Aki Mechanisms

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...