کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5842364 | 1560636 | 2012 | 5 صفحه PDF | دانلود رایگان |
AimsAcetaminophen is a safe antipyretic and analgesic drug within the clinically recommended dosage range, but overdose can cause fatal liver and or kidney damage. Most of the nonsteroidal anti-inflammatory drugs (NSAIDs) exert their analgesic effect via inhibition of cyclooxygenase, which also results in a reduction of renal blood flow. Therefore, the use of NSAIDs in pain treatment for chronic kidney disease (CKD) patients is of particular concern. Acetaminophen lacks the anti-inflammatory and anti-coagulatory properties of the NSAIDs. In this study, we investigate whether acetaminophen has an impact on the progression of renal failure.Main methodsAcetaminophen (150Â mg/kg/day or 750Â mg/kg/day) or indomethacin (5Â mg/kg/day) was orally administered to adenine-induced chronic renal failure model rats for 4Â weeks. The plasma concentrations of acetaminophen and its metabolites were measured during the treatment period; renal function and oxidative stress in the rats were also monitored.Key findingsIndomethacin significantly decreased the survival rate of renal failure model rats. In contrast, both low (150Â mg/kg) and high (750Â mg/kg) doses of acetaminophen improved the survival rate. The progression of renal failure was attenuated by acetaminophen (750Â mg/kg) after administration for 2Â weeks. The metabolites of acetaminophen were found to accumulate in plasma. Plasma glutathione concentration had significantly recovered after acetaminophen administration.SignificanceAcetaminophen has no effect on the progression of renal damage in adenine-induced renal failure model rats. This result is in part due to acetaminophen's antioxidant activity. These results suggest that acetaminophen is a suitable analgesic agent for treating CKD patients.
Journal: Life Sciences - Volume 91, Issues 25â26, 17 December 2012, Pages 1304-1308