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.
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.
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.
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.
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!
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