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.
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