• Zeinab Karimi, Pooran Ghahramani, Fatemeh Masjedi, and Vahideh Yavari.
• Shiraz Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: zkarimi@sums.ac.ir.
• Am. J. Med. Sci. 2024 Dec 7.

BackgroundAllopurinol, a xanthine oxidase inhibitor, recovers histological alterations and renal dysfunction induced during renal ischemic-reperfusion injury. This study investigated the cross-talk between the allopurinol and soluble Klotho.MethodsRats were randomly divided into three equal groups (n=8 per group): The sham-operated group without renal ischemia, the BIR (bilateral ischemia-reperfusion) group which underwent renal ischemia, and BIR+Allo (allopurinol) group which was pretreated with allopurinol (100 mg/kg- gavage) 30 min before the renal ischemia. After recovery from the anesthesia, all animals were placed in metabolic cages to collect their urine in 24 h. After 24 h, plasma was extracted from blood samples taken from the tail vein-plasma and urine samples were saved at -20°C. Kidneys were harvested and weighed. The left kidney was dropped in the buffer of 10% formalin for H&E staining, and the right kidney was located in liquid nitrogen and saved at -80°C for the oxidative stress analysis.ResultsAfter renal ischemia-reperfusion, serum creatinine, blood urea nitrogen, xanthine oxidase, and total oxidative stress levels significantly increased. However, plasma Klotho level and total antioxidative capacity decreased in the BIR group. There was a reverse correlation between Klotho and xanthine oxidase levels. The pre-treatment with allopurinol increased plasma Klotho, induced a protective effect on renal histopathological changes, and corrected functional biomarkers.ConclusionOur result showed that allopurinol enhanced antioxidative effects by increasing Klotho activity. Therefore, Klotho may be involved in the protective effects of allopurinol on the renal injury induced by BIR.Copyright © 2024. Published by Elsevier Inc.

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