sulindac and Acute-Kidney-Injury

Sulindac is a long-acting nonsteroidal anti-inflammatory drug (NSAID) widely used for the management of osteoarthritis, rheumatoid arthritis, ankylosing sponydlitis, and acute gouty arthritis. Reports of sulindac toxicity in the literature are rare. We report the case of a 22-year old male with a history of bipolar disorder who was brought to the emergency department after ingesting approximately 15 g of sulindac in a suicide attempt. He was found to have acute kidney injury and hyperbilirubinemia. Despite aggressive fluid resuscitation, his renal function progressively worsened requiring the initiation of hemodialysis. Ten days following ingestion of sulindac, he began to develop ischemic skin changes with a gangrenous appearance in his hands and feet. He continued to receive supportive treatment, and his acute kidney injury, hyperbillirubinemia, and ischemic skin necrosis eventually resolved. Clinicians should be aware of this long-acting NSAID and its ability to cause prolonged multisystem organ dysfunction.

Topics: Acute Kidney Injury; Anti-Inflammatory Agents, Non-Steroidal; Bipolar Disorder; Drug Overdose; Fluid Therapy; Humans; Hyperbilirubinemia; Ischemia; Male; Necrosis; Renal Dialysis; Resuscitation; Skin; Skin Diseases; Suicide, Attempted; Sulindac; Young Adult

Acute renal dysfunction has been described as a feature of acute overdoses of the nonsteroidal anti-inflammatory drugs benoxaprofen, fenoprofen, ibuprofen, mefenamic acid, piroxicam, suprofen, and zomepirac. The cases reported here include renal impairment after acute overdoses of another three nonsteroidal anti-inflammatory drugs: diclofenac (one case), naproxen (two cases), and sulindac (five cases). The eight patients presented with lumbar pain and oliguria and had protein and erythrocytes in the urine. Serum creatinine was increased to a maximum of 190-932 mumol/L. Renal impairment was generally transient but in one case was treated by hemodialysis and one by continuous arterio-venous hemofiltration dialysis. In all cases of significant acute overdose of nonsteroidal anti-inflammatory drugs, the risk of acute renal dysfunction must be considered.

Topics: Acute Kidney Injury; Adolescent; Adult; Alcoholic Intoxication; Creatinine; Diclofenac; Drug Interactions; Female; Humans; Male; Middle Aged; Naproxen; Sulindac

Four elderly patients developed nephrotic syndrome while receiving sulindac. Sulindac treatment had commenced 4-12 months prior to presentation with the nephrotic syndrome. Two patients also developed oliguric renal failure. Renal biopsy in one showed minimal change nephropathy and in three cases membranous nephropathy. Interstitial nephritis was present on renal biopsy in all cases. The nephrotic syndrome and renal failure resolved in all cases after withdrawal of sulindac. Two patients received steroid therapy and improvement in renal function and disappearance of proteinuria seemed to be temporarily related to steroid therapy in both cases. Despite the fact that sulindac is less likely to cause renal failure due to inhibition of renal prostaglandin secretion this report shows that sulindac treatment can be associated with renal failure and the nephrotic syndrome.

Topics: Acute Kidney Injury; Aged; Aged, 80 and over; Female; Humans; Indenes; Male; Nephrotic Syndrome; Sulindac

Topics: Acute Kidney Injury; Aged; Arthritis; Female; Gout; Humans; Hyperkalemia; Indenes; Recurrence; Sulindac

Urinary excretion rates of prostaglandin (PG) E2, PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane (TX) B2 were evaluated in three groups of cirrhotic patients [without ascites (group 1, 13 cases), with ascites and normal renal function (group 2, 15 cases), and with ascites and renal failure (group 3, 5 cases)] and in 14 healthy controls. All urinary arachidonate metabolites were significantly increased in group 2 patients. Patients with renal failure showed lower PGE2, PGF2 alpha, and TXB2 values than those from group 2; PGF2 alpha values were also lower than controls. Platelet TXA2 production during whole blood clotting was significantly reduced in all groups of patients. Administration of low-dose aspirin and sulindac, two cyclooxygenase inhibitors selectively sparing renal cyclooxygenase activity, effectively inhibited platelet TXA2 production without affecting urinary TXB2 excretion, thus ruling out platelets as a possible source of urinary TXB2. We conclude that patients with ascites and normal renal function show an overall activation of the renal PG system. Renal production of vasodilating PGE2 and PGI2 may be involved in supporting renal function in these patients. A reduced platelet synthesis of proaggregatory TXA2 also occurs in cirrhotic patients. This may play a role in the bleeding tendency of cirrhosis.

Topics: 6-Ketoprostaglandin F1 alpha; Acute Kidney Injury; Adult; Aged; Arachidonic Acid; Arachidonic Acids; Aspirin; Blood Platelets; Creatinine; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Epoprostenol; Female; Humans; Kidney; Liver Cirrhosis; Male; Middle Aged; Natriuresis; Prostaglandins E; Prostaglandins F; Renin-Angiotensin System; Sulindac; Thromboxane A2; Thromboxane B2

Topics: Acute Kidney Injury; Aged; Cholestasis; Female; Humans; Indenes; Nephritis, Interstitial; Sulindac

Topics: Acute Kidney Injury; Humans; Indenes; Sulindac