Renal damage: a possible role of diclofenac induced injury associated with altered acid phosphatase and collagen content in Balb/c mice

Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the most popular classes of drugs with anti-inflammatory, analgesic and antipyretic effects. NSAIDs interfere with certain metabolic pathways which are involved in formation of prostaglandins. The prostaglandins have been assigned many physiological roles including renal metabolism. Diclofenac, a NSAID, is prescribed for its anti-inflammatory and analgesic actions during different type of bone and muscle injuries. We hypothesized that other than treating different ailments, the drug can have some detrimental effects on kidney by possibly suppressing renal prostaglandins. To test this, Balb/c male mice were exposed to diclofenac sodium at dose rate of 10 mg/ kg/ body wt from 10-30 days. Collagen content of kidney was analyzed by estimating hydroxyproline content. Acid phosphatase was localized in renal tissue histochemically. Further, acid phosphatase was also assayed biochemically. A noteworthy hike in collagen concentration was noticed in diclofenac treated kidney throughout the study period (p < 0.05). Histochemical sections revealed initial decrease in acid phosphatase content with some localized areas of enzyme activity. Change in acid phosphatase content was accompanied by many pathological abnormalities. These findings were corroborated by biochemical results too.