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Renal tubular acidosis
Minimal change disease
Focal segmental glomerulosclerosis (NORD)
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Acute tubular necrosis
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Nephroblastoma (Wilms tumor)
Posterior urethral valves
Hypospadias and epispadias
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
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|Blood urea nitrogen||36 mg/dL|
|Dysmorphic red blood cells||Absent|
|Sodium (UNa)||15 mEq/L|
|Fractional excretion of sodium (FENa)||<1%|
|Urine osmolality||650 mOsm/kg|
postrenal azotemia p. 626
postrenal azotemia p. 626
Tanner Marshall, MS
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.
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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