prerenal azotemia


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Related to prerenal azotemia: postrenal azotemia

non·re·nal az·o·te·mi·a

, prerenal azotemia
nitrogen retention resulting from something other than primary renal disease.

prerenal azotemia

Renal underperfusion Nephrology The most common form of acute renal failure, characterized by ↑ nitrogenous waste, due to ↓ blood flow to the kidney Lab ↑ nitrogenous wastes–eg, creatinine and urea, which act as poisons when they accumulate in the body, damaging tissues and compromising organ function Risk factors ↓ blood volume–eg, dehydration, prolonged vomiting, diarrhea, bleeding, burns, etc; pump failure–eg, CHF, shock, kidney trauma or surgery, renal artery embolism, and other types of renal artery occlusion. See Renal failure.

azotemia

an excess of nitrogen-containing compounds in the blood. See also uremia.

postrenal azotemia
is caused by reduced renal blood flow caused by increased pressure within the renal collecting system, e.g. hydronephrosis and urine retention from a variety of causes.
prerenal azotemia
is due to extrarenal causes that reduce renal blood flow and glomerular filtration, e.g. dehydration, shock, reduced cardiac output, decreased plasma albumin osmotic pressure.
primary renal azotemia
results from loss of renal functional parenchyma.
References in periodicals archive ?
Determining the fractional excretion of sodium (FENa) is valuable in differentiating between acute tubular injury and prerenal azotemia (the presence of increased amounts of nitrogenous substances in the blood, consistent with renal failure) (Corwin, Schreiber, & Fang, 1984).
The patient presented with mild prerenal azotemia which resolved overnight with IV hydration; his maximum serum creatinine level of 1.
Differential diagnosis of prerenal azotemia from acute tubular necrosis and prediction of recovery by Doppler ultrasound.
With acute obstruction the urinary chemistry values are similar to those in prerenal azotemia.
Serum chemistry determinations revealed prerenal azotemia and hepatopathy by elevated liver enzymes and prolonged prothrombin time.
He also developed fecal incontinence, oliguria and prerenal azotemia secondary to decrease fluid intake and gastrointestinal losses.
Mortality rate was 26%; human T-lymphotropic virus (HTLV-1) infection, chronic alcoholism, eosinopenia, sepsis, and prerenal azotemia on admission were poor prognostic factors.