Salsalate exacerbation of chronic renal insufficiency. Relation to inhibition of prostaglandin synthesis.
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 arteriosclerotic cardiovascular 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 F1 alpha decreased more gradually as the dose of salsalate was increased. Renal function appeared to decline in parallel with the decrease in 6-keto-prostaglandin F1 alpha 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.
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000378:metabolism; D000368:Aged; D001168:Arthritis / Q000188:drug therapy; D015232:Dinoprostone; D004198:Disease Susceptibility; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000652:urine; D011460:Prostaglandins F / Q000652:urine; D012459:Salicylates / Q000009:adverse effects*
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D012459:Salicylates; D015232:Dinoprostone; C014182:salicylsalicylic acid; C100006:prostaglandin F1