Pathophysiology of Ischemic/ Toxic Acute Renal Failure

摘要: An adequate blood flow through the renal cortex and sufficient hemodynamic pressure in glomerular capillaries are both critical prerequisites for normal filtration. If either a fall systemic or circulatory failure (due to acute myocardial infarction other heart disease) reduction of volume depletion secondary hemorrhage fluid loss from burns, vomiting, diarrhea, excessive sweating, etc.) occurs, perfusion is reduced filtration decreased. Homeostatic mechanisms body conservation then activated with an increase antidiuretic hormone aldosterone secretion enhancement reabsorptive activity tubular epithelium. Reduction urine output results, while urinary excretion nitrogenous end products increases plasma concentrations urea creatinine. In this “functional” phase (ARF) [1] extrarenal functional insufficiency [2] (the so-called “prerenal azotemia” ARF”), kidney not damaged integrity preserved: tubules, fact, retain sodium avidly concentrate urine; thus, becomes hypertonic, low concentration markedly fractional (FENa). cardiac restored values, function rapidly returns normal. hypotension, sustained failure, hypovolemia) maintained even worsened, “organic” damage ensues “acute necrosis,” ATN, “intrinsic ARF”) which oligo-anuria associated ability epithelium, resulting isoosmotic increased filtered (FENa>l%). patient survives (with help dialysis) despite function, recovery volume, usually occurs within 10 15 days, but sometimes 30 days more after onset [3].