Acute Kidney Injury (AKI) | Etiology, Pathophysiology, Clinical Features, Diagnosis, Treatment

what's up ninja nerds in this video we're going to be talking about acute kidney injury if you guys want to follow along some really helpful comprehensive notes illustrations go down to the link below to take you to our website get that stuff it's really going to help you to understand this topic also if you guys like this video you benefit from it makes sense please hit that like button comment down in the comment section and most importantly subscribe all right let's talk about aki all right ninja so let's talk about aki so acute kidney injury

is whenever the kidneys obviously have been injured through particular causes that we'll pretty much spend a decent amount of time talking about but whenever the kidneys are injured the kidneys are responsible for being able to excrete particular metabolic waste products urea creatinine but whenever the kidneys are injured their ability to excrete creatinine their ability to excrete urea maybe decreases a little bit and so as a result the patient may develop an increase in their bun or an increase in their creatinine as a result of some type of particular injury and we'll talk about pre-renal aki

intra-renal aki and post-renal aki the other thing that may actually happen as a result of the kidney being injured is not just an increase in these metabolic waste products because of the decreased ability of the kidney to excrete these substances or filter them but also the ability to make urine maybe goes down and so what happens is as a result they develop a decrease in their urine output now the particular causes are easily remembered as pre-renal intrarenal and post-renal aki now pre-renal aki is that the patient develops an increase in their creatinine and increasing the

bun or a decrease in their urine output as a result of some type of issue where the blood flow the blood flow to the kidney so we think about pre-renal the blood supply to the kidney is actually reduced in some way shape or form there is a reduced blood flow now what could be the causes for something having reduced blood flow reduced perfusion to the actual kidney the easiest one to remember is that there is a decrease in the actual blood volume okay so there's a decrease in the blood volume if you have a decrease

in the blood volume there's potentially a decrease in the actual blood pressure decreased perfusion to the kidney and therefore decreased ability to excrete metabolic waste products and make urine what are particular easy things to remember as causes of a decreased blood volume one of the easiest things to remember is actually whenever there's not a problem where your total body volume levels are lower but it's actually where you have a maybe a normal total body volume but the amount of volume in the blood vessel the effective arterial blood volume is lower what are conditions where the

effective arterial blood volume is lower but you actually have a total normal body volume conditions that are usually like hypovolemic related or you're third spacing a lot of fluids what are what are some examples of these one of the big ones is when someone has chf you know when someone has really significant heart failure they have chf the pumping function of the heart is decreased so maybe the left ventricle is all jacked up it's not pumping well it's not having a good cardiac output what happens when you have a reduction in the cardiac output because

maybe a person has chf and their ejection fraction is really low so in other words the volume of blood that they're pumping out the percentage of blood the pumping out of the ventricles is much lower what may result in a low cardiac output if you have a low cardiac output that leads to a low mean arterial pressure which is your perfusion pressure if you have reduced perfusion to the kidneys what happens reduced blood flow to the kidneys and as a result this can lead to acute kidney injury via the increase in bun increasing creatinine and

decreasing urine output so chf would be an example of where maybe they have a total body volume that's actually normal but the amount of volume that's actually being circulated through the blood to the kidney is lower and this is actually one example we actually give a particular name to this whenever the heart is responsible for this aki it's actually called cardio renal syndrome i want you guys to remember that okay so cardiorenal syndrome is when a person has some type of cardiac cause usually chf that leads to this aki okay beautiful what's another particular cause

where you actually have a decreased total effective arterial blood volume another example of this would be someone who has what's called liver failure so if someone has very severe let's say liver failure so significant liver failure you know what the liver is actually responsible for making proteins you know there's a protein that the liver makes it's called albumin and albumin is a beautiful protein imagine this protein gets excreted into the blood right and here's this protein what it does is imagine imagine albumin is like a little water sucker right it's pulling and keeping water inside

of the blood vessel right so imagine this is like a little kind of like it's asthmatic gradient really it keeps and pulls water into the actual the vasculature so what happens is if someone has liver failure their ability to make proteins decreases so what happens to the albumin production it drops what happens to the ability to pull water into the blood vessel or keep it in the blood vessel it decreases and so as a result less water is actually being held with inside of the vasculature and instead it actually may we do call this when

some of the fluid actually doesn't stay in the vessel but it kind of sits in the interstitial spaces it's called third spacing so they might actually start having less fluid less effective arterial blood volume let's write that down so what's the result out of this this is resulting in a decreased effective arterial blood volume and so what happens is as a result you have less actual like volume of blood within the vessel and that lowers your mean arterial pressure and that lowers the perfusion to the kidney which can lead to a aki okay so we

actually whenever somebody has severe liver failure this could actually be a cause due to hypoalbumineria there's another condition where you actually do the same thing except you don't actually it's not an issue of production it's because the kidneys are injured and they start actually having excretion of lots of albumin so lots of albumin ends up in the urine okay so you have albuminuria or protein urea and a lot of it and what happens is because you're just getting rid of tons of albumin what happens to the albumin levels in the blood it's the same kind

of effect less albumin is in the blood because more of it's in your urine you have less ability to hold on to the fluid your effective arterial blood volume drops and that can lower your map and it can lower the profusion to the kidney leading to an aki what is this called this right here is called nephrotic syndrome so nephrotic syndrome is usually where they have protein urea lipid urea they have hematuria they also have a lot of edema hypertension things of that nature as well all right so again just wanted to make sure you

guys understand that so far we have chf leading to it low perfusion to the kidney right cardio renal syndrome liver failure nephrotic syndrome these are leading to low albumin within the blood hypoalbuminemia right whether it be actually decreased production or you're actually getting rid of a lot of albumin into the urine there's another condition which can actually lower your effective arterial blood volume and it's because you're again third spacing a lot of fluids you know in a patient who has what's called pancreatitis so acute pancreatitis there's so much inflammation that whenever there's all of those

cytokines and proteases that are being released it causes these blood vessels to become super leaky and so your total volume actually could be normal but your actual vessels are so leaky that they actually start having some of the fluid that is in the plasma leaking out of the blood vessel and so a lot of the fluid starts to sit outside of the vasculature what is this called third spacing so it actually does what as a result having severe pancreatitis you have third spacing of fluid which leads to a low effective arterial blood volume less perfusion

to the kidney leading to a kidney injury so this is another condition can actually do this you know when you have a really really bad bacterial infection within the blood and it's actually causing significant vasodilation increased capillary permeability and it's usually due to a really nasty infection of source that's causing hypotension it's causing fever what is this sepsis right so if someone is actually having severe sepsis particularly with shock so septic shock they may start having significant vasodilation increased capillary permeability third spacing a lot of their fluid lowering their effective arterial blood volume lowering their

mean arterial pressure lowering their perfusion to the kidneys again leading to an acute kidney injury we're so good we can make sense of this stuff in engineers okay so what i want you to remember is low blood volume leading to an aki these are some of the things that i want you guys to think about and two of these is usually due to your third spacing fluids whether it be low albumin or a lot of capillary permeability or the other one is you're just not perfusing the kidneys because not a lot of it is actually

leaving the heart and because of the heart having severe failure instead you could third space but where would a third space if you had left ventricular failure into the lungs pleural effusions pulmonary edema if you had right side heart failure where would a third space into the abdomen into the legs so it's the same kind of concept okay beautiful let's talk about another situation now this problem is actually where you have a low total body volume where you're losing tons of volume from the body and it's not actually a low effective arterial blood volume it's

just low total volume what are conditions where you could actually you know it's like exorcist and you're just vomiting severe vomiting right and severe vomiting if you're vomiting a lot you're getting rid of a lot of fluid that's fluid that could be potentially absorbed across the gi tract and so that's a decreased fluid intake in that sense or if you're peeing out your butthole and you have diarrhea that's again volume that you're not having a lot of time of motility there's little absorption that's actually occurring and you're losing a load a lot of total volume

from the body so severe vomiting severe diarrhea what's another thing that could actually be due to what if you're not just taking as much water or fluids as you should be in and so there's actually just a decreased intake so sometimes if you have a severe dehydration due to decreased intake that may also be a potential cause so again vomiting diarrhea is you're losing it from the gi tract or you're not taking in as much another thing you know whenever somebody's like severely sweating like sweating hard you're having a lot of evaporative cooling effect here

so excessive sweating what would be conditions where you could be excessively sweating maybe hyperthermia maybe fevers in situations where there's really really significant sweating you could be losing fluid a lot of losses from the actual skin another one where you actually have lots of evaporative kind of losses of fluids because of the loss of the skin barrier being intact severe burns severe burns usually like third degree okay these are things to think about you know what another one is sometimes we do this to patients unfortunately they're a little bit fluid overloaded or maybe we are

trying to give them a little bit of lasik because they're a little bit swollen or they're giving them furosemide and when we give them the furosemide or we give them some type of diuretic maybe we just give a little bit too much of a diuretic and we don't keep an eye on it and because of that they start just peeing loads and because they're peeing loads and loads of fluid guess what this fluid is whenever you use something like diuretics particularly furosemide loop diuretics it's more of a dilute urine but either way you're losing a

lot of fluid that's a total volume loss there so excessive diuretic use or that you know someone actually having a lot of diuretics could be one of the causes for their dehydration or their total volume loss another one believe it or not is if you actually have blood loss you know blood actually is a good chunk of our when we lose blood we're losing red blood cells white blood cells you're also going to be losing some platelets those are your like your formed elements right but what's one of the biggest components of blood when we

talk about blood we have red blood cells which is the erythrocyte layer then you have the buffy coat which is your white blood cells and platelets but what's like 55 of your blood plasma plasma is a part of our blood volume so whenever you have someone who's actually bleeding like maybe they have some type of um bleed from someone in in this case let's just say that they have some type of a urogenital bleed of some kind right if there's blood loss that blood loss you're actually losing plasma and that could be another potential cause

of them having a total volume loss all right so we have a total effective arterial effective arterial blood volume is low or third spacing of fluid these are above causes and then these ones are you actually have a total volume loss from the body but either way the whole concept is the same that if you actually think about it the same way if a person is having all of these particular conditions whether they're losing fluid from the gi tract from the skin excessive diuretic use or blood loss you're lowering what inside of the blood the

total blood volume inside of the blood is reduced if you lower the blood volume that will actually lower your blood pressure particularly the mean arterial pressure less perfusion to the kidneys and as a result inducing aki okay beautiful that is by far going to be the most common cause that i want you guys to remember the other two causes that i want you guys to think about is potential causes of a pre-renal aki again something before the kidney usually it's the blood vessels that are being affected that are perfusing the kidneys one is there's actually

some type of large vessel blockage of some kind so the large vessels that actually supply the kidneys what are the vessels that supply the kidneys the renal arteries right so let's say that you have some type of blockage of the renal artery what would be a condition which would put you at a susceptibility where you can throw clots and it can go anywhere it could maybe go to the brain it could go to the kidneys it could go to the spleen it could go to your gi tract it could go to a limb what is

that condition afib so you know in a patient who maybe has afib atrial fibrillation and they throw off a clot they embolize and that clot which was in the heart goes and embolizes inside of one of the renal vessels this can lead to a renal embolus so this is a potential thing to think about if you have a really significant renal blockage you're reducing blood flow to the kidney or not just a renal embolus but you know there's patients who get a lot of fatty plaques with inside of these let's actually kind of write down

let's let's say you have a person here as like a nice like fatty plaque because they don't take care of themselves they got a lot of renal artery stenosis and a patient who has what's called renal artery stenosis you know and actually particularly to be important here it's usually bilateral so whenever they have both vessels that are really really hurting because you still get a little bit of flow here right in a real embolus you might have a complete blockage of flow and a renal artery stenosis is just narrow so you may still get a

little bit of flow to the kidney but if you have bilateral kidneys you have a significant reduction in blood flow to both the kidneys and therefore you'll definitely develop a severe aki you know there's another condition i'm going to just draw another vessel here but it's imagine here you have another vessel and it's actually really kind of like thick and narrowed and dilated portions this also can really really affect blood flow to the kidney you know there's a condition where you have kind of this imagine like a beady kind of appearance of the vessel it's

called renal artery fibro muscular dysplasia okay so it's kind of like a dilated narrow dilated narrow dilated narrow portion of the renal artery believe it or not renal thyroid muscular dysplasia can actually significantly reduce blood flow to the kidneys as well so a big thing to think about is a large vessel blockage renal artery embolus renal artery stenosis or renal fibromuscular dysplasia all right so the last thing that i want you guys to think about for renal particularly pre-renal aki is not we've talked about the total volume loss we talked about a large vessel blockage

but what else what if we actually get into like some of the smaller vessels of the kidney you know the renal artery will give off branches eventually it'll from you know that you'll have like your your arcuate you'll have your lobar arteries your arcuate arteries there you have the cortical arteries and then you have the afferent arterial right well the afferent arteriole eventually feeds into this tuft of capillaries called the glomerulus and then from the glomerulus it exits out via the efferent here right so we have what's called the afferent arterial blood will come in

should usually get filtered at this actual capillary tuft here called the glomerulus and then exit out via the efferent arterial what if i actually caused significant at widespread multiple glomeruli because this is where the filtration is happening right what if multiple afferent arterioles i really squeeze them super hard i squeeze the living crap out of these things so i clamp down on the afferent arterial and if i clamp down on the afferent arterial what would happen to the blood flow that's actually going through here it would decrease well in the same way let's say that

i come over here and i talk about the efferent here what would happen if i actually dilated the efferent arteriole then a lot of blood would be able to easily leave out of the vessel so a lot of blood would leave out of the vessel and if a lot of blood eat leave out of the vessel that's less time here in the glomerulus and actually if you dilate it it lowers the pressure so it's easier for blood to leave out so what can happen is we can have certain things that can cause renal artery the

afferent arterial to undergo constriction and then the efferent arterial to undergo dilation and if you constrict it there's less blood that's going into the actual glomerulus so less filtration and if you dilate the efferent arterial more blood is able to exit easily and it lowers the pressure inside of the glomerulus which lowers filtration so the effect of both of these things can lead to a low glomerular filtration rate that's going to lead to less excretion of nitrogenous waste products and low urine outputs so what kind of things can cause this i'm glad you asked you

know there's a condition called hepatorenal syndrome it's kind of similar to someone having severe liver failure so let's say that someone has really really bad liver failure right whenever you have really bad liver failure there's a condition that can happen as a result of this called portal hypertension it's basically you know there's veins that actually come to the liver from your gi tract they're called the hepatic portal circulation right and you're supposed to be able to take blood via the hepatic portal circulation take it to the liver and then what happens is there's another big

vessel here called the ivc the liver will actually clean all the blood that's coming via the hepatic portal system and then once it cleans it it puts it into the inferior vena cava to go to the right heart and then distribute to the lungs get oxygenated and so on and so forth and the patient who has hepatic portal hypertension these vessels are so fibrotic and there's so much inflammation in the liver that it reduces the portal blood flow and so the liver says oh man i'm not getting enough blood to be able to deliver to

the ivc so what i'm going to do is i'm going to start releasing some chemicals i'm going to start releasing some vasodilators okay some vasodilators and the hope is that these vasodilators will counteract this actual high pressure and so if i counteract the high pressure i'll get more blood flow hopefully going through the liver and then getting filtered into the ivc but you know what actually happens as an unfortunate result you do cause some splenic vessel vasodilation but these vasodilators actually get into your systemic circulation and when they get into the systemic circulation guess what

they do to multiple blood vessels in your systemic circulation it causes the systemic vessels to undergo a vasodilatory effect what happens when you vasodilate multiple systemic vessels well it's going to actually lower your blood pressure you know when your blood pressure lowers and actually kind of lowers your effective arterial blood volume when you lower your systemic blood pressure what does your body try to do in response it says hey blood pressure is low i need to try to increase the blood pressure so i can perfuse vital organs and i need to constrict the vessels to

organs that are viewed as non-vital guess what the kidney unfortunately is viewed as non-vital in low blood pressure situations so when this happens this low blood pressure will actually cause intense renal artery and afferent arterial vasoconstriction and so it'll stimulate this vasoconstrictive mechanism which reduces the significant amount of blood flow to the glomerulus reducing your glomerular filtration rate and another thing that also happens is whenever you have low blood pressure you know it actually activates what's called the renin angiotensin aldosterone adh system and you know what they do what are they supposed to do they're

supposed to cause a little bit of renal artery vasoconstriction that worsens that and then also you know adh and aldosterone they're supposed to reabsorb sodium and reabsorb water if you reabsorb these that means less of it's in the urine that lowers your urine output even more because you're reabsorbing whatever little gfr you had whatever little urine that you were going to make now the adh and aldosterone that you just had produced you're going to reabsorb that little sodium in water and so this is going to lower your urine output even more okay so unfortunately this

is what happens as a result to try to be able to preserve your blood pressure but it can unfortunately affect the kidneys a little bit and this condition where the liver directly affects the kidney or indirectly affects the kidney through these mechanisms is called hepato renal syndrome and again this can also coincide with what we talked about above having low albumin so you can kind of get a double whammy with this kind of effect now what are the things can actually cause constriction of the affair and arterial you know there's drugs that we love to

pop a lot whenever we're in a lot of pain insides so nsaids believe it or not have a pretty significant aphid arteriolar effect and vasoconstriction so that can actually kind of reduce your gfr and another one is what's called tacrolimus it's actually what we use whenever someone gets like a kidney transplant and you're supposed to help prevent rejection but it's a calciner inhibitor so these are the kind of drugs that would particularly affect the constriction effect other things believe it or not is you know when you have very very high calcium levels super super high

calcium levels and whatever the condition may be that actually causes this hypercalcemia maybe it's a malignancy maybe it's a parathyroid hormone that's being uh too high either way high calcium loves to act on those affair and arterials and high calcium a lot of calcium gets into those actual smooth muscle cells induces the vasoconstriction also reactivates the renin angiotensin aldosterone system and that can cause this intense renal artery vasoconstriction but there's other things that you want to think about you know there's some nasty little drugs sometimes they're they're not nasty but they can be effect you

know they can have some nasty effect on some people is um you use it for blood pressure and sometimes they can cause a little bit of a nasty effect they're good in patients with high blood pressure who also have diabetes who have heart failure and they're called ace inhibitors or angiotensin recepton receptor blockers these ones particularly work by inhibiting angiotensin ii angiotensin too you know what it does in the efferent arterial it causes vasoconstriction because if you constrict the efferent material what would that do it would actually lower the amount of blood that's leaving the

glomerulus it would also increase the pressure within the glomerulus what would that do if you increase pressure and you have less blood that's leaving the layers it would cause higher glomerular filtration rate you'd be able to make more urine right if i give a drug that's actually going to cause vasodilation of the efferent material it's opposing angiotensin ii and therefore it's going to cause dilation reducing the gfr so that is kind of that sometimes the unfortunate effect of ace inhibitors and arbs okay we have done hit up the pre-renal aki causes let's now talk about

the intra-renal aki causes all right so the next one that we're going to talk about is intra-renal aki right so now it's it's pretty easy to understand now when we talked about pre-renow it's a problem with blood flow right it's an issue with blood flow there's a reduced blood flow to the kidney but an intra-renal aki the person is having again low urine outputs or having high bun high creatinine but it's not due to an issue with the blood flow it's an issue with the kidney itself so the kidney tubules the small little vessels like

the glomeruli are affected in some way shape or form but yeah that's kind of the big thing is it's actually a kidney injury particularly something wrong with the renal parenchyma whether it be the small little blood vessels or whether it be the actual kidney tubules what are the particular things that i want you guys to remember by far the most common cause of intrarenal aki is what's called acute tubular necrosis often referred to as atn okay a t n acute tubular necrosis has a couple different causes one is it actually could be due to significant

reduction in blood flow so you know whenever somebody has a pre-renal aki right they have very little blood flow so one of the other ones to think about with intrarenal ki someone has very very low blood flow for long periods of time so low blood volume for a long period of time it's not corrected right especially someone with sepsis hey look at that perfect someone who has sepsis severe sepsis that goes on for long periods of time it really really lowers your effective arterial blood volume and if it's not effectively treated that reduces significant amount

of blood flow to the kidneys and guess what the little kidney tubules those little cells they depend upon oxygen as well to be able to work and if you're not giving oxygen to these poor little guys what's going to happen they're going to undergo ischemia what happens if ischemia is not actually reversed it undergoes necrosis and the tissue cells die and the kidney cells themselves lose the ability to perform their functions and we'll talk about what that is so that's one big thing to think about is someone having a very low blood volume for a

long period of time one of the best examples is actually septic shock worked out perfectly all right the second thing is medications okay so certain types of drugs and there's a lot of them i am not going to go through every single drug i don't want you to focus on that i want you to know some of the big ones to think about and and the particular ones to think about is actually antibiotics um so two of the antibiotics that i actually do want you to remember here is what's called aminoglycosides and another one called

vancomycin these are pretty common drugs that we have you know we prescribe a lot especially vancomycin and that's a definitely one that can actually cause an acute kidney injury it actually directly damages these beautiful cute little proximal and convoluted tubular cells and different types of tubular cells with inside of the actual nephron it damages those little guys and so their inability to reabsorb and secrete and perform those normal functions another one is antivirals actually believe it or not antivirals you know there's um acyclovir that we actually can prescribe in certain types of infections acyclovir is

actually kind of a nasty one as well so these are some there's also other drugs like methotrexate and many many many different types of drugs but these are kind of the big ones that i want you guys to remember one more we actually kind of give a lot is contrast die so sometimes if someone is actually getting contrast radioiodine contrast stuff like that contrast dyes actually may have a little bit of an effect on the kidney tubules as well and cause direct injury so again remember these drugs are nephrotoxin so they actually cause direct injury

to these actual kidney tubular cells okay so we have reduced blood volume we have drugs that directly damage the kidney tubules you know what else can actually directly damage these kidney tubules you know that whenever somebody has a lot of damage to red blood cells what does that call when you like pop these little suckers open and you release out a lot of hemoglobin that gets released out freely circulating that's a nasty little son of a gun sometimes sometimes if it actually gets down here into the kidney tubules it actually can again cut it can

get taken off into the hemoglobin and the iron can actually get taken up into these actual acute the tubular cells and cause direct nephrotoxic injury you know not just hemolysis but you know there's a protein similar to hemoglobin but it's actually kind of in our skeletal muscle cells and whenever our skeletal muscle cells get all jacked up in a condition like rhabdo you know someone has rhabdo myolysis they have their injury to the actual skeletal muscle whether it be a crush injury whether it be trauma whether it be overexertion seizures all that good stuff it

starts spilling out tons of myoglobin and that myoglobin starts getting into the bloodstream and it actually starts getting taken into the kidney tubes and it gets taken up into these kidney tubular cells and causes a direct nephrotoxic injury boom shabam you know another condition you know whenever someone has a nasty cancer so let's say that you have a can you have a bunch of cancer cells you know this is a pretty common sometimes like leukemia lymphoma stuff like that but you have tons of cancer cells and you're actually getting chemo and what happens is the

chemo is designed to be able to kill these sons of guns but what happens is when you kill a bunch of cancer cells they spill out some of the actual metabolic waste products and you know what one of those nasty ones is uric acid and whenever you have lots of uric acid that gets spilled out believe it or not it actually does to cause direct nephrotoxic injury to these poor little tubular cells and their ability to be able to reabsorb urea and excrete creatinine and reabsorb sodium and water all that stuff's all jacked up you

know there's another condition you know in other conditions called multiple myeloma you know multiple myelomas whenever you have these plasma cells we'll put multiple myeloma and what happens is these plasma cells they produce tons of like kind of like proteins right but one of the proteins that they actually produce is called a bence jones proteins and these bench jones proteins actually will get taken through the blood taken to these actual tubular cells within the kidney and cause direct injury to the tubular cells these are the bench jones proteins so again these are the things that

i really want you to remember there's one other thing i don't think it's super hail because you don't see it that often hopefully but people who actually unfortunately this can be come up in a clinical vignette is when a child gets a hold of like antifreeze ethylene glycol and it can cause visual changes as well but this also has the ability to cause direct nephrotoxic injury okay so again if you damage these kidney tubules their ability to be able to reabsorb secrete substances and the ability to actually help to play a role within glomerular filtration

becomes very very effective and we'll explain that pathophysiology a little bit later all right so we got the causes for acute tubulin necrosis which is the most common type for intrarenal aki what's another one that i want you guys to think about the next one not so common but again something to think about is called acute interstitial nephritis this is also referred to as a i n now acute interstitial nephritis is actually whenever you have damage or injury to the kidney tubules and it's a lot of inflammation of the kidney tubules and the actual interstitium

around the kidney tubules okay what kind of condition would cause a lot of inflammation so let's actually do this in a different color let's do like pink or something so what condition would cause a lot of inflammation of the interstitium so the spaces between the blood vessels and the actual kidney cells or the tubular cells or a lot of inflammation directly of these kidney tubular cells imagine them really sad and crying what would be some conditions well first thing is drugs it's always drugs right so what are some one of the big ones is actually

going to be your beta-lactam antibiotics so your penicillin antibiotics these are big the other one is ppis believe it or not so proton pump inhibitors these are also some ones that actually can cause a little bit of injury as well there there is other ones i don't want us to get hung up too much on these but yeah ppis beta-lactams those are some of the ones that i want you to think about you know there's other conditions they're like infiltrative diseases they're inflammatory kind of conditions where you can get you know the condition called sarcoidosis

where you have a lot of these like inflammatory granulomas that get deposited into tissues guess what if it gets deposited into the area around the interstitial spaces or near the actual kidney tubular cells this can be enough to cause interstitial nephritis or maybe another condition called amyloidosis amyloidosis where there's actual proteins that get kind of deposited into this area you know there's another condition when actually patients have a lot of autoimmune disorders there's a condition it's called systemic lupus erythromytosis and this kind of condition have lots of antibodies and these antibodies that they're actually producing

can cause damage to the actual tubular cells and cause inflammation around the interstitial and even another condition called shogren syndrome right but you know what else infections infections whether it be bacterial right legionella streptococcus viral infections like cmv hepatitis viruses different types of fungal infections as well but infections in general can actually cause injury to these actual tubular cells inflammation of the tubular cells and a lot of interstitial inflammation and again think about it like this these this interstitium and the tubular cells if they're inflamed their ability in being able to reabsorb substances being able

to excrete creatinine and their ability that affects the actual filtration pressures all of that stuff is going to be altered okay so we have acute tubulin necrosis acute interstitial nephritis what are the last two components here that i want us to think about here so there's two other ones that i want you to think about that are actually kind of involving a little bit more of the structure called uh the you know we have what's called the glomerular basement membrane so you have these like capillaries here okay this is your glomerular capillaries then you have

what's called the glomerular basement membrane and then you have cells you know you have some some cells here if i were to actually kind of draw them they're little foot cells and they kind of look like little you know weird-looking things here these are called podocytes right so you have podocytes you also have other cells called mizangio cells if i were to draw them i'll just draw them kind of like this purplish color here so you have these things called mesangial cells they're all over the place but you know whenever someone has an inflammatory condition

you know there's kind of an inflammation of all of these areas inflammation of the mesangium inflammation of the glamorous basement membrane inflammation and damage of the podocytes right you know there's a condition where you have like these antibodies and and antigen deposition into these areas you know there's a condition where you actually kind of cause inflammation of the glomerulus and the glomerular basement membrane and the mosain gm cells and all that kind of those accessory cells we call this glomerulonephritis we're just going to represent that as gn and there's so many different types we'll have

to talk about this in a separate video so we're not going to spend the time going over all of these but just remember this could be a particular cause of aki because it's going to affect the ability for the not just the damage not just the effect it's going to affect the glomerular filtration rate but also it may cause some damage to some of the structures that are involved within the filtration and reabsorption of substances so again one of the big things to think about here is that if you damage the actual glomerulus it can

actually affect the glomerular filtration rate all right so glomerulonephritis would be another one the last one again these aren't these these last two that we're talking about they're not super big i don't want you guys to spend too much time thinking about them but it's just something to have in the back of your mind but you know in a condition where you have a lot what's called thrombotic micro angiopathies there's a bunch of these again i don't want you to go to go too ham on them but something called ttp thrombotic thrombocytopenic papera another condition

called hemolytic uremic syndrome another condition called a disseminated intravascular coagulation and sometimes even in patients who have what's called hypertensive crisis right and these situations you can kind of get a lot of like small little thrombi so a lot of thrombi that kind of deposit with inside of the fair interior the glomerulus and it really kind of causes a lot of inflammation and damage to structures within this area and this can lead to a reduction in glomerular filtration rate sometimes this can also be seen in conditions like vasculitis as well so big thing to think

about for intra-renal aki what i really want you guys to spend most of your time remembering is particularly the intra-renal aki a little bit on the acute interstitial nephritis but don't go too ham on remembering glomerulonephritis and thrombotic microangiopathies and vasculitis okay now that we got that done let's talk about the last type of aki post renal aki all right the last type of aki is a post renal aki so post renal aki is obviously we're getting pretty good at this stuff right pre-renals reduce blood flow intrarenals there's something wrong with the actual renal parenchyma

most common is acute necrosis and post renal is it's after the kidney because most likely ureter bladder prostate area urethra something in that part of the urogenital tract is actually being affected okay and so we like to think about you know something that's actually happening after the kidney and this issue after the kidneys what's actually leading to an accumulation of urea an accumulation of creatinine and a reduction in urine output what are some conditions that you guys should think about well i like to think about this as something that's usually above the bladder right so

some kind of issue down from the ureter all the way till we get to the bladder and then something at the bladder down to at least the level of the urethra so what are some things that can actually happen it's actually not that bad right so it's something that's involving the ureters something involving the ureters has to be wrong here and you know what's really easy is something like a kidney stone so sometimes having what's called renal calculus right could be a cause so some type of kidney stone you know what else could be another

particular cause that you got to think about sometimes is if there's some type of large kind of like intra-abdominal tumor some type of large maybe it's a colorectal cancer maybe it's some type of retroperitoneal mass or something of that nature but there's some large tumor that's actually causing compression and if it's compressing down on the actual ureter it again is kind of like in the same way resembling like a kidney stone okay in these kinds of situations usually it actually needs to be a pretty significant like effect to actually cause that much of an acute

kidney injury and so usually having like a kidney stone in one ureter or tumor only compressing one ureter isn't going to do it too often and so sometimes this would need to be a bilateral effect if you had a bilateral renal calculi or you had a significant tumor that was compressing maybe both of the actual ureters this would definitely produce a very significant type of post renal aki okay so that covers those two not too much right not too bad it's actually one of the easiest ones the other one is actually going to be somewhere

at the bladder and urethra level okay so the bladder the bladder neck and the urethra so what could be some issues that would actually cause this you know in males they have um a pretty good sized little donut shaped structure here and sometimes if it gets really really like large which can't happen it's called a condition called benign prostatic hyperplasia that can actually cause if it gets really really big it may actually cause compression of the urethra the prostatic urethra which actually causes kind of an out low outlet obstruction here and again less actual urine

coming from the bladder will be able to exit out through the urethra and then the overall effect is that this could actually cause some type of reduction in urine output and if it causes the backflow backflow black flow all the way up to the kidney tubules that kind of pressure build up it can cause an acute kidney injury other things that can actually cause an outlet obstruction there not just bph but if someone has some type of prostate cancer so something is similar to that but like prostate cancer or they have some type of urethral

injury you know sometimes if you have like a significant type of like urethral stricture of some form and you know one more sometimes in patients who get foley catheters they get catheters and the catheters may be not functioning for some reason it could actually cause less urine to become coming out via the foley if the foley is not functional and again that can cause the pressure to build up back through the ureters back into the kidney so we can say a non-functional foley which isn't too common to be honest with you but again something to

think about all right the other thing that you want to be thinking about is maybe it's actually not something that's causing like an obstruction whether it be bph prostate cancer urethral stricture or non-functional foley maybe it's actually something wrong with the bladder it's just not really good at being able to contract and if the bladder's not contracting with it really well it just isn't able to empty contents out what is the actual condition in which the bladder isn't really good at being able to empty things out maybe there's something wrong with the nerves that supply

the bladder or maybe there's something wrong with the actual muscle that the muscle just doesn't want to contract or maybe the actual urethral sphincters just don't want to react as much you know a condition called a neurogenic bladder and again this could be due to a neural issue this could be do something to like some type of uh issue of like multiple sclerosis parkinson's disease strokes it could be neuropathy a bunch of different things but there's some type of issue where the detruster muscle just isn't contracting as much or the urethral sphincter is over contracted

okay you know another kind of condition is actually not conditions but medications that kind of replicate this where medications that are used for patients who are actually having incontinence they actually act they actually wet themselves right they have a hard time being able to prevent themselves from actually having episodes of of incontinence and so because of that we give them medications to be able to prevent the incontinence but as an end result it actually causes maybe the bladder to just not contract enough or maybe cause the sphincter to tighten up too much and so instead

they actually don't make urine and it causes retention and so medications that are designed to be able to treat incontinence maybe they start leading to retention and the best ones to remember here is what's called your anti cholinergic medications okay these are things like um we have drugs like what's called oxybutynin tolterridine sulfinosin things of that nature okay that covers all of the aspects of the causes of post renal aki and all the causes in general of aki now what we need to do is we need to create a bridge we need to understand how

these causes lead to an acute kidney injury how that acute kidney injury leads to clinical manifestations lab values different complications so on and so forth let's talk about that all right so let's talk about the pathophysiology now when we talk about the pathophysiology we'll go through these and kind of talking about pre-renal intra-renal and then we'll quickly talk about post-renal aki okay and the reason why is we're going to kind of explain a little bit more about the lab stuff the diagnostics the things that you really need to know for your exams so pre-renal aki

right when someone has a pre-renal aki we already know all the causes there's a reduction in blood flow right and the reduction in blood flow leads to a reduction in the gfr now what i want you to remember is in someone who has what's called a pre renal aki right there is a reduction in the gfr and all of these you're going to have some reduction in gfr so there's there's less filtration right less filtration that's occurring here between the glomerulus and the bowman's capsule now whenever you filter substances you can filter things like urea

and you can filter things like creatinine right now in someone who has a pre-renal aki it's the primary reduction in blood flow there's nothing wrong with the actual renal parenchyma okay if it's at the renal parenchymal level then you're at an intra-renal aki but in a pre-renal aki these tubular cells are functional they're working well there's no issues with these cells so their ability to reabsorb substances and excrete substances is completely intact so what happens is you have this excretion of urea and creatinine but it's a little bit lower in general okay so we can

already say that the blood whenever you have less filtration right there's a low g f r there's less filtration of urea so you already might have a little bit more urea in the blood and you already might have a little bit more creatinine than the blood that you prefer because of this low gfr but the kidney tubular cells are intact they're working so you know what that means is your kidney tubular cells whenever you get urea down here urea is actually a reabsorbable substance in like the proximal convoluted tubule and so urea as long as

these kidney tubules are functional should be able to be reabsorbed back into the blood right so that should be intact if these kidney tubes are intact so you should be able to reabsorb urea if the kidney tubules are intact now if the kidney tubules are also intact they're supposed to excrete creatinine and so if these kidney tubes are working they should be able to take the creatinine and excrete it into the kidney tubules right and so what is kind of happening out of this is that you have creatinine that you're excreting so it should lower

the creatinine within the blood so what do we kind of see out of all of this the creatinine and the urea generally will increase a little bit because of a low gfr but because the kidney tubules are intact in a pre-renal aki you could reabsorb urea and you should be able to excrete creatinine so what truly happens to the actual total concentration of urea in the total concentration of creatinine effectively the total concentration of urea actually will go up okay but the actual concentration of creatinine it won't go up too much they only may actually

go up just a teensy bit because just not as much of it is actually being filtered across the actual glomerulus so we can say that when you compare if you were to compare a ratio to the blood urea nitrogen to the creatinine what would it look like so the bun over the creatinine now you look at that ratio the bun is super high right because you're reabsorbing urea and you're having less filtration of urea the creatinine though it's just a little bit high because you have less less of it being filtered but you're actually secreting

it because you have functional tubular cells so the bun to creatinine ratio we actually say is greater than or equal to 20 to 1. so 20 bun to 1 of creatine usually the ratio is greater than or equal to that for the bu and creatinine ratio then if you also took a look at the urine if you actually calculated and looked at the urine and said how much urea is actually in the urine there is very little urea that's actually in the urine because you should be absorbing the urea because you have intact kidney tubules

here's another thing that's important whenever you have intact kidney tubules and you have urea that's actually being reabsorbed you know sodium and water so let's say here we have sodium and water whenever there's sodium and water you know sodium and water actually like to follow urea so whenever there's urea reabsorption there's also sodium reabsorption and sodium that actually when it follows kind of the urea and the waterfall is the urea you actually get an increase in the sodium reabsorption and an increase in the water reabsorption but there's one more thing i want you guys to

think about you know when you have a low gfr a low gfr will lead to kind of a a low sodium chloride concentration that should trigger your actual macula densa cells to tell the affair and arterial particularly the jg cells to start releasing renin and then it'll tell ren and hey renin there's low blood flow low glomerular filtration low sodium chloride i think you actually need to figure out a way to increase the blood pressure so you can increase the profusion to the kidneys you should activate the renin-angiotensin aldosterone adh system and so you know

what happens is this low gfr will actually trigger a stimulation of the renin angiotensin aldosterone adh system and you know what happens whenever you have an increase in aldosterone and an increase in adh you reabsorb your sodium in the blood and you reabsorb water within the blood so not only are sodium and water following urea during reabsorption but the iranian angiotensin aldosterone adh axis is being stimulated because of the low gfr and triggering sodium and water to be reabsorbed and this only works why because the kidney tubules are intact if the kidney tubules were damaged

this wouldn't matter because you could be releasing these hormones all the way but if the kidney isn't responding to adh and aldosterone because those kidney tubes are damaged it won't matter but we are reabsorbing lots of sodium and water and so the sodium and water will go up in the blood in attempts to be able to increase your blood volume increase your blood pressure that you can increase your gfr what happens though to the sodium and the water within the actual urine so the sodium the sodium concentration let's actually put like the sodium concentration goes

down and the water actual concentration also will go down and then if you actually look we have something called the fractional excretion of sodium which is basically how much sodium is actually excreted in the urine and compared to how much is filtered and that is going to be a low amount we actually say less than one percent when you actually look at the urine so the amount of sodium that's actually excreted into the urine comparison to the amount that's filtered is less than one percent so these are some of the things that you want to

think about and because there's very little water inside of the urine the urine is very concentrated and so we say that the urine osmolality will almost be greater than 500. so some of the things that i want you guys to think about for pre-renal aki is that the kidney tubules are intact remember that so they can reabsorb and they can secrete substances you have a low gfr because of a low blood perfusion that leads to more urea more creatinine accumulating in the blood because you're not actually filtering them but since the kidney tubules are intact

you can reabsorb more urea and you can excrete creatinine so because of that the bu and creatinine ratio will be greater than or equal to 21. you also because you're reabsorbing urea urea can act as kind of like a gradient molecule that can pull sodium and water so you reabsorb sodium and water but on top of that when you have low gfr it should trigger the activation of the renin-angiotensin aldosterone adh system and because the kidney tubules are intact they respond to that and reabsorb sodium reabsorb water so you get more of that in the

blood to augment your blood volume and your blood pressure therefore your gfr but less of the sodium less of the water end up in the urine so you end up with concentrated urine uranus greater than 500 higher this number is the more concentrated it is less water there is your sodium inside of the urine is actually going to be low because you're reabsorbing it so the fractional excretion of sodium is getting less than one percent the urine sodium is low usually like less than like 20 and the amount of urea is also low okay that

is pre-renal aki let's now talk about intra-renal aki now an intra-renal aki what kind of happens here this is an interesting one so intra-renal aki there is some type of kidney tubular injury these kidney tubules be all jacked up they're not good at performing their function anymore which is being able to excrete and reabsorb whatever the cause may be that we talked about they're damaging these tubules you know what happens when you damage these kidney tubules the kidney tubules imagine them kind of like flaking off imagine these like like these cells like flake off you

have a bunch of them and because they're dying they start flaking off because you're trying to regenerate new cells to re-epithelialize those kidney tubules and what happens is whenever they die off they kind of leave all of these cells that kind of clump up and produce like a really thick kind of like block uh cast kind of structure all right so you get like this thing called a here we'll have the urine here but well they have this thing this is called like a cast a cast is basically like it's a clump of these cells

that kind of form to the shape of the tubular lumen we actually call it like muddy brown cast but either way these casts that we have here are actually a result of all of these tubular cells dying off because of whatever the offending agent was whether it was some type of nephrotoxin or endogenous kind of process or you know low blood volume over a long period of time but either way there's injury now these casts what do they start doing if you had something that's supposed to filter across here and there's supposed to be fluid

that moves down so imagine filtrate should move down and it should eventually end up through all the kidney tubes into the urine imagine you have a blockage all of these casts are blocking up a part of the tubule what does that do to the back pressure what happens to the back pressure now well now the pressure will start rising it'll increase the pressure within the tubular system now what do things whenever you have things that want to move right if i had things that wanted to move from the glomerulus into the actual capsular system and

then into the tubules what does it want to move from well filtration glomerular filtration rate is dependent upon a bunch of different pressures right for example the hydrostatic pressure inside of the vessel the osmotic pressure in the vessel the hydrostatic pressure in the capsule and the osmotic pressure in the capsule imagine that the capsular hydrostatic pressure is super high it's going to now cause things like filtrate that wants to move from the glomerulus into the actual capsule to be affected because things want to move where you always want to move from high pressure to low

pressure that's the desire but what if the pressure is now not as low as you prefer it's higher it's going to decrease the actual glomerular filtration the amount of substances that will be excreted so this will be affected significantly and that will reduce the gfr now if you reduce the gfr you have less filtration of what kind of substances waste products and so you may accumulate a little bit of urea and you may accumulate a little bit of creatinine right that's what makes sense kidney tubules are they working can they excrete can they reabsorb nope

so guess what happens the urea that you have here it was supposed to get reabsorbed can it get here to here no because these kidney tubules are all jacked up they can't perform the function of reabsorption anymore so do you reabs absorb a lot of urea into the blood no so there's actually no effect of kind of like that significant urea reabsorption okay that's a big big deal okay that actually should make sense right now the next question is can we excrete creatinine so can these kidney tubule cells take the creatinine that's in the blood

put them into the tubular cell and then into the urine no because the ketos would be all jacked up so because of that what happens to the creatinine in the blood it builds up because we can't excrete it and so as a result what happens to the creatinine the creatinine starts going up because we can't excrete it now if you look at the ratio between the bun and the creatinine which one's higher now if we think about it well the creatinine wasn't actually filtered as much urea wasn't filtered as much but when we talked about

reabsorption not really much urea was reabsorbed but tons of creatinine was actually retained because you couldn't excrete it so because of that look at these arrows there's way more creatinine in the blood than there is actually urea so the bu and creatinine ratio will actually be less than or equal to 15 to 1. okay all right beautiful so we understand that now what actually will happen then if you can't reabsorb urea what happens to the urea in the urine does it go up yeah because you can't reabsorb it so you pee it out you get

tons of urea in the urine okay beautiful another thing if you're not reabsorbing urea can you reabsorb sodium and water by via the osmotic gradient nope that's all jacked up and so now less sodium and less water get reabsorbed because normally this wants to follow the urea but it can't because urea is not being reabsorbed the other thing we have low gfr man we're so good in engineers when you have a low gfr what should this do should stimulate the random angiotensin aldosterone adh system and you should have the production of aldosterone you should have

the production of adh this should want to reabsorb sodium this should want to reabsorb water well you make these hormones but are the kidney tubules actually functional that they can respond to the aldosterone and they can respond to the adh no they'd be all jacked up this process doesn't happen and so you actually don't reabsorb sodium and you don't reabsorb as much water so where does the sodium in the water go into the urine my friends and so you end up with a lot of water in the urine and a lot of sodium in the

urine when you have lots of uh like water in the urine what do we actually say then about osmolality what will it be the urine osmolality will actually be a little bit more dilute in comparison so less than 350 and the sodium there's a lot more sodium that's actually being excreted in comparison to the amount that was actually filtered so what do we say about the fractional excretion of sodium it's greater than two percent okay so that actually should make sense all of this stuff cool you know what else is this really intrarenal aki really

affects not only the excretion of creatinine but also it affects a lot of the processes of sodium reabsorption potassium excretion acid excretion drug excretion so this one can really have some significant deleterious effects leading to a lot of complications that we'll talk about below all right so post renal aki now the reason why i don't want to go too crazy on the path of fizz is that again you're not going to really need to know this too much for your exams because it varies a lot of this pathophys so but we'll quickly quickly explain it

so post renal aki here's the way i want you guys to remember it okay post renal akis is it's kind of like intra-renal aki right there there's let's actually kind of elongate this tubule here a little bit so imagine i kind of elongate this tubule but again remember this is after the kidneys so just remember that this is after the kidneys we're thinking about this tubule being a continuation into like the ureter there's some kind of obstruction or there's something that's obstructing the flow of filtrate and urine throughout the actual kidney tubules right but it's

somewhere beyond the kidney what happens is similar to what happened in the aki part intra-renal is that normally you want fluid to be able to filter across and move down easily without any kind of um obstruction or resistance but if you have something that's causing an obstruction like a renal tumor i mean something like a a renal calculus or a tumor that's compressing down on the ureter or you have some type of bladder outlet obstruction like severe bph this may actually cause the pressure to increase and so again if we cause the pressure in the

capsule to rise what would happen to the glomerular filtration rate as a result it's very simple right you obviously want things to move from areas of high pressure to areas of low pressure but whenever the capsular hydrostatic pressure is high it's going to lower the actual net filtration pressure and therefore the glomerular filtration rate and so you have less filtration that's going to be occurring so we have a low gfr right and that's going to be the result of this certain type of obstruction okay now as a result we already know that if you have

less gfr you end up with a little bit of an increase in urea a little bit of an increase in creatinine because you're not filtering off as much of that across the glomerulus are the kidney tubules are intact they are the pressure's built up but it's not enough to actually cause injury to these kidney tubular cells yet so the kidney tubular cells are intact if they're intact what do you do you're able to take any of the urea reabsorb it you're able to take any of the creatinine and excrete it and so you have low

creatinine within the actual blood effectively right if these are intact you can do that function also since the urea is getting reabsorbed the kidney tubules are intact sodium and water can also be reabsorbed and because the kidney tubules are intact guess what else when you have a low gfr you stimulate the renin angiotensin aldosterone adh system right and if that has functional kidney kidney tubular cells aldosterone and adh as long as the kidney tubule cells are functional will increase sodium and will increase water and guess what the kidney tube does are functional and so because

of that if you actually look at the urine guess what you'll reabsorb as long as this is present you'll reabsorb sodium and water and so what happens to the amount of sodium and water that's actually present within the urine it's low low sodium low water you're able to reabsorb urea so what happens to the urea concentration their ureas low this should look familiar doesn't it it looks just like pre-renal aki that's what i want you to remember in the early stages of post-renal aki so i want you to remember early in the early stages of

post-renal aki it can resemble pre-renal aki where they're bun creatinine creatinine is low bun's elevated right so they have a elevated bu in to creatinine ratio that's greater than or equal to 20 to one they have a fractional excretion of sodium that's less than one percent they have a urine osmolality that's greater than 500 and they have a low urea that's all i want you to remember now what do you think happens in later stages guys in the later stages of someone with a post renal aki let's kind of elongate that tubule just a little

bit you elongate the tubule a little bit right and just imagine that this is some kind of obstruction that's taking place again we're kind of like shorthanding this obstruction but you have a tubule that's actually blocked there all right so we have this obstruction here right and again this is either like a significant renal calculi or some type of tumor or there's significant bph and this has been occurring over a longer period of time well the pressure now is going to increase even more it was already a little high enough to reduce the glomerular filtration

rate but now the pressure starts really increasing that it actually starts exerting some really significant effects on these kidney tubers and imagine it like this imagine the kidney tube just ballooning out right so imagine here i had a kidney tube that was like this and then after a while it starts kind of ballooning out like this because of all the pressure and as it starts ballooning out guess what kind of is supposed to be running here your blood vessels these poor little guys start getting compressed and if they start getting compressed you're going to start

reducing the poor little blood flow to these kidney tubules right and they're not going to get their oxygen and they're going to start dying off if the kidney tube you'll start dying off all these poor little guys and you have all of this high pressure system within the kidney tubules again you're still going to have this low glomerular filtration rate because again you have high pressures within the capsule it's lowering the net filtration pressure so you're still going to have a low gfr and again same concept you'll have an increase in urea you'll have an

increase in creatinine but the kaden tubos are damaged if they're damaged and they're not actually working as well because you have so much obstruction that's causing so much pressure to squeeze on the vessels and reduce the oxygen supply and start causing damage can you actually reabsorb urea no can you excrete creatinine no so creatinine starts building up urea doesn't actually accumulate as much in the blood and because of that guess what not as much sodium and water comes over so less sodium and less water will move over also normally what happens when you have a

low gfr it should stimulate the renin angiotensin aldosterone adh system if aldosterone and adh are present and the kidney tubules work they should increase sodium if adh is present in the kidney tubules work this should increase water reabsorption but are the kidney tubules working no they're all jacked up can you reabsorb sodium and water no and so effectively what happens as a result what happens then as a result to the actual urine if we were to kind of look at like this you actually look at here we'll do it like this that way we can

make some room here what happens to the amount of urine sodium the urine sodium will be high what happens to the amount of water it'll be high because you're not reabsorbing it via this process and you're not reabsorbing it via this process what happens to the urea well you can't reabsorb it so the urea goes up what happens to the fractional excretion of sodium it goes up greater than two percent what happens to the water leading to the osmolality of the urine it actually does what well there's actually more water if there's more water it's

more dilute so the urine osmolality will be less than 350. my gosh if this doesn't look like something i've seen before it's intra-renal aki so you know what i want you guys to remember to take away from all of this i know it was a roundabout way of getting there but post renal aki in the early stages looks just like pre-ringling api and the later stages looks just like intravenous aki because again what happens to the bu and creatinine ratio in this point what happens really quick b you in creatinine where's the urea what does

it look like here well you re you don't filtrate as a lot as much of it and you don't reabsorb it so it's only a little bit elevated creatinine you don't excrete it and you don't filter it so it's super elevated and so the creatinine ratio will be less than or equal to 15 to one this should look exactly like intriguing like i so what i want you to remember for the pathophysiology is we understand pre-renal we understand intra-renal we understand all of the diagnostic aspects of it the clinical applications of it how this leads

to decreased urine out but so on and so forth but post renal like in the early stages it looks like pre-renal and the late stages it looks like intra-renal agile the last thing that i want to talk about is complications that can happen as a result of someone having a significant acute kidney failure and when i talk about acute kidney failure this is really mainly intra-renal aki that's going to produce these nasty complications not as much pre-renal aki and nowhere near as much as post-renal akin so what are some of these complications that i want

you guys to think about well you know whenever the kidney's all jacked up and it's not able to particularly again i want you to really remember intra-renal aki the kidney's injured it's not able to do what to the urea it's not able to really kind of like reabsorb the urea but it's also having a difficulty being able to filter the urea and so what happens is you may develop a little bit of urea buildup when urea builds up in the blood enough that it actually starts causing azotemia azotemias whenever you have elevated levels of blood

urane nitrogen creatinine but whenever that azotemia starts actually leading to nasty effects adverse effects on the body it's called uremia so understand azotemia uremia not the same thing azotemia has just increased like urea nitrogenous waste products in the blood uh uremia is the effect of azotemia causing nasty adverse effects what are some of those adverse effects of uremia well you know uremia likes to cause platelet dysfunction what the heck are your platelets involved in they're involved in clotting right so if someone actually has uremic dysfunction this can lead to i mean they have elevated uremia

uric acid and creatinine that's actually causing nasty metabolic effects on the body it can lead to platelet dysfunction and platelet dysfunction can lead to bleeding oh that's not good right what else you know elevated levels of urea also love to cause inflammation of the pericardial cavity and so the pericardial cavity that normally is responsible for having just a little bit of fluid in it starts to become super infant inflamed and there a ton of fluid can start to develop what do we call that well first off the inflammation of it is called pericarditis but whenever

it's really inflamed it tries to increase the secretion of serous fluid and that serous fluid can lead to what's called a pericardial a fusion okay so you can have platelet dysfunction leading to bleeding pericarditis leading to pericardial fusion and worst case scenario cardiac tamponade and what else this is really nasty on the neurons it really affects the neurons and can cause the neurons to become super agitated to the point where they can have excess firing and this can lead to seizures if it's really high but it also can lead to what's called encephalopathy where patients

become confused they become having an altered mental status they're disoriented you know what else it actually can do too besides the encephalopathy is it can actually cause asterixis you know if you take someone's hand you try to extend it they start kind of like beating like this so it can cause something called asterixis okay but these are some of the nasty kind of encephalopathic effects that you may have on the central nervous system as a result of uremia so one of the big complications is the nasty effects of uremia what else the kidneys they're so

good at being able to maintain our acid-base balance you know whenever the kidneys are naturally really functional and we need to be able to maintain our acid-base balance our kidneys should be able to excrete protons in the urine whenever we're in an acidotic state but if the kidneys are damaged you know protons are actually secreted primarily through an active process by the proximal convoluted tubule distal convoluted tubule portions and so what happens is if your kidney tubules are injured in an acute tubular necrosis your ability to excrete protons decreases and because of that the amount

of protons that accumulate within the blood go up what does this call whenever you have lots of protons that accumulate in the blood acidosis but if it's an acidosis and it's not due to a respiratory issue it's actually due to the kidneys or some type of other thing besides the lungs being involved what is this called a metabolic acidosis so this can lead to what's called a metabolic acidosis and what's the nasty effect of metabolic acidosis it can cause arrhythmias it can cause hypotension it can actually cause vasopressors to be not non-effective they're really nasty

stuff man a lot of electrolyte shifts as well okay so we have metabolic acidosis and uremia is another potential complication what else you know the kidneys are also good at being able to kind of get rid of excess fluid so they maintain our fluid balance not just acid-base balance but also fluid balance and so normally if for example our blood pressure was higher our body would try to say okay let's make a lot of urine right or if i needed to get rid of some sodium i need to get rid of some water and stuff

like that my body would my kidneys would be able to respond to that but if the kidneys are injured and they're not able to respond appropriately to hormones not able to kind of manage the normal water balance because the kidney tubes aren't just working very well what may happen to the amount of urine that you make what's the common theme of aki decrease urine output right if there's a decrease in the urine output you're not having as much fluid that's actually being released from the body and so effectively you may have more volume in the

body let's just use the example of water if you have a lot of water within the body because you're not getting rid of it because the kidneys aren't working well what happens to the overall fluid volume in the body become kind of volume overloaded and if you lead to volume overload what can that present as well it can present as edema right maybe in the lungs pulmonary edema maybe within the peripheral tissues leading to peripheral edema right so lower extremity edema maybe some abdominal ascites associated effects like that right so that's one of the big

things to think about so not only can an intra-renal aki particularly but akis in general complications can lead to uremia can lead to metabolic acidosis and volume overload what else i'm glad you asked you know drugs drugs are responsible a lot of drugs are actually renally excreted so they're excreted primarily in like the proximal convoluted tubule it's an active process but if the proximal convoluted tubular cells are jacked up and they're not able to take these drugs and excrete them into the actual urine what happens well they're not excreted because the kidneys aren't working well

to be able to excrete those drugs and so what happens to the actual drug concentration in the body it increases oh my gosh what happens if the drug concentration increases it depends what if you are taking an anticoagulant your kidneys all jacked up and now you got heparin that's actually accumulating tons and tons within the body oh no oh no what happens you can potentially develop a bleed you can become hypokind of coagulable and so because of that you can develop bleeds or what if you're taking a benzodiazepine for a little bit of anxiety but

you got jacked up kidneys and because of that you're not able to excrete a little bit of that benzodiazepine it accumulates it causes a significant amount of sedation or respiratory depression that can happen as well so you have to be thinking about that so another thing is it can lead to drug accumulation as well all right what else the last one that i want you guys to think about you know the kidneys are good at being able to maintain not only acid-base balance not only fluid balance not only a drug excretion not only removal of

nitrogenous waste products but also electrolyte balance you know the biggest one that i really want you to think about potassium so normally the kidneys are good at being able to excrete potassium into the urine when it needs to right so it's normally responsible for excreting potassium right but if the kidneys are injured especially in an intra-renal aki is it gonna be able to excrete potassium no so what happens to the amount of potassium that accumulates within the blood and ends up higher and if you have hyperkalemia especially really high levels that has some very deleterious

effects on the heart it can lead to some significant cardiac arrhythmias okay so it can lead to some cardiac damage it can lead to a lot of different arrhythmias right it may lead to bradycardia it may lead to some type of junctional rhythm it may lead to particularly maybe even some type of a heart block and maybe even put a patient into like v-fib so that's the big things to be able to think about so whenever somebody has this significant kind of hyperkalemia we know hey man there's a really bad kidney injury so what are

the complications that i really want you to remember that are associated with someone having a significant aki uremia metabolic acidosis volume overload drug accumulation and electrolyte abnormalities particularly hyperkalemia but if you want to go the extra nine yards you can also say hyper phosphatemia and then sometimes it can even have effects on sodium sometimes you may have some sodium retention sometimes you may actually get rid of a lot of sodium and so that could also affect your blood pressure as well okay i hope that part makes sense now what i want us to do is

finish up talking about the diagnosis of akis differentiating which one it actually is and then treatment all right ninja so we're at the diagnosis right so what we want to do is we want to talk about how do i know if somebody has an aki that's the first thing how do i know it's an aki second thing is how do i know which type of aki it is how do i know if it's pre-renal injury you know post-renal or if it's like chronic kidney disease and it's you know it's maybe an acute on chronic kidney

injury so that's something to think about obviously one of the easiest things is knowing a patient has a history of chronic kidney disease and then seeing that they have an aki could be a sign of acute chronic but nonetheless how do i go about diagnosing ak and then trying to figure out which one it is well first we have to know what is the actual true definition of an aki and the best one is the the kdigo guidelines and so the kdigo guidelines looks at uh particularly two things one is it says let's take a

look at what the creatinine is so the creatinine is usually elevated right in an aki according to the k-digo so we say this is the k-digo guidelines or the generally the most widely used ones so whenever the creatinine is elevated we know that there's an acai but like how much like at what point do i actually know that this is an aki well there's kind of a couple of definitions and there's a lot of staging we're not going to go through all of them i don't think it's necessary i want you guys to just remember

like two points about the creatinine when the creatinine increases we say if it's greater than or equal to 0.3 milligrams per dl usually within like the first like 48 hours so if we see an increase of 0.3 or more milligrams per deal of their creatinine let's say they came into the hospital two days later it was it was 1.0 and then now it's 1.3 that could be a sign of an aki an early stage right or we say we know what their baseline is and it's greater than 1.5 times their baseline creatinine and the higher

you go up the more severe it is for example if we say it's 1.5 to 1.9 times the baseline creatinine it's kind of like a stage one and then if you go to like two to three and then greater than three the more you go up the more times the baseline creatinine go up the more severe the aki okay and so generally we kind of say 1.5 greater than that at least you at least have a stage 1. so it goes 1.5 to generally 2 2 to 3 greater than 3. okay so these are kind

of two ways that we can look at it in response to creatinine the other way is urine output what's their urine output look like and the easiest way i like to remember that is that they're making less than 0.5 ccs per kilogram of body weight right and this is generally per like hour and we say that if it's at least for greater than or equal to six hours the longer you go obviously the worst case scenario it is so for example we say if it's greater than or equal to six hours that's like a stage

one if you're going up above 12 hours it might be a stage two if you're going up to 24 hours you're completely a nerd you're not making any urine then that's going to be getting into the severe stages third stage of aki so these are kind of your basic definition of aki so if i had a patient come in i'm looking at their actual labs you're more likely to diagnose it off the cranium oh their creatinine went up by 0.3 in the past 48 hours or they have 1.5 or greater times the baseline creatinine within

the past seven days that's also an aki or if they're in the hospital and you actually have like a foley catheter and they're monitoring their urine output daily you're seeing oh they've been making very little urine over the past 6 hours 12 hours 24 hours or they're not making any urine those can be signs of an aki so that's the first thing is this would be aki the next thing we have to say is okay what's the cause of the aki that's what i really want to get down to so the first thing that you

can do believe it or not it's a really quick easy thing is we can quickly rule out post renal it's usually the easiest one to rule out and one of the ways that you can do that is you can actually obtain like a renal ultrasound so you want to go through their history you want to go through your physical exam but a renal ultrasound versus like maybe a ct scan of like the abdomen and pelvis would be a way that you can quickly go about doing this okay so let's say that i got a renal

ultrasound or a you know ct of the abdomen pelvis and when i did i see that the person had some hydro nephrosis in other words it looked like their kidney was like ballooning up and we'll take a look at an image of a hydrogen of roses in a second but if they did have signs of hydronephrosis oh there's some plumping up of those good old kidneys the only reason that it would plump up or get filled with like fluid is that there's something that's causing an obstruction in the ureter or downstream from that and so

that may lead you right into saying ooh they may have a post renal aki and then you can start looking at their history oh do they have a history of bph oh do they have a history of prostate cancer are they taking any medications like totality and sulphinus and oxybutynin discontinue those you know do they have a neurogenic bladder is there a cause for them having this that they actually you know have some type of issue where they have a spinal cord injury they have parkinson's disease they have multiple sclerosis and that's the reason why

they have this neurogenic bladder you know do they have a kidney stone okay i got to fix the kidney stone do they have a tumor in their abdomen you can further evaluate that kind of based off of quickly looking do they have a renal ultrasound or a ct abdomen pelvis that shows significant hydronephrosis other things that you can easily do is check like a bladder scanner right that can maybe show that they have retention oh maybe there's something that's actually distal around the bladder neck or beyond that that's actually causing this so there's things that

help us to realize this but again quick easy one is checking a renal ultrasound ct audio and pelvis and again other things that you can add on that are commonly utilized is you can consider something like a bladder scan as well because this can help you to determine from like the neck down usually at the level of the bladder and down if there's something else wrong okay beautiful now that we've determined that we've kind of already said okay it's post renal aka and then we can go down the list of all the things ticking them

off oh it's not this it's not this it's not this or it's this okay we do the renal ultrasound or the ct abdomen pelvis and we see that there is actually no hydronephrosis so there's no or negative hydro nephrosis well then the next thing we can say is okay there's no hydronephrosis do they have is this just a chronic kidney disease do they have a history of chronic kidney disease hmm okay what if they did what if they have a history of ckd and then you also get the ultrasound of the ct of the abdomen

and pelvis and you see that they have very small atrophic kidneys in that situation you might say oh this may be ckd and that's it all right so sometimes you just have to kind of go through that list all right so we have a patient who has some signs of aki we got the real ultrasound we got hydronephrosis ooh maybe it's post renal go through all their particular history and physical exam medication list oh they don't have hydro well do they have a history of ckd that you can think of do they have small atrophic

kidneys it's probably just ckd and that's right the way they have this azotemia okay what if they have completely normal like looking kidneys like on the ultrasound they have normal looking kidneys so normal kidneys like they look completely normal there's no abnormal abnormalities no structural abnormalities no hydronephrosis they're not small they're not atrophic there's nothing like that they're just normal good old kidneys okay well in that case what's the next test that i do this is not something that we classically do in practice but it's what you're going to be needing to know for your

exam and your boards is that we may go to doing what's called a urinalysis so a ua with microscopy and you might do this with microscopy okay when you do a urinalysis with microscopy what you're looking for is particular things that may pop up right if so for example let's say that you had an abnormal urinalysis an abnormal urinalysis and let's just say for example you got white blood cell casts that show up in the actual ua you have some bacteria that show up within the ua you have your leukocyte esterase that are positive you

have nitrites that are positive what may that be due to oh i may be good to a good old infection right maybe you have some type of pylonephritis sometimes that can cause an acute kidney injury right because we said infections may lead to like some type of acute interstitial nephritis maybe right all right or maybe sepsis sometimes you can get euro sepsis right but another thing is what if we had someone who had white blood cell casts you know this is one we didn't talk about you know in acute interstitial nephritis you get a lot

of inflammation but you know the particular types of cells that love to migrate to the area of the kidney tubules when there's lots of inflammation because it's a hypersensitivity reaction eosinophils eosinophils love to come to that area and so some of the eosinophils when they come into the area of the actual kidney tubules and interstitial fluid around the kidney tubules they get lost into the urine sometimes so you get white blood cell casts and what's called eosinophils in the urine we call that eosinophiliuria okay what could that be indicative of acute interstitial nephritis right acute

institutional fighters what do you got to think about drugs ppis right particular types of beta-lactams do they have an infection is there some type of bacterial fungal viral do they have sarcoidosis amyloidosis do they have lupus things of that nature okay what else what if i had some red blood cell casts and i had some dysmorphic red blood cells right and let's say that this person also has protein urea lipid urea they got some really weird like looking lipid casts and stuff like that what could that be what could that be glomerulonephritis maybe so if

it is you're suspecting glomerulonephritis or kind of maybe like a vascularity of some relationship this isn't where you end unfortunately you may have to go the level of like it's called a renal biopsy and then when you renal biopsy and do serology tests that may lead you to say oh this is either glomerulonephritis versus some type of vasculitis okay now we've gone that way we say okay abnormal ua it showed potentially pilo or it should acute interstitial arthritis or show glomerulonephritis or vasculitis what if you had somebody who had these things called muddy we already

talked about these before but muddy brown cast this is kind of like one of those buzzword terms you don't want to forget muddy brown cast that clogged up the kidney tubules caused the increased pressure and intra-renal aki acute tubular necrosis right we talked about that one acute tubular necrosis this is most specific and whenever you have acute necrosis what kind of aki is that intrarenal aki what were all of these that we talked about glomerulonephritis versus vasculitis this was kind of a particular type of intrarenal aki ain is an intra-renal aki pyelonephritis may lead to

an intra-renal aki and then this also may lead to an intra-renal ki so whenever you're going to this point here where you've got near normal kidneys you're at the ua with microscopy you're trying to differentiate is this an intra-renal or a pre-renal aki okay we've gotten to that part what if the ua that we got is completely normal they are like a normal urinalysis it's completely normal all right if you have a normal ua the next thing you go to is you check what's called urine electrolytes okay you check the urine electrolytes because this may

help to differentiate some of the pre-renal insurance like hi big thing to remember this is not commonly clinically used actually some of the guidelines say not to use the urine electrolyte studies because they're not super effective in differentiating pre-renal and adrenal ki but it's something that you need to know for your exams so if you check the urine electrolytes okay let's take for example we have a patient who has a urine sodium that is low they have a phenol that is less than one percent they also have a urea a urine osmolality that's greater than

500 and their urine their urea concentration within the urine their fractional excretion of urea is also going to be low what does this make you think of pre-renal aki right this should make you think of pre-renal aki and then you have to get down to the bottom of it you get okay is this pre-renal aki that this patient has is it due to what's going on is there some type of volume issue so in other words you got to determine okay is this some type of issue where they have their what's called hypervolemic right and

this is usually those cases of like chf hepatorenal syndrome nephrotic syndrome things of that nature or is this a case where they're actually like hypovolemic their total body volume is low and those were your burns your vomiting your diarrhea right it was the diuretic use blood loss so on and so forth now in the other part of the test you have someone that actually has a urine sodium that's opposite that's actually high greater than 40 generally a fractional excretion of sodium that is greater than 2 percent a urine osmolality that's less than 350 and a

urea excretion that's actually higher what would this make you think of an intra-renal aki so this would make you think about acute tubular necrosis all right so let's talk about the treatment of acute kidney injury now we talked about the diagnosis above now again keep in mind that when we talk about the diagnosis this is the way that you would go about in a textbook kind of way that's not always the way that we actually go through in a clinical scenario so remember the urinalysis urine electrolytes at that part it's not always like that in

the clinical scenario and actually the guidelines say that you shouldn't actually stick to utilizing the urinalysis and the urine electrolytes is differentiating the two between intra-renal and pre-renal and so we'll briefly talk about the actual true like best clinical way about going about this evidence-based practice but also making sure that we're hitting the things that you need to know for your exams so when i talk about differentiating pre-renal and entrepreneurial ki it's actually kind of how they respond to treatment therapies is really the best way looking at their history looking at their physical exam as

well so let's say that i have a patient who i suspect has a pre-renal aki right and and i know that they have an underlying history of heart failure right i know that they have an underlying history of heart failure they have signs of heart failure they have a particular physical findings of heart failure and they have a low ejection fraction if that's the case then i know that this person would not respond to fluid that would actually maybe even make them a little bit worse it would actually cause them to maybe develop a little

bit more pulmonary edema but the problem is is that again pre-renal we think about low blood volume low blood flow so we constantly say give fluid in a person like this it actually might not help it actually may make worse because it might not augment their blood pressure and these individuals you actually want to try to get rid of some of that excess fluid pull it into the vasculature get rid of it out of that third spacing fluid and so in these patients with cardiorenal syndrome it's actually best to consider something like diuretics for the

hypovolem hypovolemic state that they're in and all that third spacing of fluids and the second scenario you also want to try to augment their blood pressure not with fluid but with inotropic agents give them drugs that will actually cause their heart to contract a little bit more if they need a little bit of work so giving them an inotropic agent or a vasopressor of some kind dobutamine milranone digoxin maybe even something like norepinephrine or epinephrine those things may give it a little bit more kick and increase the profusion to the kidneys right so that's one

way we try some diuretics we try an ionotrope we increase their blood pressure a little bit and we pull off excess fluid and their creatinine improves their urine output improves hey that was their cause of the aki pre-renal if they have a patel renal syndrome so you know that they have an underlying history of liver failure and hepatic portal hypertension and we know that they have this issue of low albumin but we can make sense of this as their potential cause in that situation you actually want to trial something called octreotide and octreotide is basically

it inhibits that splenic vessel it inhibits those vasodilatory chemicals and so it inhibits the effect of dropping systemic blood pressure right and then you can also give another drug that tries to be able to cause systemic vasoconstriction rather than just solely renal artery vasoconstriction and this is called midadrene so midadrene will cause systemic artery vasoconstriction octagotide will actually inhibit those vasodilator chemicals that are released by the liver and that's another problem with the liver if it's damaged it doesn't make albumin so it doesn't keep fluid inside of the vessel and so in those cases you

can also give them albumin to be able to keep some of that fluid inside of the blood vessel as well okay so that's what we do for a patterinal syndrome okay so if you tried some octotide submitted drain some albumin and it improved oh that was the cause all right cool sepsis they have sepsis you maybe see signs of hypotension they have fever they have positive blood cultures uranalysis whatever it may be you find a pneumonia a septic focus somewhere and you obviously have evidence of sepsis and septic shock and these patients you have to

treat their underlying cause of sepsis maybe that requires antibiotics and maybe you have to augment their distributive shock their low blood volumes because they're third spacing fluids with iv fluids in this case and maybe you have to give them some vasopressors to be able to increase their blood pressure so give them fluids to try to keep their effective arterial blood volume up and give them vasopressors to be able to squeeze on those vessels to increase the pressure to increase the perfusion to the kidneys and then antibiotics to treat the underlying cause for hypovolemia where they're

just they have low volume states encourage fluid intake give them iv fluids if need be or po intake have them just drink some fluids and if that's the case if you have them drinking more fluids and it's increasing their blood volume increasing their blood pressure they're perfusing the kidneys they're making more urine they're getting rid of the excess urea and creatinine it improved their renal function so sometimes one of the easiest ways to determine if it's pre-renal and intra-renal is you can look at their history and say okay i think that they would respond to

some fluid i give them fluid they improve oh maybe it was a pre-renal of a hypovolemic category oh i'm going to give them fluid they didn't really get any better actually made them a little bit worse okay let's try some diuretics and some blood pressure augmentation oh that got them better oh maybe it was a pre-renal they could have a cardiorenal type or maybe hepatorenal syndrome or maybe a septic kind of patient so that's kind of the way that we go about this an intrarenal aki it's actually a little bit different these patients that's usually

because of some type of offending agent whether it be a drug whether it be some type of like you know process that we talked about with atn ain and glamailonephritis and thrombotic microangiopathies atn is the biggest one that i want you to remember what actually is the best test is giving them what's called frozamide seeing how they respond to frostbite if their kidneys are working and they're not damaged they'll make urine but if you give them ferociamide and they don't make any urine or they make very little urine their kidneys aren't working and it's likely

an intra-renal aki that's a quick easy test right it's called the furosemide stress test it was validated in studies and so what we do is with atn we have to figure out what the underlying cause is so what's the biggest one those nephrotoxins stay away from those sons of guns right stay away from the contrast i have able reduce the concentration of the vancomycin discontinue if it's not necessary consider another antibiotic instead of aminoglycosides right those are things to think about the other thing is is there anything what about hemolysis treat the underlying cause of

the hemolysis if they have rhabdo what do you do for rhabdo though rhabdo in early stages before it really hits the kidneys you may be able to augment that with iv fluids they may actually improve a little bit of iv fluids for a patient with tumor lysis syndrome what do you give them you give them something to tie up that uric acid resburicase actually and then maybe if somebody has like multiple myeloma you actually have to give them like chemotherapy so again it's treating the underlying cause but remember that atm is probably one of those

that if it's not treated if it's not reverse if you don't fix the underlying cause it actually could potentially progress to a very severe renal failure that requires dialysis actually okay acute interstitial arthritis it's again discontinuing the nephrotoxic agents right so getting rid of um you know beta-lactam antibiotics ppis right different things like that um it's also considering you know is there any underlying infection treat the infection is there any type of inflammatory process sarcoidosis amyloidosis lupus something like that maybe they may respond to a little dose of steroids right um thrombotic microangiopathies and glamorous

arthritis you have to treat the underlying disease you have to figure out what was the actual cause is it hus is it ttp is it hypertensive crisis is it nephrotic syndrome nephritic syndrome all of those things that's not something that we're going to go into right now but sometimes these are you know kind of like autoimmune diseases so they might respond to steroids plus or minus what's called d-mars so things like methotrexate mycophenolate cyclospora and things like that right okay last but not least is post-renal ak which is going to be the least common but

again we go through that process there is an hydronephrosis think about their medication history think about their medical history go through those things and think about it right so if a patient has a post renal aki and you suspect it and you think oh they have bph that's probably why what can i do to help someone with urine retention from severe bph i can give them things called alpha one blockers tyrazosine prazisin tamsilosim those basically work on the sphincter and cause that sphincter to do what relax a little bit so that you can get the

urine out of the bladder sometimes you may even try what's called five alpha reductase inhibitors finasteride deuterostide right those help to be able to kind of decrease the stromal development of the the actual prostate gland take a long time though but sometimes in the interim because these do take a decent amount of time to work you may have to do what's called catheterization okay so may have to do what's called a catheterization and this may be something like what's called a foley catheter or intermittent kind of straight catheterization to be able to relieve that urinary

retention what if they have like a tumor well you gotta figure out what the underlying cause of the tumor is then it can be treated do they have a kidney stone sometimes with stones you can actually put in a stent they may pass it on their own sometimes if it doesn't work with the stint maybe you have to do what's called a perk percutaneous nephrostomy sometimes that might actually work and then again discontinuing the offending medication what are the most common uh medications that i want you guys to remember the anticholinergics right tulteradine sulfenasan oxybutenin

getting rid of those medications that are used to treat incontinence but actually there's maybe just too much of the dosage or for whatever reason it's causing a little bit more retention unfortunately okay another thing make sure that if they have a foley catheter make sure that sound of a gun is actually working and it's flushing and it's actually appropriately get draining urine and there's not something that's actually causing obstruction it's kinked it's not in the right place sometimes that's the simplest thing to actually fix okay you have a patient that you've gone through you determine

what kind of aki they have you treated it but they have such significant kind of complications associated with it and what's the one that most likely will lead to these nasty complications that we talked about intrarenal aki it's by far the most common so in intra-renal aki what happens is the kidneys become so dysfunctional that they respond and not being able to secrete protons and this leads to a significant acidosis or they have significant inability to be able to excrete particular types of electrolytes and you know which one is the biggest one potassium is enough

severe hyperkalemia or they're actually having high levels of drugs so intoxication we'll say and this is usually due to high drug accumulation or maybe they took some drug and they weren't able to actually reverse it or maybe there was no kind of ability for charcoal lavaging and at this point in time the drug accumulation is so high you have to put them on dialysis or they're so volume overloaded because their kidneys just aren't able to maintain that fluid balance well or you have really really bad uremia uranium encephalopathy uremic pericarditis or platelet dysfunction it's all

jacked up now in those kinds of situations and the kidneys aren't working you have to create a kidney for them and that's where basically imagine here imagine here's our blood vessel right so imagine for a second this is the superior vena cave and this is the inferior vena cava and imagine you take a catheter right so here's like a catheter and this catheter i'm going to have it pull blood from the inferior vena cava right pulling blood from the inferior vena cava and then here i'm going to have one that kind of takes it back

to the superior vena cava okay imagine this thing runs through kind of like a like a colander right here like imagine this okay imagine there's like a little colander here and what happens is i'm going to take and remove blood from the actual ivc okay so blood's going to be coming from the ivc and this blood's going to be nice and dirty it's going to have lots of acid like lots of protons lots of abnormal electrolytes that are accumulated in excess potassium maybe drug accumulation maybe an excessive amount of fluid that they have that you

want to pull off or maybe they have lots of urea and creatinine that's building up you pull that out of their actual venous system and into this kind of like uh structure here this colander and what happens is this colander has an ability to remove imagine there's like a little tube here there's like a little tube here and there's like little holes along the length of this what happens is as this is actually running through this colander to kind of get back to the venous circulation which will go this way it pulls off some of

that excess fluid some of that excess acid some of the excess electrolytes some of the drugs all of those different things and it gets kind of sucked out of that and then what happens is this thing this colander is so cool that it also has the ability to put some fluid back in put some actual solutes back in some albumin back in and help to just make sure that the blood is the way it should be nice and clean and then it sends it back to the superior vena cava what's this called this is called

dialysis and so dialysis is one of the ways that we may have to treat a patient who develops this very severe acute kidney injury and what are the ways that we can do this you know there's two ways continuous renal replacement therapy which is what it sounds like you're continuously doing dialysis over a long period of time and very slow intermittent hemodialysis you're doing it like every other couple days okay for continuous renal replacement therapy this is for patients who are really kind of like hemodynamically unstable so for example you may only pull off 50

cc's of fluid every hour 100 ccs of fluid every hour and the patient can tolerate that because if you pull a lot of fluid off at once what may you do to their blood pressure drop their blood pressure what if the person's already hypotensive you pull a little bit too much fluid and you drop their pressure crt continuous renal replacement therapy allows for very slow pulling off of fluid which is very good in patients who are a little already hypotensive and hemodynamically unstable for intermittent hemodialysis you actually take off more larger volumes of fluid significant

fluid shifts so if that's the case you would want someone who's a little bit more hemodynamically robust or hemodynamically stable that they could tolerate pulling off like a liter of fluid in one day okay and in a short period of time like a couple hours and so if they can tolerate that you'd go with intermittent hemodialysis if they're a little bit more shocky hemodynamically stable hypotensive continuous renal replacement therapy may be the way to go and then eventually once they become more hemodynamically stable you may just switch them to doing intermittent hemodialysis every couple days

and then maybe every once a week if they start improving okay so this is the basic conversation that we're going to talk about with acute kidney injury [Music] you