What is the pathophysiology of intrarenal azotemia?

Updated: Apr 24, 2020
  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Intrarenal azotemia, also known as acute kidney injury (AKI), renal-renal azotemia, and (in the past) acute renal failure (ARF), refers to elevations in BUN and creatinine resulting from problems in the kidney itself. There are several definitions, including a rise in serum creatinine levels of about 30% from baseline or a sudden decline in output below 500 mL/day. If output is preserved, AKI is nonoliguric; if output falls below 500 mL/day, AKI is oliguric. Any form of AKI may be so severe that it virtually stops formation; this condition is called anuria (< 100 mL/day).

The most common causes of nonoliguric AKI are acute tubular necrosis (ATN), aminoglycoside nephrotoxicity, lithium toxicity, and cisplatin nephrotoxicity. Tubular damage is less severe than it is in oliguric AKI. Normal output in nonoliguric AKI does not reflect a normal GFR. Patients may still make 1440 mL/day of urine even when the GFR falls to about 1 mL/min because of decreased tubular reabsorption.

Some studies indicate that nonoliguric forms of AKI are associated with less morbidity and mortality than is oliguric AKI. Uncontrolled studies also suggest that volume expansion, potent diuretic agents, and renal vasodilators can convert oliguric AKI to nonoliguric AKI if administered early.

The pathophysiology of acute oliguric or nonoliguric AKI depends on the anatomic location of the injury. In ATN, epithelial damage leads to functional decline in the ability of the tubules to reabsorb salt, water, and other electrolytes. Excretion of acid and potassium is also impaired. In more severe ATN, the tubular lumen is filled with epithelial casts, causing intraluminal obstruction and resulting in a declining GFR.

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