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Turkiet — Turkish Statistical Institute. This article has been cited by other articles in PMC. Ryssland — Federal state statistics service.

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Voluntary Register of Works. Gazette of Patents and Trademarks. Most likely, the formation of immune complexes in NSAID nephropathy is secondary to the increased permeability to macromolecules and does not necessarily contribute to the renal damage. More complexes may be formed the longer time the increased permeability persists and more easily in patients with a hyperreactive or dysregulatory immune system. That proteinuria was associated with treatment time, but not with amount of glomerular deposits, although the two latter were associated with each other, also indicates that lymphokine production is more important for the creation of proteinuria than the formation of immune complexes.

In accordance, a large number of clinical and experimental observations have shown that even pronounced MGN may appear without inducing proteinuria or renal failure [ 85 ].

Most important in the management of NSAID nephropathy is to discontinue treatment with the offending drug. A worsening of renal function was seen in all patients who continued NSAID treatment, and with few exceptions all patients improved after discontinuation of the drug, in most cases with total remission.

The nephritides seen after treatment with NSAID are not necessarily separate entities distinctly demarcated from each other and with separate mechanisms, but rather a continuous spectrum of renal responses to a state of hypersensitivity against the drug. The clinical, laboratory and pathologic variations are most likely determined by the type and strength of the immunologic response and the length and magnitude of the drug exposure.

The milder and more protracted course in NSAID-induced nephropathy compared with drug-induced ATIN may be due to a delay of the immunologic reactions induced by the offending NSAID itself causing the immune system to work ineffectively and in slow-motion. I thank Drs R. Schillinger for providing supplementary data. National Center for Biotechnology Information , U. Br J Clin Pharmacol. Author information Article notes Copyright and License information Disclaimer.

Received Apr 20; Accepted Sep This article has been cited by other articles in PMC. 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.

Methods To isolate the renal effects of NSAID from other pathogenic conditions the following criteria for inclusion of a case report were used: Statistics As almost all data were dichotomous it was necessary to use non-parametric statistics. Table 1 Grouping of the patients according to various parameters. Open in a separate window. Table 2 Number of patients with signs or symptoms of systemic hypersensitivity. Biopsy findings The renal biopsy was studied by light microscopy LM in all patients, by immunofluorescence microscopy IM in 75 patients, and by electron microscopy EM in 64 patients.

Light microscopy In 67 patients the glomeruli were normal. Table 3 Number of patients by type of nephritis. Electron microscopy This was performed in 63 patients.

Follow-up The glomerular function at follow-up, a few days to 10 years after discontinuation of NSAID median 4 months , was reported in 86 patients. Associations Associations between all parameters in Table 1 and the major subgroups were calculated, as were associations between each parameter. Discussion The peculiar syndrome of acute or subacute tubulointerstitial nephritis associated with the nephrotic syndrome seen after NSAID treatment has given rise to much speculation about the underlying mechanisms.

Conclusions The nephritides seen after treatment with NSAID are not necessarily separate entities distinctly demarcated from each other and with separate mechanisms, but rather a continuous spectrum of renal responses to a state of hypersensitivity against the drug. Acknowledgments I thank Drs R. Tables with more comprehensive information can be acquired from the author. Renal effects of drugs that inhibit prostaglandin synthesis.

Garella S, Matarese RA. Renal effects of prostaglandins and clinical adverse effects of nonsteroidal anti-inflammatory agents. Renal syndromes associated with nonsteroidal antiinflammatory drugs. N Engl J Med. Carmichael J, Shankel SW. Effects of nonsteroidal anti-inflammatory drugs on prostaglandins and renal function. Pirson Y, van Ypersele de Strihou C. Renal side effects of nonsteroidal antiinflammatory drugs: Am J Kidney Dis. Glomerular and interstitial disease induced by nonsteroidal anti-inflammatory drugs.

Acute interstitial nephritis with glomerulopathy due to nonsteroidal anti-inflammatory agents: Reversible membranous nephropathy associated with the use of nonsteroidal anti-inflammatory drugs. Non-steroidal anti-inflammatory drugs and renal failure.

Progression of minimal-change glomerulopathy to focal glomerulosclerosis in a patient with fenoprofen nephropathy. Reversible renal failure and nephrotic syndrome without interstitial nephritis from zomepirac. Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs. Vasculitis with alclofenac therapy. Reversible renal failure and nephrotic syndrome associated with nonsteroidal anti-inflammatory drugs. Mefenaminsäure Ponstan -induzierte akute interstitielle Nephritis mit reversiblem, schwerem, nicht-oligurischem Nierenversagen.

Reversible membranous nephritis associated with diclofenac. Nephrotic syndrome induced by tolmetin.

Renal failure and nephrotic syndrome associated with sulindac. Reversible rapidly progressive renal failure with nephrotic syndrome due to fenoprofen calcium. Dhar SK, Yum M. Acute tubular necrosis and minimal-change glomerulopathy associated with fenoprofen therapy.

Toxicite aigue de la glafenine glifanan Acta Clin Belg. Nephrotic syndrome associated with use of the nonsteroidal anti-inflammatory drugs. Case report and review of the literature. A possible T-lymphocyte disorder. Indomethacin-associated acute renal failure. Reversible acute interstitial nephritis associated with indomethacin. Israel J Med Sci. Acute nephrotic syndrome with reversible renal failure after phenylbutazone.

End-stage renal failure caused by regular use of anti-inflammatory analgesic medication for minor sports injuries. S Afr Med J. Renal effects of fenoprofen. Membranous glomerulonephritis in rheumatoid arthritis not related to gold or D-penicillamine therapy: Association with reversible renal failure and acute interstitial nephritis.

Flurbiprofen-associated acute tubulointerstitial nephritis. Akute interstitielle Nephritis mit oligurischem Nierenversagen nach Phenylbutazon-Medikation. Short-term niflumic-acid-induced acute renal failure in children.

Naproxen-associated renal failure in a child with arthritis and inflammatory bowel disease. Naproxen-induced nephropathy in systemic lupus erythematosus. Fenoprofen-induced acute interstitial nephritis presenting with nephrotic syndrome. Nephrotic syndrome associated with sulindac. Association of renal papillary necrosis and ankylosing spondylitis.

Pathophysiologic mechanisms of acute renal failure, hyperkalemia, tubular nbecrosis, and proteinuria. Acute interstitial nephritis in a patient with aspirin hypersensitivity. Zomepirac, interstitial nephritis, and renal failure. Ibuprofen-associated lipoid nephrosis without interstitial nephritis. Renal disease and use of topical non-steroidal anti-inflammatory drugs.

Tolmetin-induced acute renal failure. Naproxen nephrotoxicity in a 2-year-old child. Am J Dis Child. Nephrotoxicity from nonsteroidal anti-inflammatory drugs.

Nephrotic syndrome associated with nonsteroidal anti-inflammatory drug use in two children. Granulomatous interstitial nephritis after nonsteroidal anti-inflammatory drugs.

Reversible membranous glomerulonephritis associated with ketoprofen. T and B lymphocyte subsets in fenoprofen nephropathy.

Membranous nephropathy associated with diclofenac. Recurrence and specificity of nephrotic syndrome due to tolmetin. Tolins JP, Seel P. Ibuprofen-induced interstitial nephritis and the nephrotic syndrome. Sulindac-induced acute interstitial nephritis. Salsalate and minimal-change nephrotic syndrome. Minimal change glomerulonephropathy associated with nonsteroidal antiinflammatory drugs. Persistent renal failure following administration of naproxen.