Acute Renal Failure Due to Nephrotoxins

Authors:
  • NHNorman K. Hollenberg
    Norman K. Hollenberg
  • DADouglass F. Adams
    Douglass F. Adams
  • DODonald E. Oken
    Donald E. Oken
  • HAHerbert L. Abrams
    Herbert L. Abrams
  • JMJohn P. Merrill
    John P. Merrill
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Abstract
Seven patients with nephrotoxin-induced acute renal failure had characteristic renal hemodynamic and angiographic abnormalities identical to those found in patients with acute renal failure due to shock and hemolysis. The abnormalities include the absence of recognizable cortical arterial vessels and the cortical nephrogram, delayed transit of contrast medium through the kidney and disappearance of the rapid — or cortical — flow component of xenon washout from the kidney. These observations suggest a persistent homogeneous reduction in renal cortical perfusion sufficient to induce the cessation of glomerular filtration and thus account for the failure of renal function. The similarity of the hemodynamic pattern in patients with acute renal failure of widely different etiology suggests a pathogenetic final common pathway involving undefined mediators that induce severe, sustained preglomerular vasoconstriction.

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