Nephrotic syndrome and acute interstitial nephritis associated with the use of diclofenac
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 . 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. "
ABSTRACT: The aim of this study was to investigate effects of subchronic exposure to sublethal levels of diclofenac on growth, oxidative stress, and histopathological changes in Danio rerio. The juvenile growth tests were performed on Danio rerio according to OECD method number 215. Fish at the age of 20 days were exposed to the diclofenac environmental concentration commonly detected in the Czech rivers (0.02 mg L(-1)) and the range of sublethal concentrations of diclofenac (5, 15, 30, and 60 mg L(-1)) for 28 days. A significant decrease (P < 0.01) in the fish growth caused by diclofenac was observed in the concentrations of 30 and 60 mg L(-1). The identified value of LOEC (lowest observed effect concentration) was 15 mg L(-1) of diclofenac and NOEC (no observed effect concentration) value was 5 mg L(-1) of diclofenac. We did not find histopathological changes and changes of selected parameters of oxidative stress (glutathione S-transferase, glutathione reductase) in tested fish. The environmental concentration of diclofenac in Czech rivers did not have any effect on growth, selected oxidative stress parameters (glutathione S-transferase, glutathione reductase), or histopathological changes in Danio rerio but it could have an influence on lipid peroxidation.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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ABSTRACT: Human and veterinary pharmaceuticals have been shown to occur in considerably high amounts in sewage treatment plant (STP) effluents and surface waters. The non-steroidal inflammatory drug diclofenac represents one of the most commonly detected compounds. Information concerning possible ecotoxicological risks of the substance are rather scarce. So far there are no data available on its possible effects in fish after prolonged exposure. In order to evaluate sublethal toxic effects of diclofenac in fish, rainbow trout (Oncorhynchus mykiss) exposed to diclofenac concentrations ranging from 1 μg/L to 500 μg/L over a 28 day period were investigated by histopathological methods. In addition, diclofenac residues in various organs were analyzed by means of gas chromatography/mass spectrometry (GC/MS).The histopathological examinations of diclofenac-exposed fish revealed alterations of the kidney such as an hyaline droplet degeneration of the tubular epithelial cells and the occurrence of an interstitial nephritis. In the gills, the predominant finding consisted in a necrosis of pillar cells leading to damage of the capillary wall within the secondary lamellae. The lowest observed effect concentration (LOEC) at which both renal lesions and alterations of the gills occurred was 5 μg/L. In contrast, the light microscopical examination of the liver, the gastro-intestinal tract, and the spleen did not reveal any histopathological alterations neither in diclofenac-exposed fish nor in solvent controls or control individuals.Chemical analysis showed a concentration-related accumulation of diclofenac in all organs examined. The highest amounts could be detected in the liver, followed by the kidney, the gills and the muscle tissue. Dependent on the diclofenac concentration used, the bioconcentration factors (BCF) were 12–2732 in the liver, 5–971 in the kidney, 3–763 in the gills, and 0.3–69 in the muscle respectively. From the present findings it can be assumed, that prolonged exposure in environmentally relevant concentrations of diclofenac leads to an impairment of the general health condition of fish.Aquatic Toxicology 06/2004; 68(2):141-150. DOI:10.1016/S0166-445X(04)00096-7 · 3.45 Impact Factor