Clinical meaning
Acute kidney injury mechanisms reflect disruption of renal hemodynamics, tubular function, or glomerular integrity. Prerenal AKI results from decreased effective circulating volume or impaired renal autoregulation: the kidneys normally maintain constant GFR across a MAP range of 80-180 mmHg through afferent arteriolar vasodilation (prostaglandins) and efferent arteriolar vasoconstriction (angiotensin II). NSAIDs inhibit prostaglandin-mediated afferent vasodilation; ACEIs/ARBs block angiotensin II-mediated efferent vasoconstriction -- either can precipitate AKI when renal perfusion pressure is marginal. Intrinsic AKI involves direct renal parenchymal damage: acute tubular necrosis (ATN) is the most common intrinsic cause, resulting from ischemic or nephrotoxic injury to tubular epithelial cells. Ischemic ATN follows a predictable course: initiation (tubular cell injury), extension (ongoing hypoxia and inflammation), maintenance (tubular obstruction from necrotic debris, backleak of filtrate through damaged tubules, and vasoconstriction from tubuloglomerular feedback), and recovery (tubular cell regeneration). Nephrotoxic ATN from contrast media involves direct tubular toxicity, medullary vasoconstriction, and reactive oxygen species generation -- the clinician implements prevention protocols (isotonic saline hydration pre- and post-procedure, avoidance of concurrent nephrotoxins, use of lowest contrast volume necessary; N-acetylcysteine benefit is controversial). Acute interstitial nephritis (AIN) is a hypersensitivity reaction most commonly triggered by medications (antibiotics, NSAIDs, proton pump inhibitors) -- classic triad of rash, fever, and eosinophilia occurs in only 10% of cases; urinalysis showing WBC casts and eosinophiluria supports the diagnosis. Treatment is withdrawal of the offending agent, with consideration of corticosteroids for severe or persistent cases.