Diclofenac-induced biochemical changes in nephrotoxicity among male Albino rats

Abstract

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with adverse renal effects caused by the reduction in synthesis of renal prostaglandins in sensitive persons or animal species, and potentially during long-term use in non-sensitive persons if resistance to side effects decreases with age. The effects of diclofenac sodium on the kidneys were studied during 4 1/2 hours in eight patients with normal renal function. Urinary output decreased within 10 min after the injection, and maximally by 80%. The renal plasma flow and the glomerular filtration rate initially diminished significantly, by 35%, but began to increase after only 2 hours. The dominant and persistent effect was a reduction of free water clearance, with maximum fall from 5.9 to 0.08ml/min after 2 1/2 hours. Aim: The aim of this study was to evaluate the effects of diclofenac-induced acute nephrotoxicity using biochemical parameters in rats.Methods: 12 male Wistar rats allotted in 4 equal groups were intraperitoneally injected with 0, 10, 50 and 100mg/kg diclofenac, respectively and 12 hours after injection, blood serum samples were collected for assessment of basic renal function test parameters such as urea, creatinine, and uric acid, sodium, Potassium.Results: Rats treated up to 50mg/kg diclofenac were considered to be within normal range in rats. By increase in dose more than 50mg/kg showed significant increases in uremia were evidenced in intoxicated animals. Observed specifically in group IV Rats.Conclusions: In this study, uremia, as an indicator of kidney damage, was significantly increased depending on dose. Diclofenac may cause kidney damage depending on dose and this effect may also be observed. NSAIDs-induced nephrotoxicity may be due to the inhibitory effect of these drugs on prostaglandin synthesis, thus causing kidney ischemia.