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0:03
On the nefrology ward, two people came in. The first one is 55-year-old Matilda, who came in with oligura, fever, and a rash on her arm. Matilda also has a history of taking NSAIDs for her knee pain. The second one is 34year-old George, who came in with oligura hypotension tacocardia and cold extremities. George says that he's also been having diarrhea for a few days now. Bun and creatinine levels were high for both of them. Both Matilda and George have renal failure.
0:38
Now renal failure is when the kidneys are not functioning properly. Before talking specifics, let's remember some basic renal physiology. Now the kidney's job is to regulate what's in the blood. So they might remove waste or make sure electrolyte levels are steady or regulate the amount of water and even make hormones like ariththropoin which stimulate red blood cell production. All right. So blood gets into the kidney through the renal artery into clumps of arterials called glomemeuli where
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filtration happens. After filtration the stuff that gets filtered out which is called the filtrate moves into the renal tubules where reabsorption and secretion of fluid and electrolytes happen. Along with fluid and electrolytes though waste containing compounds are also filtered like ura and creatinine although some ura is actually reabsorbed back into the blood whereas only a tiny bit of creatinine is reabsorbed. In fact in the blood the normal ratio of blood ura nitrogen or bun to creatinine
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is between 5 and 20 to1 meaning the blood carries 5 to 20 molecules of ura for every one molecule of creatinine. And this is a pretty good way to assess kidney function. So when we want to check renal function, we look at BUN and creatinine levels. And if there's something wrong, then levels of both BUN and creatinine will be high. Enjoying our osmosis videos? Unlock your full potential with an Osmosis subscription. Get unlimited access to every Osmosis feature and
2:12
resource with a free 7-day trial. Now back to renal failure. There are two types of renal failure, acute and chronic. Acute renal failure is also called acute kidney injury. This is when the kidney is not functioning at 100%. And that decrease in function develops relatively quickly, typically over a few days. In this case, the individual typically presents with oligura, even anura, and levels of bun and creatinine will be high. Then there's chronic kidney failure
2:46
which is now called chronic kidney disease. This is when the kidney function gradually decreases over a minimum of 3 months. This is usually caused by hypertension, diabetes mellus or congenital renal conditions. Both acute and chronic renal failure have some pretty dire consequences. A lot of things that the kidneys normally excrete are now stuck in the body. First, hydrogen ion secretion is impaired and this can lead to metabolic acidosis. Secondly, potassium excretion is also
3:19
impaired and this can lead to hyperc calmia. Now, in certain cases like heart failure, pulmonary edema or hypertension, the kidney will retain more water and sodium. So, the individual can present with peripheral or perorbital edema. Next, there's uremia which is caused by the accumulation of uremic toxins including ura itself. Symptoms include nausea and anorexia. Another sign of uremia is bleeding and easy bruising and that's due to platelet dysfunction. There's also uremic paricarditis which
3:54
is the inflammation of the paricardium. Next there's uremic neuropathy affecting the central and peripheral nervous system. Clinically there's progressive encphylopathy and that causes asteris which is a tremor in the hand when the wrist is extended just like a bird flapping its wings. Finally, renal failure can also increase lipid synthesis in the liver causing hyper lipidmia especially hyper triglyceridemia.
4:24
Now chronic kidney disease can lead to even more problems over a long period of time. If a child is affected, it can lead to growth retardation and developmental delay, especially in individuals that had to undergo dialysis. Another important fact for your exams is that there's also ariththropoin deficiency and this leads to anemia. Finally, there's renal osteodistrophe and this happens for a number of reasons and it's important to memorize all of them. First, the kidneys cannot excrete
4:54
phosphate leading to hyperphosphatmia. Next, the kidneys are needed to convert 25 hydroxy vitamin D to active 125 dihydroxy vitamin D or calcatrial, which is the active form of vitamin D, which helps with intestinal calcium reabsorption. As a result, there'll be hypocalcemia. Now, since there's too much phosphate and too little calcium, this can affect the bones and they can become thinner and more prone to break. Hyperphosphate and hypocalcemia also triggers the
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parathyroid glands to release more parathyroid hormone which is a hormone that causes increased bone breakdown to release more calcium. Finally, the extra phosphate in the blood can also bind to calcium and they can deposit in various tissues like the vascular tissue. Okay, now that we've gone over the general pathology, let's look at some specific causes of acute kidney injury. There are three types of acute kidney injury or AKI. prenal AKI, intrarenal AKI, and post-rrenal AKI.
6:00
With prenal AKI, the cause is decreased blood flow into the kidneys. Now, since less blood's going to the kidneys, this means that less blood is being filtered. So, there's a decrease in the glomemeular filtration rate or GFR, which is how much blood, usually in milliliters, the kidney filters through the glomemeuli per minute. If less blood is being filtered, that means that less ura and creatinine are filtered out and more stays in the blood. So levels of bun and creatinine will be high.
6:32
Also with less blood being filtered, the kidneys activate the renan angotensin system which causes aldoststerone released by the adrenal glands. This hormone tells the kidneys to reabsorb sodium. When sodium gets reabsorbed, water gets reabsorbed as well. Water and sodium reabsorption is also tied to ura reabsorption. So in this situation, ura gets reabsorbed and so even more ura gets into the blood resulting in a bun to creatinine ratio of greater than 20 to1.
7:01
Now looking at the urine more sodium is being retained. So the urine sodium is usually less than 20 mill equivalents per liter. The ratio of sodium excreted to total sodium filtered or fna is usually less than 1%. And finally that urine is more concentrated because less water is excreted. So typically the urine's greater than 500 millos moles per kilogram. Prennal AKI can happen in hypoalmic states like an acute hemorrhage, gastrointestinal losses like diarrhea
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and vomiting and renal losses like with diuretics. All this can lead to hypoalmic shock. In a hypoalmic state, the individual presents with tacocardia, hypotension, reduced skin tur and cool extremities. Now, prenal AKI can also happen with hypervalmic states where there's a low effective circulating volume. One example is severe systolic heart failure leading to not enough blood getting pumped to the kidneys. When this happens, it's called cardioral syndrome.
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Finally, systemic vasoddilation like with sepsis can lead to prenal AKI. Next, there's intrinsic or intrarenal AKI which is due to damage to the tubules, the glomemeilus or the kidney interstitium, which is the space between tubules. In general, with intrarenal AKI, there's kidney damage causing them to lose the ability to filter blood and secrete or reabsorb materials like normal. If ura is not reabsorbed, less ura stays in the blood relative to creatinine and the bun
8:39
to creatinine ratio falls to less than 20 to1. Also, renal tubule cells cannot reabsorb sodium, meaning the urine sodium goes above 40 mill equivalents per liter and the fea goes above 2%. And finally, since water is not being reabsorbed as much, urine osmolality falls below 350 millos moles per kilogram. All right. Now, the most common cause of intrarenal AKI is acute tubular necrosis or ATN, which causes damage to the tubules. Often, ATN is due to eskeeia from a prenal acute kidney injury. On
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your tests, make sure you don't confuse this with prenal AKI where there's decreased filtration of blood, but the kidneys are not damaged. In ATN, there's severe eskeeia leading to the death of tubular cells. The proximal tubular cells and the thick ascending limb cells are highly susceptible to injury and that's because these cells receive their blood from vaserecta which are tiny capillaries located in the medela of the kidney. In this particular zone, the blood flow is
9:44
relatively slow to allow for the countercurren multiplication mechanism to work properly. The other way tubules can be damaged is via nephrotoxins like contrast dyes, amoglycosides, antibiotics, cysplatin, heavy metals like lead, myoglobin from damaged muscles like in rabdtomyolysis, ethylene glycol or radiocontrast dye and hemoglobin ura that's usually associated with hemolytic anemia. The proximal tubial cells are particularly susceptible to nephrotoxin injury.
10:21
Now ATN usually has three stages. The first one is the inciting event or the trigger that causes damage to the tubules. Next there's a maintenance phase also called the aliguric phase which usually lasts from 1 to 3 weeks. This is when the kidneys are not working. And here there's a risk for developing electrolyte disturbances like hypercalemia because potassium is not effectively secreted, metabolic acidosis because acid secretion is impaired and uremia which is when there's too many
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waste products retained. Finally, there's the recovery phase which is when the kidneys start working because the tubular cells begin a process of re-epithelization, meaning new functional cells are born. As a result, creatinine and BUN levels fall and there's polyura. Also, for your tests, remember that in this phase, there's a risk for developing hypocalemia because too much potassium is excreted. This time, there can be wasting of other electrolytes or minerals as well. Remember for your
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exams that on microscopy there are muddy brown granular epithelial cell casts along with renal tubular epithelial cells. All right, moving on to another cause of intrarenal AKI, which is acute interstitial nefritis. This is an inflammation of the renal interstitchum over the course of days to weeks. It's thought to be a type 1 or type four hypersensitivity reaction and is typically a response to a medication like NSAIDs, in which case it's called analesic neuropathy, penicellin,
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rafampen, proton pump inhibitors, and diuretics. After the sessation of the offending medication, symptoms of acute interstial nefritis typically resolve completely. In rare cases, the inflammation in the interstitium can be caused by systemic infections like infections with myopplasma or autoimmune conditions like shogrin syndrome, sarcoidosis or systemic lupus hematitosis. It can be asymptomatic but for your exams remember that can also present symptoms like fever, rash, hematuria,
12:26
pyura and costtovertebral angle tenderness. With acute interstitial nefritis the blood count shows eosinophilia and the urine microscopy shows white cells, white cell casts and red blood cells. Another type of intrarenal AKI is acute glomemelon nephritis which is when the glomemerieli are damaged by inflammation. Acute glomemeular nephritis can be caused by rapidly progressive glomemeular nephritis which is when the inflammation in the glomemeilus is so severe that it breaks the glomemeular
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basement membrane and as a result the kidney function decreases rapidly in a matter of days to weeks. Another cause of acute glomemeular nephritis is hemolytic uremic syndrome which is caused by bacteria like e.coli0157H7. for your exam. Remember that it's characterized by hemolytic anemia, thrombocytoenia, and acute kidney injury. Another clue is that the person might have had bloody diarrhea for a few days prior to the oligura. Next up, there's diffuse cortical necrosis, which is when there's
13:29
generalized cortical infuction of both kidneys. This happens because of a combination of vasospasm and disseminated intravascular coagulation or DIC where tiny thrombi blocks some of the arteries in the kidney and so the kidneys don't get any blood in that area. This can be associated with abstetric complications like abruptio placenti where there's massive blood loss that can lead to both vasospasm and dic. It can also be associated with septic shock which also causes DIC.
14:00
All right. Next, there's renal papillary necrosis where the renal pilli are damaged and tiny parts of them can be eliminated in the urine. So, they're sloughing of the renal pilli. This is usually a consequence of eskeemia because the arteries supplying the renal pilli are tiny. So, they're prone to obstruction. Now, renal papillary necrosis can be associated with cickle cell disease because the abnormal red blood cells can build up and obstruct the arteries that supply blood to the renal pilli.
14:29
It can also be due to acute pyonfritis because the inflammation can obstruct those arteries. Another cause is the use of NSAIDs because they block the synthesis of prostaglandins that keep aphrant arterials dilated. In other words, lack of these prostaglandins causes vasoc constriction of the apherant arterial and therefore decreased glomemeular filtration rate. So when there's reduced blood flow through the renal artery which is particularly common in the elderly and individuals with underlying
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heart, liver or kidney disease, vasoc constriction of the apherent arterial can lead to renal papillary necrosis. Finally, diabetes mellus can lead to papillary necrosis due to the vascular damage it induces. Let's move on to post-renal AKI which is caused by an obstruction in the outflow of urine from the kidneys which causes a buildup of urine that backs up into the kidney. Now BU to creatinine ratio FEA and urine sodium largely depend on if the tubules are working or not. So for
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your test simply remember that these three parameters can vary. Just as with the others, less water and fluid being reabsorbed causes the urine to be less concentrated and urine osmolality falls below 350 millos moles per kilogram. Postrenal AKI is most frequently due to benign prostatic hyperplasia or prostatic cancer in a male, both of which lead to compression of the urethra. This can lead to frequent urination but a slow urinary stream and a low volume of urine excretion.
16:01
Finally, there are kidney stones that can get stuck in either urer or in the urethra. Now, if only one urer is obstructed, it's called unilateral obstruction and the other kidney is working fine, then renal function is usually preserved. But if both uriters are obstructed, it's called bilateral obstruction. All right, as a quick recap, consequences of renal failure include metabolic acidosis, hyperc calalemia, sodium and water retention, hyper lipidmia and uremia for both acute and
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chronic kidney failure. Chronic renal failure leads to growth retardation and developmental delay along with ariththropoin deficiency and renal osteodistrophe for chronic kidney disease. All right. Now, acute kidney injury can be prenal when there's decreased blood flow to the kidneys. Labs here show high levels of BUN and creatinine. BUN to creatinine ratio of greater than 20 to1. Urine sodium is less than 20 mill equivalents per liter. FNA less than 1% and urine osmolality
17:02
greater than 500 millos moles per kilogram. Intrarenal AKI due to damage to the tubules, the glomemeilus or the kidney interstitium. Labs show high levels of BU and creatinine. Bun to creatinine ratio less than 20 to1. Urine sodium above 40 mill equivalents per liter. FENA goes above 2% and urine osmolality falls below 350 millos moles per kilogram. Causes of intrarenal AKI include ATN, acute interstatial nefritis and acute glomeular nephritis. With postrenal AKI, there's an
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obstruction in the outflow of urine. Labs show urine osmolality below 350 millosm moles per kilogram, but the other values might vary depending on if there's damage to the kidneys themselves. Okay, so back to our cases. Matilda came in with oligura, a fever, and a rash on her arms. And the lab showed that she had high levels of BUN and creatinine. Oh, and she's also taking NSAIDs. Further lab work showed that she also had eosinophilia, bun to creatinine ratio less than 20 to1, urine sodium
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above 40 mill equivalents per liter, fea above 2%. And urine osmolality below 350 millos moles per kilogram. She also had pyura and white cell casts. So we can say that Matilda has a case of intrarenal AKI caused by interstitial nefritis which in turn is caused by NSAIDs. So this is analgesic nefropathy. In this case, NSAIDs are stopped and the problem eventually resolved. Next, there's George that came in with oligura hypotension tacicardia and cold extremities and has also been
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having diarrhea for a few days. BUN and creatinine were high and further lab work showed BU to creatinine ratio greater than 20 to1 urine sodium less than 20 mill equivalents per liter FNA less than 1% and urine osmolality greater than 500 millos moles per kilogram so it's a case of prenal AKI caused by diarrhea we should rehydrate him
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