Postrenal azotemia

Definitions & Key takeaways

Postrenal azotemia is a condition characterized by an excessive level of nitrogen-containing waste products in the bloodstream (azotemia) due to obstruction of the urinary tract. Postrenal azotemia can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Postrenal azotemia can lead to kidney failure if left untreated. Treatment typically involves medical or surgical interventions to remove the obstruction.

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Introduction0:00–0:39

Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function develops relatively quickly, typically over a few days.
Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function.
AKI can essentially be split into three types, prerenal AKI meaning the cause of kidney injury’s coming before the kidneys, postrenal AKI—meaning after the kidneys, or intrarenal AKI—meaning within the kidneys.

Physiology0:39–2:01

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 overall amount of water, and even make hormones - the kidneys do a lot of stuff!
Blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where it’s initially filtered, with the filtrate, the stuff filtered out, moving into the renal tubule.
Sometimes fluid or electrolytes can move back from the filtrate into the blood - called reabsorption, and sometimes more fluid or electrolytes can move from the blood to the fitrate - called secretion.
Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed.
In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good diagnostic for looking at kidney function!
Ultimately the filtrate is turned into urine and is excreted from the kidney through the ureter, into the bladder, and peed away.
Meanwhile, the filtered blood drains into the renal vein. Alright, so with postrenal AKI, there’s some obstruction to the outflow from the kidneys.

Causes2:01–2:51

Reduced flow can be a result of something compressing the ureter like intra-abdominal tumors, or compressing the urethra further down, like from benign prostatic hyperplasia—a noncancerous growth of the prostate gland, both of which sort of pinch the ureter or urethra shut.
Also though it could be some blockage inside, like kidney stones getting stuck in the ureter or urethra, which actually plug it up.
Now, if only one ureter’s obstructed, called unilateral obstruction, and the other kidney’s working fine, then renal function’s usually preserved.
If, say, both ureters are obstructed, called bilateral obstruction, or the urethra gets blocked, then we’ve got a recipe for postrenal AKI.

Pathophysiology and diagnosis2:51–5:36

Whatever the obstruction is, it ultimately causes this buildup of urine and pressure that backs up into the kidney; all the way to the millions of tiny renal tubules.
Normally, filtratration moves fluid from the relatively high pressure arteriole to the low pressure renal tubule, but this backup causes an increase in renal tubule pressure, which reduces the pressure gradient and lowers the amount of fluid that filters across which lowers the glomerular filtration rate, or GFR, which is how much blood the kidneys filter in mL through their glomeruli per minute.
This means that less waste products like urea and creatinine are filtered out of the blood, meaning more stays in the blood, which leaves people with azotemia or high levels of nitrogen-containing waste compounds in the blood, as well as oliguria—low levels of urine.
Now if we follow the stuff that does make it into the tubule, which also includes things like sodium and water, it turns out that the high pressure tubular system essentially forces more reabsorption of sodium, water, and urea, but not much creatinine because remember little to no creatinine gets reabsorbed.
Now this increased urea reabsorption relative to creatinine increases the BUN to creatinine ratio in the blood, typically making it greater than about 15 to 1.
Also, while the tubules aren’t functioning normally and reabsorbing appropriately, the urine sodium is typically less than 20 mEq / L, since most of the sodium’s being reabsorbed, which means that the fraction of sodium excreted to sodium filtered, or FENa is usually less than 1%, And finally since most of that water and fluid is being reabsorbed as well, the urine’s typically pretty concentrated, usually greater than 500 mOsm / kg.
Alright so I say “normally” because, over time, the increased pressure damages the epithelial cells responsible for reabsorption in the tubules.
When that happens, less and less urea gets reabsorbed back into the blood and instead stays in the tubule and then gets dumped out into the urine, and this causes the BUN:Cr ratio to fall below 15 to 1.
Also, in the same way, less sodium is reabsorbed, so more gets excreted and urine sodium goes above 40 mEq/L and FENa goes above 1% in mild cases, but in severe cases it can go above 2%.
Finally, just as with the others, less water and fluid being reabsorbed causes the urine to be less concentrated, and urine osmolality falls below 350 mOsm/kg.

Review5:36–6:15

Alright, so as a quick recap, postrenal acute kidney injury is where the kidneys aren’t functioning at 100%, and this is due to some obstruction in the ureters that blocks the flow of urine.
Now that you know all about postrenal AKI, check out these other two videos on prerenal AKI and intrarenal AKI! Thanks for watching, you can help support us by donating on patreon, or subscribing to our channel, or telling your friends about us on social media.