prerenala

Prerenal refers to kidney dysfunction caused by reduced blood flow or perfusion before the kidneys, leading to azotemia without intrinsic kidney damage early in its course. In the context of acute kidney injury (AKI), prerenal azotemia is typically reversible if perfusion is promptly restored; prolonged hypoperfusion can progress to intrinsic renal injury such as acute tubular necrosis.

Common causes include volume depletion from vomiting, diarrhea, hemorrhage, or inadequate fluid intake; decreased effective circulating volume from heart failure, cirrhosis with ascites, nephrotic syndrome, or sepsis; and drug effects that impair renal perfusion (for example, diuretics, ACE inhibitors, or NSAIDs in susceptible patients). Other contributors include renal artery stenosis and perioperative hypotension.

Pathophysiology centers on reduced renal perfusion triggering compensatory mechanisms that conserve volume and maintain GFR. The kidney increases sodium and water reabsorption, and angiotensin II-mediated efferent arteriolar constriction helps sustain glomerular filtration. Laboratory features reflect intact renal parenchyma unless injury progresses: BUN-to-creatinine ratio commonly >20:1, urine osmolality often >500 mOsm/kg, and fractional excretion of sodium (FeNa) usually <1% (though diuretics can confound this; FeUrea <35% may be used as an alternative).

Diagnosis involves clinical context, laboratory data, and exclusion of postrenal obstruction or intrinsic renal disease. Imaging, such as renal ultrasound, may be used to assess obstruction and anatomy when indicated.

Management focuses on restoring renal perfusion and addressing the underlying cause. This typically includes cautious administration of isotonic fluids for hypovolemia, optimizing hemodynamics in heart failure or cirrhosis, avoiding nephrotoxins, and treating contributing conditions. Prognosis is generally favorable with timely correction; prolonged or recurrent prerenal states can lead to irreversible kidney injury.

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