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Article
September 1987

Salsalate Exacerbation of Chronic Renal Insufficiency: Relation to Inhibition of Prostaglandin Synthesis

Author Affiliations

From the Regional Kidney Disease Program and Department of Medicine, Hennepin County Medical Center, and School of Medicine, University of Minnesota, Minneapolis.

Arch Intern Med. 1987;147(9):1674-1676. doi:10.1001/archinte.1987.00370090150026
Abstract

• Nonacetylated salicylates have not been reported to cause the hemodynamically mediated acute renal failure associated with nonsteroidal anti-inflammatory drug therapy. A 73-year-old woman with a creatinine clearance of 0.33 mL/s (20 mL/min), hypertension, and arterioscleroticcardiovascular disease developed reversible renal insufficiency when her dose of salsalate was increased to 4.5 g/d (serum salicylate concentration, 2.22 mmol/L [30.7 mg/dL]). Under close observation the patient was re-treated with lower doses of salsalate while renal function and the urinary excretions of prostaglandins were monitored. The excretion of prostaglandin E2 decreased abruptly while the excretion of 6-keto-prostaglandin F decreased more gradually as the dose of salsalate was increased. Renal function appeared to decline in parallel with the decrease in 6-keto-prostaglandin F and recovered rapidly after discontinuation of salsalate therapy. Nonacetylated salicylates can cause a hemodynamically mediated acute renal failure in patients at risk for this nephropathy.

(Arch Intern Med 1987;147:1674-1676)

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