increases your systemic vascular resistance I'm sorry decreases your systemic vascular resistance that's the amount of resistance to blood flow that you have and if that happens what that does is the combination of a reduced uh svr and a reduced cardiac output leads to a reduction

in your blood pressure you can remember this all based upon the formula that blood pressure is equal to cardiac output times spr acidosis can do both of these things it may stimulate a reduction in contractility and it may stimulate vasod dilation of your vessels and so it can worsen hypotension and another little thing that I like to add on in patients with ICU as acidosis gets worse it reduces the response to medications that we use to push patients blood pressure up known as vas oppressors okay cool let's move to the next thing which is hyperkalemia

hyperkalemia we see this in a bunch of different patients but again I'd say the big thing for this is that we see this in patients with severe Aki the reason behind this is that as a patient has hyperemia their GFR reduces and as their GFR reduces again we already know this that they're going to have less filtration as I have less filtration I don't secrete out as much potassium and so blood is going to run through here which is going to be rich in potassium and there's going to be less filtration of that potassium so

there'll be less potassium that's present in the urine and more potassium will stay within the bloodstream and so what you'll start to experience with these patient is that they'll have less potassium in the urine and more potassium that actually is going to rise up in their bloodstream because I'm not able to filter it because of the reduction in GFR why is potassium being so high a bad thing as potassium starts to rise at least greater than six M equivalent per liter we start to see cardiac events this may may potentially suppress the AV node and

these patients can have what's called an AV block so I would be worried and I would be on the lookout for some type of like AV block which is a heart block but the other thing it can do is it can precipitate very interesting and high Feld ECG changes that we need to be able to recognize and recognize quickly because sometimes this is the only thing that hyperemia may give us before we get that lab value back one is you want to look for Peak t- waves all right that's these very very large t-waves very

very large pointy t-waves after that you want to go backwards I like to remember go one up two backwards I'm going to elongate I'm going to elongate my PR interval and so I start seeing the PR interval get a little bit longer and that's how we get the AV blocks right that's how we get those AV blocks so the P interval will start getting longer so I go up left down the p-wave starts to disappear that's again how we get the blocks interesting right so then absent p waves or loss of p waves this is

when we start seeing patients develop things like second degree moits 2 and third degree blocks the last one is I Go Again up left down right I'm going to widen my QRS interval and as a patient starts widening their QRS interval to greater than 120 milliseconds so you see a increase in their QRS interval this is when you start to see some downfalls what do I mean this is when I start seeing the patients start to go into what's called a sine wave pattern and these sine wave patterns can quickly break down and cause a

patient to develop asy or ventricular fibrillation so hyperemia is at very high risk for cardiac arrest very important to recognize that okay so you may see the high potassium or you may see the ECG changes be aware of that in the clinical vignette all right next one's hyperemia same concept it's not too hard to imagine as blood is flowing blowing through here as a patient gets severe acute kidney injury and they drop off their GFR guess what one of the biggest things that is getting filtered across the actual glal filtration membrane it's water and sodium

and so what happens is is if I'm not filtering off the water the water will actually start staying in the bloodstream and eventually the water levels will go up and up and up and so I will maintain I'll increase my amount of water and I may even increase a little bit of my sodium retention but primarily water and sodium retention what that's going to do is is that's going to pump up the patient's blood volume when you pump up the blood volume there's a lot of different things that we can see with regards to complications

all right one is we can see that the blood volume if it's really high what happens is you start seeing fluid that starts exuding and leaking out of the pulmonary capillaries into the actual alveoli for example let's say oop sorry guys let's say some of that fluid starts leaking out here what is this called pulmonary edema and then maybe even some of the fluid starts leaking out here into the plural cavity What's this called plural affusions and so that's a big thing to be able to remember for these patients that that they are very high

risk for things like pulmonary edema and also what's called plural effusion iions why is this important to realize well one thing is that with these patients they may have these findings on chest x-ray but the other thing is is that if you have some type of fluid that's logging up the alveoli or in the plural cavity it's compressing the alveoli what's going to happen to your ventilation you're going to have an impairment in ventilation and so these patients often times can have hypoxia so they may present in a bunch of different ways one of the

things i' would be looking out for is is the patient exhibiting some type of reduction in their O2 so in other words are they having hypoxia I would also be looking for any features of disia right are they having any shortness of breath and then sometimes they can even present with proxis or nternal disia or ethopia but look for shortness of breath look for any evidence of hypoxia or crackles rails and oscilation or a chest x-ray that confirms this this is the big one this is the that can cause a lot of problems the second

one is if fluid kind of like clogs up within the extremities so if fluid starts kind of logging up in the legs and into the interstitial spaces this can start causing things like pedal adeema pedal adeema or peripheral edema is also important because this can kind of present with that pitting sign and so you want to look for evidence of pitting that could be present so look for any kind of evidence of pittings what does that mean meaning that if I press down on these patients legs of Edema it'll leave in the indentation for a

couple seconds swelling of the legs shortness of breath maybe even hypoxia evidence of crackles rails on oscilation and maybe on x-ray we see some evidence of pulmonary Demar fusions the last thing is when a patient has an increase in their blood volume they're filling their ventricles more right so you should get an increase in the Venus return theoretically if I increase my Venus return right I theoretically have a larger indolic volume and I have more blood that I can pump out of the heart into the systemic circulation and that should theoretically do what increase my

blood pressure right and so sometimes these patients can have very high blood pressure whenever they're super hyperic again the concept behind this is that you're increasing their IND diastolic volume which then increases their stroke volume or their cardiac output and then that is what leads to their very very increased blood pressure so again whenever you fill their tank up you can increase their indolic volume increase their stroke volume cardiac output and that is the mechanism in itself that is causing the patient to have high blood pressure all right so look for that the other thing

I actually like to also consider is that when a patient is having lots and lots of water as compared to them having sodium and they really up their blood volume sometimes patients can develop what's called hyperic hyponatremia so that's one other thing that I'd like to add into the mix as well all right that covers hyperemia again please don't recognize this because this kind of complication here can be very detrimental as well as the hypertension last one is the scary one ureia now when I say a patient gets complications of uremia this is a couple

different things here so again when a patient has a drop in their GFR they lose the ability to filter waste products one of those waste products tends to be Ura so as their GFR starts to FL fall off they start to retain and retain and retain and retain more of that blood Ura nitrogen when that beIN starts to go up this is when we start seeing potentially complications now this term in itself is called azotemia where there's an increase in The Bu but when The Bu is high enough that it's causing complications that is then

referred to as ureia so what are some of the potential complications one is so this may have an effect on our central nervous system and it may do this it may cause swelling of the brain but one of the big things here is that it actually can cause an altered mental status one of the biggest things is it can cause confusion or it may even cause things like lethargy all right so severe tiredness that's one really big one the other one is I look for what's called negative myoclonus or a big heavy term here uh

we call this asterixis and asterixis is kind of a flapping trimor if you will for example take a look at this image here as you can see what asterixis indicates so you see how that there's that flapping triem and the hands are completely extended that's a very very important sign now this isn't always only seen in ureic enop this can be seen in other forms of encylopaedia nausea and vomiting so I would watch out for nausea vomiting altering levels of consciousness and flapping Tremors the other thing here is it loves the paric cardium and it

can really really tick off the pericardium and when it ticks off the pericardium it can cause inflammation of the pericardium what is this called when you cause inflammation of the pericardium this is called pericarditis and so pericarditis is another pretty common uh complication that we can see in patients who have this underlying uremia so with pericarditis you can see a couple different things one is chest pain two friction rub three is they may have a par paracardial affusion and then four is you can see ECG changes so again what would it be the biggest one

is the classic chest pain the kind of pain that is really really bad and sometimes when you have the patient lean forward it kind of feels a little bit better it also radiates to the trapezius is that other common term you have a friction rub so when you listen to their heart on oscilation you may hear that friction rub that's potentially present the third thing is that they may have a affusion that's present on an echo and so if they have an infusion that's present on an echo that could also suggest this especially in the

context of you having a very high bu and an acute kidney injury and lastly they may have ECG changes and the classic ECG changes is that they have diffuse St elevation and PR segment depression so look for these cuz it kind of represents or mimics a stemi but look for that diffuse St elevation the concave appearance as well as PR segment depression the last thing here is that it also can cause platelet dysfunction so this one's really interesting so platelet dysfunction we see this because what happens is when your Ria is really really elevated you

know what's these playlists are supposed to do let's say here you have an area of injury right so here's an area of injury within the blood vessel normally platelets should come and they should block up that hole right and they should form what's called a platelet plug right because they're trying to plug this up to induce hemostasis this is normal this is what you want but when a patient has uremia what it does to the platelets you know the platelets they're supposed to um secrete chemicals like ADP thromboxane A2 uh serotonin all of these things

that they release and also um they also Express other things that help them to stick right they're supposed to secrete these and they're also supposed to express things like fibrinogen and Von wild Bron Factor all that stuff like that when you have a patient with ureia they block all these granules from being able to degranulate and so now the pletes can't communicate with one another they're dysfunctional in that sense and so if you have an injured blood vessel like this guess what these platelets will not stick to the area they're going to cruise right on

by because of that this puts the patient at high risk of bleeding right and so plel dysfunction can look a lot of different ways one is it could present with bleeding and this bleeding it's not usually like full-fledged like oh my gosh they're dying no it's sometimes it's like nose bleed so EP staxis maybe some gingival bleeding uh they may have vaginal bleeding they may have gi bleeding so it can vary um the other thing is that they could if the bleeding is severe they could potentially present with um anemia as well so these are

the things to definitely be considerate of if a patient comes to you and they have a very very elevated bu along with features of incopy pericarditis or features of platelet dysfunction this is enough for me me to dialyze a patient all right so be aware of that my friends we've talked about the complications guess what time to move on to how do we really put all this together and diagnose the type of Aki or the cause of the Aki in this patient how do we really diagnose Aki first off diagnosing the Aki and then figuring

out the cause of the Aki so first look for the creatinine so if they present in the vignette that a patient has a maybe a prior creatinine and now it's greater than 0.3 from that two days ago or it's an oliguria per se so they're not producing as much urine and they give you a true volume maybe something like this based on their body weight or another rule of thumb is less than 400 milliliters within a 24-hour period if you see these you should start thinking okay this is an acute kidney injury then what I

need to think about is okay is it post-renal intrarenal or pre-renal the reason why I want you to start thinking about this is because postrenal is oftentimes the easiest one to diagnose right it's cuz I want to get a renal bladder ultrasound if I do that I'd be able to see what do I see hydrosis oh I can see that in proximal and distal obstructions do I see Hydro urer I can see that I'm proximal in distal obstructions and do I see an enlarged bat bladder that would be more in distal obstructions and then look

at their history right so I'm thinking it's a postrenal AK if I see any of these findings here you can see look at this look at the the kses they're huge and look at the thickness now this is a water log kidney so then I have to start thinking about okay what's their present ation and then again add on to this do they have a normal or empty bladder it's probably a proximal obstruction also do they have flank pain do they have hematuria do they have any kind of nause and vomiting this would be a

very common scenario for you know bilateral nephrolithiasis another one is that their is their platter huge so and one of the things that we can do is we can do what's called a postvoid residual we tell the patient to pee and then what we do is we look at their bladder before they pee and then we look at their B bladder after they and if their postvoid residual is greater than 200 mls and their bladder looks like this like a golf like a huge melon then this is definitely a suggestive more of a distal obstruction

another thing that we can do is we can just insert a Foley and if their urine output improves significantly with Foley catheterization it's usually suggestive of a distal obstruction but again history is Paramount here listen to them do they have flank pain hematuria do they have nausea vomiting and maybe if you look further and you say oh there's a stone there that would suggest bilateral nephrolithiasis if they have BPH if they have some type of concern for a neurogenic bladder and they improve with a fly catheter it's likely a distal obstruction and then done that's

the diagnosis you've moved forward with no evidence of obstruction now you're at the intrarenal and pre-renal this is a little bit more challenging now I will say pre-renal accounts for 60 to 70% of the cases so often more than not it's prerenal but it's still important that you evaluate these patients for the exam we love to say get a urine sodium a urine creatin in the the reason why is is if you look at this plus their serum creatinine so you get a renal function panel plus a uran osmolality this will give you the phena

and this will give you what their ADH levels are kind of looking like all right and how well the kidneys are responding to ADH so let me give you a kind of a concept here we now think okay I get this let's say that the fena which is the fractional excretion of sodium is low it's less than 1% that means that the kidneys are reabsorbing pretty much all the sodium they can this means that they are trying to improve their effective arterial blood volume the best that they can and the kidney tubules aren't injured this

tells me it's prerenal the other thing is if the urine osmolality is affected as well that could be a reason but let me explain the fena we know that a patient has low renal profusion and pre reenal Aki they activate the renin system Angiotensin one forms angiotensin two forms Heen increases the production of aldosterone from the adrenal gland and aldosterone goes to the distal tubal and increases sodium reabsorption right there boom there's increasing sodium it also does what Angiotensin 2 acts on the proximal tubules increases sodium reabsorption all right less sodium is going to be

in the urine and then on top of that if I have less sodium in the urine that means that I'm going to have a lower phena because fena is looking at the urine sodium and the serum sodium as well as the urine creatinine and the serum creatinine and so if my amount of sodium that's present in the urine is lower my fena is lower now another concept here is that ad ad is also hyper produced here and what happens is when ADH is highly produced it goes to this collecting duct and increases water reabsorption if

I increase water reabsorption what's going to happen I'm going to have less water in the urine if I have less water in the urine what happens to my urine osmolality it goes up and the concept behind this is that my urine is more concentrated because I'm trying to pull as much fluid as I can into the circulation so that's the concept here and if the urine osal is greater than 500 that's what we consider to be elevated this tells me that the tubules are responding and that the body is trying to hold on to sodium

and water to improve their effective arterial blood volume that's likely pre-ural Aki however this is not perfect in a perfect in in a clinical world this is not perfect often times what I found as a clinician is that when the fenina is less than one it could be any Aki all right it's it's not perfect another thing to consider that we like on the boards is the buing creatinine ratio ADH also not only reabsorbs water it also reabsorbs Ura and if we reabsorb a lot of Ura what happens to the amount of Ura that presents

in the urine it's lower so what happens to the Ura in the bloodstream it goes up and the amount of Ura that we have to creatinine becomes higher with that ratio greater than 20 to1 and so that's another way that we look at this intrarenal Aki is very interesting and these patients often times their fena greater than 2% that means that they are not reabsorbing the sodium now let's explain why in this particular situation maybe the patient has a reduction of GFR because there's nefron injury all right what happens usually that increases random production Angiotensin

one Angiotensin 2 supposed to cause aldosterone to be high but again these cells are damaged even if aldosteron is present are you going to be able to reabsorb sodium no so sodium doesn't get reabsorbed here all right if Ang ton two is present and it goes to the proximal tubular cell to reabsorb sodium but the tubular cells are damaged are you going to reabsorb sodium no so then what happens to the sodium in the urine it goes up what happens to the vena it goes up that's the concept when we really only see this in

ATM because this is the one that causes direct tubular cell injury this is the one that causes primarily tubular cell injury plus it's about 85% of the cases for intrarenal Aki all right let's do the water part we also know that you're supposed to make ADH and ADH should go here and work on this collecting but if the cells are damaged can it respond no so you can reabsorb the water no so what's going to happen to that water it's going to go in the urine what's going to happen to the UR osmolality it's going

to be lower less than 350 and that's the Conant so if you do see a patient with a feni greater than 2% and a low urine osmolality for the most part it is ATN that's a consistency that we've seen as clinicians and the last thing is that you know again ADH does help to reabsorb Ura but if this is damaged is it going to be able to do that no so Ura goes up in the urine and usually The Bu and kening are should tends to be lower right right maybe like less than 20 to1

so like 15 to1 and so this is the concept but what I really want you to think about here even easier than this is that you can have Angiotensin 2 and ADH and aldosterone be elevated but it doesn't matter because the damaged tubules are unable to respond to these hormones anyway so even if they were elevated you wouldn't be able to reab absorb that sodium in water regardless so that's the concept of why sodium and water gets dumped into the urine is that they're just not capable of reabsorbing them all right so this is a

really nice way of being able to think about this in a vignette what I find though as a clinician that's a little bit easier to differentiate between these two is what's called a feride stress test so what you do is you give the patient who has aligera a very large dose of feride maybe one gram per kilogram when you do that you look at their urine output and if they're able to make more than 202 hours it tells me it's likely a pre Ral if they can't it tells me that their kidneys are just not

able to respond to the drug and that they are not working the tubular system is off and that usually suggests an intrarenal Aki but this is something I like to think about in the clinical world just to add that to you guys' uh you know repertoire either way let's go back when we look at these patients what I found that is very very very helpful especially within the intrarenal Aki Camp as a your analysis with the pre-renal camp it's just a really good history so let's let's kind of dig into that let's say that we

get a good history of physical exam when we look at their volume status if I see a patient who's like very very hypotensive they're critically ill I'm thinking about shock start thinking about septic shock cardiogenic shock hypmic shock if I see a patient who's like hyperemic per se maybe um I'm sorry hypovolemic per se so in other words they have decreased uh you know skin turg dry mucous membranes maybe they have a history of diarrhea iresis vomiting uh a lot of dehydration then I'm thinking about hypovolemia if a patient has you know maybe for example

hyperemia they have peripheral edema pulmonary edema on top of that maybe they have some aites maybe they have some jugular Venus distension some hypertension but on top of that they have history of CHF I can think about cardiorenal syndrome if they have curosis I can think about hepatorenal syndrome so that's something to think about in that camp and then last if the patient really doesn't appear like they're hypovolemic they don't appear hypervolemic they appear kind of UIC but they're on specific medications maybe ineds tacro arbs ACE inhibitors that's when I'm going to start thinking about

medication related so renal Vaso constrictive mechanisms all right now that's the best way I think to to approach pre-renal with ininal there's actually a lot of utility heavy heavy utility to a UR analysis with microscopy and then a hmp you can never go wrong so what I want you to look for here is let's say that a patient has prolonged low blood pressure so they've had hypotension they've been exposed to aminoglycosides vanoy and contrast ey they have rabdo homolysis they have tumor liis syndrome or they have multiple Myoma in combination they have muddy Brown cast

that's ATN especially with this finding here you got this it's ATN especially with this as well if a patient has recent medications plus fever rash and elevated Ur urani oils think about Ain all right so recent medications fever rash urine oils Ain if the patient has let's say a pulmonary renal syndrome they have hemoptisis and hematuria on top of that with that hematuria they have things like red blood cell cast lots of protein UA you think about glomulin nefritis think about things like ankov vasculitis think about things like your anti-gbm disease or good pasture syndrome

and then maybe like your immune complex disease like lupus nefritis all right my friends we went through a lot of the aspects here with really figuring out how to diagnose Aki it really comes down to a renal bladder ultrasound is it postrenal or not if it is not then what do you do then you say get the urine sodium urine creatinine figure out your fena if the fena is low Ur osmolality is high maybe it's prerenal look at your history look at your volume status if the fena is high uros mity is low it's probably

intrarenal ATN most likely get your Ur analysis in your history to figure out which one of those intrarenal Aki really fits all right we're talking about complications now really with acute kidney injury the reason why I focused on complications because you have to figure out how to treat these if they come up if a patient has an Aki one of the big things that you have to be thinking about is do they have metabolic acidosis the reason why is metabolic acidosis is really really important especially if the pH is less than 7.2 you should put

these patients on sodium bicarbonate to address that in Aki one of the things I like to think about in patients who have hyperemia is Loop Diuretics Loop diuretics are great drugs especially because these patients often time tend to be hyperemic to a degree with Loop Diuretics what happens is they're blocking the sodium potassium 2 chloride Cod Transporters in the ascending limb if they block that then what happens so sodium is delivered in higher amounts to the distal tubule sodium rushes in potassium rushes out and goes into the urine and you dump a lot of potassium

into the urine this is great in patients who are hyperemic as well as volume overloaded all right and they are able to produce urine the other scenario that you could consider in patients who are a little bit more like not as hyperic they're more UIC or hypovolemic is a potassium binding resin this could basically release these catons that it's bound to which then opens up a an opportunity for potassium to bind to that resin and get pooped out this is great in patients who have hyperemia that's more mild and they're not a nuic I I'm

sorry they are aeric they're not capable of producing a lot of urine so therefore Loop Diuretics won't give that much of a benefit instead use this to get it out through the stool the next thing is Loop diuretics are also beneficial in hyperia plus hyperemia and the concept behind it here is that they're blocking what they're blocking the sodium potassium two chloric transmitter you don't get as much sodium here in the the med the medulla you don't pull as much water out of the descending limb the countercurrent multiply mechanism right more water and more sodium

is delivered down here and so you're going to lose a lot of sodium and pottassium and water in the urine and that's why this is good at getting rid of Volume Plus getting rid of potassium that's why this is a great drug for that both combo scenario be careful when you have these patients who have Loop Diuretics that are using it monitor that potassium level check the ECG as well you don't want to you know Miss a patient who's getting a little bit too hypokalemic and you you're missing that all right the other thing is

that these patients if you're considering this you know patients who have you know metabolic acid do that you're treating with sodium bicarbon it's not getting better patients who have hyperkalemia that you're treating with Loop Diuretics and it's not getting better or they're having like really bad ECG changes and you're having to give them calcium insulin albuterol patients with hyperemia they're not responding to Loop Diuretics anymore you should start thinking about hemodialysis right usually we can do this with a fistula but that's more for chronic kidney disease you're going to need to take some time to

for this to form usually like two months so that's not going to be your first go this one can be a little bit faster but it has a high risk of like thrombosis or you know graph failure so this is not something that we use for acute scenarios Covena catheter is the choice um that we would utilize in acute kidney injuries that we need to begin hemodialysis unless the patient already had this present and so this is a catheter that will place usually at the bedside could be tunneled could be non-tunneled but it's going to

be for Urgent or emergent use uh for dialysis so this would be the choice if they were presented with that now we do this if they're not responding to therapy for metabolic acidosis their potassium their volume or if they have ureic complications which includes encylopedic presson but if they're having really bad uremia we just start them on dialysis all right all right now this is how I really want you to think about treating the complications what I then want to move on to is kind of really putting this in a kind a nice map thinking

about it systematically if they have a pH less than 7.2 sodium bicarb if they have hyperemia you can do a loop diuretic or potassium binding resin calcium insulin albuterol only if they have ECG changes hyperemia Loop Diuretics they're refractory or they develop uremia you dialy them the type of dialysis did you do is going to be putting in a central Venus catheter usually the IJ the type of dialysis that we use depends upon their blood pressure and if they have any cerebral edema if they do you do what's called crrt it's a continuous venovenous hemofiltration

it's used for more critically ill patient if their blood pressure is fine and they have no cerebral edema intermittent hemodialysis would be the best way to go all right so that's important now what I want you to do is think about how do we treat the underlying cause so in patients who have hypovolemia you give them fluids maybe lactat ringers normal saline improve their blood volume improve their circulation and then by doing that if you fill up their tank you're going to profuse their kidneys a little bit better and they're going to like you for

that and they're going to made more urine if the patient has some type of cardiorenal syndrome this is where Loop diuretics are great and afterload reduction is great make sense of this if I give a patient Loop Diuretics what is it going to do well it's going to reduce their volume overload that's going to reduce their central venous pressure that backf flow of blood if you do that that's going to reduce their Venus congestion and that's going to improve their renal profusion another thing is we can give afterload reduction sometimes we can do inotropes or

we can do drugs that have just afterload reduced hydrazine amlodipine inotropes like dexin dobutamine milron this is going to pump more blood out as well as reduce afterload which is going to to improve cardiac output if I increase contractility with inotropes or if I reduce afterload by reducing the systemic vascular resistance both of these things are going to do what to my cardiac output increase it and that's going to increase renal profusion so you're adjusting the Venus congestion and you're adjusting the cardiac output and that's the way that we teach this right so that's why

it's important to understand the path of Fizz because then it makes sense of the treatment hpat renal syndrome makes sense of it What was the primary thing that they were not making enough of albumin and if I don't have enough albumin what if I gave them albumin I'm going to pump it up if I give more abum what's going to happen to my ionic pressure it's going to go up am I going to hold on to water yeah what's going to happen to my circulation I'm going to fill it if I fill it will I

peruse the kidneys you beta all right what was the other problem the other problem was portal hypertension so they're releasing those systemic vasod dilators that was causing splank vasod dation what if I give them something to constrict that circulation like octreotide now it's going to squeeze on these vessels and now it's not going to divert as much blood away from the kidneys you're going to get more blood going to the kidneys well that's cool that's going to improve improve my renal profusion you know another thing those systemic vasod dilators they cause in general they cause

the patient to have a lot of vasodilation systemically so there most patients who have therosis have vasodilatory effects if I give them madrine I'm going to squeeze all of their systemic vessels if I squeeze all of their systemic vessels what's going to happen to the mean arterial pressure it's going to go up what's going to happen to the renal profusion it's going to go up so I'm I'm basically trying to Target uh kind of opposing the sympathetic nervous system remember how the sympathetic nervous system whenever it was causing renal Vaso constriction and stuff it was

taking blood away from the kidneys octreotide is going to be kind of preventing blood from being taken away from the kidneys so I'm going to get blood to go to the kidneys and I'm going to pump up the blood pressure and squeeze the systemic vessels to put P blood to the kidneys so I'm replacing what I'm losing fixing the splank vasod dilation and then pumping up the blood pressure and this is usually outpatient inpatient we use other Vaso pressors like norepinephrine turly pressing in Europe is another one that they use all right all right what

about a patient who has just Frank shock and shock we need to treat that usually we'll give them vase oppressors to squeeze their blood vessels and if we squeeze it the resistance goes up and their map goes up and so does the Ral profusion all right and we're going to get more blood flow to that kidney this is the concept that I want you to think about so if they say hypovolemia give them volume cardiorenal decongest them improve their cardiac output hepatorenal give them back albumin stop the splank vasor dilation and pump up their blood

pressure shock improve their blood pressure with vasil pressors that's it if you have bilateral renal artery stenosis open up that renal artery if it's a medication and this is always good and a patient has an acute kidney injury take these off of their medical you know uh like take them off of like their their medication list stop their ACE inhibitor stop their arbs for a bit until they improve get rid of the nids the tacro is the one thing you got to be careful if they have a transplant you might just have to reduce this

and just keep a close eye on the levels all right all right my friends let's now move on to how do we really approach this systematically do you think that the patient has CRS or HRS do they have heart failure decompensated curosis and their hyperemic if it's yes okay okay then I'm going to go ahead and avoid IV fluids don't give this patient fluids you'll worsen their hypervolemia all right if you suspect CRS it's the inotropes plus or minus the after reduction plus the diuretics to decongest them and improve cardiac output if you suspect HRS

you give malbin otide and madrin if they do not appear hyperemic all right or in this particular scenario they appear hypo or uvalic then you have to say okay give them some fluids if I give these patients fluids and you suspect that they have hypovolemia continue the IV fluids so they have diarrhea diasis dehydration poor intake okay give them some fluids and keep doing it until you improve the underlying reason of why they're losing so much if you suspect shock then you probably need to start saying okay what's the reason and treat the underlying cause

of the shock but until you do that get them on vasil pressors all right and then lastly is it medication related in this particular situation discontinue the medications if you can all right how do we now approach intral Aki this patient population is often times supportive we really don't do anything and we just allow for the tubular cells in the Glarus to heal so for example if the most common cause is ATN usually what we'll do is we'll give a little bit of IV fluids depending upon the cause if a patient has rabdo they have

lots of myoglobin tumor liis they have lots of uric acid and contrast induced nephropathy that iated contrast can be kind of nephrotoxic if it's sitting around so sometimes in these scenarios giving these patients a little bit of IV fluids can help to some degree to flush those things out into the urine and improve the flow through the kidneys but just be careful you don't give too many Ivy fluids because if these patients have a really bad acute kidney injury they'll struggle to make urine and they can get very quickly hypervolemic all right oft times though

it's just treating the underlying cause and so one of the biggest things is just discontinu ing the trigger and the most common trigger are these and so just get rid of them if you can and hold those for a while so really all you're trying to do is improve the profusion IV fluids can help um and then get rid of the nephrotoxic agent DEA so again it's pretty straightforward is it a two a tubular necrosis if it is just get the time for the kidneys to recover get rid of the underlying agents that triggered this

and just give time for the kidneys to recover and they'll get better but really just monitor them for dialysis right the big thing is if they do have what you suspect is rabdo tumor liis or contrast exposure some fluids will help it may help to flush those toxins out a little bit but if it's any other cause of ATN you just try and get rid of those nephrotoxins and prevent them from having further damage that could actually pre precipitate them to go quicker to needing dialysis if they don't have acute tubin necrosis then you just

try to figure out what's the underlying ethology if it's acute intercal nefritis guess what uh you just discontinu the offending agent sometimes steroids if it's getting really bad glarin arries depending on the type you may need to give them steroids plus an immunosuppressant like cycop phosphamide all right the last one is postrenal Aki for this one guess what bilateral nephrolithiasis if it is a proximal obstruction you're going to put a stent in or you're going to do a perk nef and so what we do here is we can say if we do a stent let's

say that there's a stone blocking here and there's a stone blocking here I'm going to run this thing up here and basically create like a little stent that opens up the uror so that the stone can pass and you'd have to do this in both another option is is you just stick a a needle into the kidney and you basically drain the urine out via this bag and then start trying to treat that stone you got to eventually get that stone out of there this is more for critically ill patients this one is going to

be for like less critically ill patients all right the other scenario is if a patient has a distal obstruction so at the at the black bladder or it's at the U bladder neck the prostate level so this stuff will not help the distal obstructions only a Foley catheter would really immediately decompress this bladder so what we'll do is if the prostate is too big if the bladder's not Contracting guess what right up there it goes and I'm going to create a little tube like via this Foley to empty the bladder and that's going to start

decompressing the URS decompressing the kidneys decompressing the bladder and that's going to immediately reduce that reduce that pressure inside the kidneys and improve filtration and so that's something that I would do in these patients also the big thing here is treat the underlying cause So eventually after you're going to have to start these guys on Alpha 1 uh drugs so maybe something like tamsulosin um Alpha 1 blockers or maybe finasterid so the um the test the five Alpha reductase Inhibitors and then sometime you're going to have to discontinue the medications if they're on in any

anticholinergics that are causing the bladder to not contract well so again think about it like this does the patient have a distal obstruction okay they do best thing to do put a fley catheter in that's really it if they have an improvement in the renal function the ear output it's likely distal obstruction by BPH neurogenic figure out the underlying cause and treat that if they do not have a disal obstruction it's probably bilateral nephro you're going to have to drain that kind of uror system the kidney somehow one way is going to be doing a

perk nephrostomy or a Ural stint either way this is the only way that you're going to drain that system and improve the renal function either way if you do a perk nef you're eventually going to have to get rid of that stone so your Ral STS are going to be a little bit better long term this is more for the critically ill to stabilize them all right my friends that was a lot on acute kidney inury I really hope that it made sense I hope that you guys enjoyed it and love you thank you and

as always until next time [Music]