What causes prerenal acute kidney injury (AKI)?

Updated: Dec 24, 2020
  • Author: Biruh T Workeneh, MD, PhD, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Prerenal AKI represents the most common form of kidney injury and often leads to intrinsic AKI if it is not promptly corrected. Volume loss can provoke this syndrome; the source of the loss may be GI, renal, or cutaneous (eg, burns) or from internal or external hemorrhage. Prerenal AKI can also result from decreased renal perfusion in patients with heart failure or shock (eg, sepsis, anaphylaxis). In patients taking calcium channel blockers, use of the antibiotic clarithromycin can result in AKI, due to a drug-drug interaction that markedly raises plasma calcium channel blocker concentrations and causes hypotension, with subsequent ischemic damage to the kidney. [5]

Several classes of medications can induce prerenal AKI in volume-depleted states, including ACE inhibitors and angiotensin receptor blockers (ARBs), which are otherwise safely tolerated and beneficial in most patients with chronic kidney disease. Aminoglycosides, amphotericin B, and radiologic contrast agents may also do so.

Arteriolar vasoconstriction leading to prerenal AKI can occur in hypercalcemic states, as well as with the use of radiocontrast agents, NSAIDs, amphotericin, calcineurin inhibitors, norepinephrine, and other pressor agents. The hepatorenal syndrome can also be considered a form of prerenal AKI, because functional renal failure develops from diffuse vasoconstriction in vessels supplying the kidney. [6]

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