Nephrotoxicity is a major complication of gentamicin (GEN). We aimed to evaluate the potential protective effect of montelukast (MK) against GEN-induced nephrotoxicity in rats. Thirty-two rats were randomly divided into four groups, each consisting of eight animals as follows: (1) the rats were control; (2) intraperitoneally injected with GEN 14 consecutive days (100 mg/kg/day); (3) treated with GEN plus distilled water via nasogastric gavage for 14 days; and (4) treated with GEN plus MK (10 mg/kg/day) for 14 days. After 15 days, rats were killed and their kidneys were taken and blood analysis was performed. Twenty-four hours urine collections were obtained in standard metabolic cages a day before the rats were killed. Tubular necrosis and interstitial fibrosis scoring were determined histopathologically in a part of kidneys; nitric oxide (NO), malondialdehyde (MDA), and reduced glutathione (GSH) levels were determined in the other part of kidneys. Statistical analyses were made by the chi-square test and analysis of variance. Serum urea and creatinine levels were significantly higher in rats treated with GEN alone, than the rats in control and GEN þ MK groups. The GSH levels in renal tissue of only GEN-treated rats were significantly lower than those in control group, and administration of MK to GEN-treated rats significantly increased the level of GSH. The group that was given GEN and MK had significantly lower MDA and NO levels in kidney cortex tissue than those that was given GEN alone. In rats treated with GEN þ MK, despite the presence of mild tubular degeneration and tubular necrosis are less severe, and glomeruli maintained a better morphology when compared with GEN group. We can say that MK prevents kidney damage with antioxidant effect, independently of NO.

Nephrotoxicity is a major complication of gentamicin (GEN), which is widely used in the treatment of severe Gramnegative infections. Reactive oxygen species are important mediators of GEN-induced nephrotoxicity. Because of the strong antioxidant properties of pomegranate extract (PE), we evaluated the protective effect of PE against GEN-induced nephrotoxicity. Thirty-two adult male rats were randomly divided into four equal groups: (1) controls; (2) treated with GEN for 14 consecutive days (100 mg/kg/day); (3) treated with GEN plus distilled water; and (4) treated with GEN plus PE (100 μL). After 15 days, the rats were killed and their kidneys were taken, and blood analysis was performed. Tubular necrosis and interstitial fibrosis scores were determined histopathologically; and biochemically, nitric oxide (NO), malondialdehyde (MDA), and reduced glutathione (GSH) levels in kidneys were determined. Urea, creatinine, Na þ , and K þ levels were investigated in the blood analysis. Statistical analyses were made by the chi-square test and analysis of variance. Serum urea and creatinine levels were significantly higher in rats treated with GEN alone than rats in the control and the GEN þ PE-treated groups. The GSH level in renal tissue of only GEN-treated rats was significantly lower than those in the control group, and administration of PE to GEN-treated rats significantly increased the level of GSH. The group that was given GEN and PE had significantly lower MDA levels in kidney cortex tissue than those given GEN alone. There was no significant difference of NO levels between the groups. In rats treated with GEN þ PE, despite the presence of mild tubular degeneration and tubular necrosis is less severe, and glomeruli maintained a better morphology when compared with the GEN-treated group. We think that PE prevents kidney damage by decreasing oxidative stress in kidney.

The simplicity of WC and BMI measurement and TG and HDL assessment, make VAI an easily applicable index for the evaluation of visceral fat dysfunction. VAI can be useful index for the evaluation and calculation of erectile dysfunction risk.

Background/Aims: KLOTHO, a type-1 transmembrane protein with glucurodinase activity, is expressed in tissues responsible for calcium homeostasis such as the kidney, parathyroid gland and the epithelium of the choroid plexus in the brain. Given the emerging evidence indicating a novel regulatory function for KLOTHO protein in renal calcium and phosphate homeostasis, the present study aims to investigate the association between KLOTHO genetic polymorphisms and kidney stone (KS). Methods:KLOTHO gene polymorphisms G395A in the promoter region, F252V in exon 2, and C1818T in exon 4 were investigated in 108 patients with renal calcium stone formation and 51 age-matched healthy volunteers with no history of renal stone formation, using polymerase chain reaction. Results: GG genotype of G395A KLOTHO polymorphism had approximately 2-fold increased KS risk compared with the homozygous genotype AA and heterozygote GA (OR 1.849, 95% CI 1.016–3.364, p = 0.044). We also found that non-A allele carriers had significantly higher KS risk associated with the KS clinical characteristics including hypercalcemia, hypophosphatemia and phosphaturia. Conclusion: Our findings suggested that the G395A polymorphism of KLOTHO gene is associated with the KSs and may act as a risk factor for the development of KS disease.

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