Recurrence and specificity of nephrotic syndrome due to tolmetin

Tietjen, David P.; Eisenhower, Dwight D.

doi:10.1016/0002-9343(89)90625-6

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“…Ninety‐seven case reports that fulfilled the selected criteria were identified [ 9–73] with a male/female ratio of 34/63, mean age 54.0 years (median 57). The indication for NSAID treatment was a musculoskeletal disorder in 52 patients, a rheumatic disorder in 30, miscellaneous disorders in eight and unknown in seven.…”

Section: Resultsmentioning

confidence: 99%

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Glomerular, tubular and interstitial nephritis associated with non‐steroidal antiinflammatory drugs. Evidence of a common mechanism

Ravnskov¹

1999

Brit J Clinical Pharma

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Aims To study the mechanisms behind NSAID-associated nephropathy. Methods Analysis of published case reports satisfying strict criteria for NSAID nephropathy. Results Ninety-seven cases with acute nephritis (AN; 19 patients), minimal change nephropathy (MC; 38 patients), membranous glomerulonephritis (MGN; 19 patients), focal sclerosis (FS; 13 patients) and other glomerulonephritis subgroups (8 patients) were identified. Hypersensitivity reactions were seen in all groups, most often in AN. Proteinuria was more severe in MC and FS than in MGN and unrelated to amount of glomerular deposits. The mean NSAID treatment time was 1.7 months in AN, 8.2 months in MC and 39 months in MGN and associated with amount of glomerular deposits, fusion of podocytes and proteinuria, and inversely associated with hypersensitivity, interstitial damage and renal failure. Rheumatic diseases were common in MGN. At follow-up 68 of 72 patients who had discontinued NSAID treatment had improved, 57 with normal renal function. Conclusions NSAID nephropathy may be caused by hypersensitivity. The reaction is milder than in drug-induced acute tubulointerstitial nephritis, probably because the offending drug inhibits the inflammatory reaction it has started itself. Heavy proteinuria is probably due to lymphokines produced as a result of the immunological response. If the allergic reaction is strong, AN is produced rapidly with severe renal failure but little proteinuria; if it is less violent, immunocompetent cells may develop to produce lymphokines and proteinuria. Immune complexes may be formed eventually, secondary to the increased glomerular permeability, more easily in patients with a hyperactive immune system and with little consequence for renal function.

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Section: Resultsmentioning

confidence: 99%

“…Also suggestive is analyses of the mononuclear, interstitial cells. In one study they were entirely T‐cells [ 26]; in another study, 80% were T‐cells and of the 20% B‐lymphocytes the great majority were IgE‐bearing [ 62] and treatment after discontinuation of the drug with another NSAID did not result in relapse [ 64, 69].…”

Section: Discussionmentioning

confidence: 99%

Glomerular, tubular and interstitial nephritis associated with non‐steroidal antiinflammatory drugs. Evidence of a common mechanism

Ravnskov¹

1999

Brit J Clinical Pharma

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Recurrence and specificity of nephrotic syndrome due to tolmetin

Cited by 1 publication

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Glomerular, tubular and interstitial nephritis associated with non‐steroidal antiinflammatory drugs. Evidence of a common mechanism

Glomerular, tubular and interstitial nephritis associated with non‐steroidal antiinflammatory drugs. Evidence of a common mechanism

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