Nephrotic syndrome and acute interstitial nephritis associated with the use of diclofenac

Department of Nephrology St. János Hospital, Budapest, Hungary.
Wiener klinische Wochenschrift (Impact Factor: 0.84). 08/1999; 111(13):523-4.
Source: PubMed

ABSTRACT Commonly reported renal complications of non-steroidal anti-inflammatory drugs (NSAID) include acute renal failure and/or acute interstitial nephritis; in rare cases a nephrotic syndrome was also observed. In most cases this was due to the development of secondary membranous nephropathy. Following withdrawal of the drug the nephrotic syndrome usually resolved rapidly. We report a 65-year-old woman who developed a nephrotic syndrome and acute renal failure during 6 months of treatment with the NSAID diclofenac. Renal biopsy revealed both, membranous nephropathy and interstitial nephritis. After discontinuation of diclofenac and treatment with prednisone 1 mg/kg/day, furosemide 400 mg/day and simvastatin at a dose of 20 mg/day, creatinine clearance gradually increased and after 5 months of treatment complete remission of the nephrotic syndrome was observed.

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    • "The possibility of nephrotoxic effects of diclofenac after chronic exposure was described by Revai and Harmos [20]. In concentrations ranging from 7 to 15 μg L−1, diclofenac exposure induced tubular necrosis in the kidneys of the rainbow trout, and hyperplasia and fusion of the villi in the intestine were detected in concentrations above 1 μg L−1. "
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    The Scientific World Journal 02/2014; 2014(7-8):645737. DOI:10.1155/2014/645737 · 1.73 Impact Factor
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    ABSTRACT: In the present study, cytopathology was investigated in the liver, kidney, gills and gut of rainbow trout (Oncorhynchus mykiss) exposed to five different concentrations (1, 5, 20, 100 and 500 μg/L) of the anti-inflammatory drug diclofenac under laboratory conditions. The lowest observed effect concentration (LOEC) for cytological alterations in liver, kidney and gills was 1 μg/L. In the gut, however, no diclofenac-induced cytopathology occurred. As the most prominent reactions induced by diclofenac (1) in the kidney, a severe accumulation of protein in the tubular cells (so called hyaline droplet degeneration), macrophage infiltration and structural alterations (dilation, vesiculation) of the endoplasmic reticulum (ER) in the proximal and distal renal tubules were observed. Furthermore, shortening of podocytes and their retraction from the basal lamina, a thickening of the basal lamina, the formation of desmosomes, and necrosis of endothelial cells in the renal corpuscles occurred; (2) in the liver, the most striking reactions were the collapse of the cellular compartmentation as well as the glycogen depletion of hepatocytes; (3) in the gills, pillar cell necrosis, hypertrophy of chloride cells, and epithelium lifting became evident in the secondary lamellae.
    Aquatic Toxicology 06/2004; 68(2):151-166. DOI:10.1016/S0166-445X(04)00097-9 · 3.45 Impact Factor
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    Aquatic Toxicology 06/2004; 68(2):141-150. DOI:10.1016/S0166-445X(04)00096-7 · 3.45 Impact Factor
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