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Pathophysiologic Mechanisms of Acute Renal Failure, Hyperkalemia, Tubular Necrosis, and Proteinuria

Wayne A. Marasco, MD, PhD; Paul W. Gikas, MD; R. Azziz-Baumgartner, MD; Robert Hyzy, MD; Charles J. Eldredge, MD; Joeffrey Stross, MD

Arch Intern Med. 1987;147(12):2107-2116.

Abstract
• Ibuprofen-associated, acute, reversible renal failure with hyperkalemia, tubular necrosis, and proteinuria developed in a patient who had no predisposing underlying disease. A renal biopsy specimen revealed mesangial hypercellularity without glomerular crescent formation. A profound interstitial nephritis with focal inflammatory cell infiltrates of predominantly mononuclear cells and neutrophils as well as focal tubular destruction was seen. Vasculitis was not observed. Ultrastructural studies confirmed the light microscopic diagnosis of a tubulointerstitial nephritis and, in addition, indicated the presence of electron-dense mesangial and subepithelial deposits. Direct immunofluorescence examination showed diffuse mesangial IgM and C3 deposition as well as vascular C3 deposition. Renal failure rapidly resolved after discontinuation of ibuprofen therapy and initiation of steroid therapy, with return to normal levels of serum creatinine, urea nitrogen, potassium, and sodium. Proteinuria also resolved.

(Arch Intern Med 1987;147:2107-2116)

Author Affiliations
From the Departments of Pathology (Drs Marasco and Gikas) and Internal Medicine (Drs Marasco, Azziz-Baumgartner, Hyzy, Eldredge, and Stross), University of Michigan Medical School, Ann Arbor.

Footnotes
Accepted for publication Aug 7, 1987.

Reprint requests to Department of Pathology, Box 0602, University of Michigan Medical School, 1500 E Medical Center Dr, Ann Arbor, MI 48109 (Dr Marasco).

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