Abstract
Introductıon Ureteral obstruction is a common pathology and caused kidney fibrosis and dysfunction at late period. In this present, we investigated the antifibrotic and antiinflammatory effects of montelukast which is cysteinyl leukotriene receptor antagonist, on kidney damage after unilateral ureteral obstruction(UUO) in rats.Mateirıals and Methods 32 rats divided four groups. Group 1 was control, group 2 was sham, group 3 was rats with UUO and group 4 was rats with UUO which were given montelukast sodium (oral 10 mg/kg/day). After 14 days, rats were killed and their kidneys were taken and blood analysis was performed. Tubular necrosis, mononuclear cell infiltration 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. Urea-creatinine levels were investigated at blood analysis. Statistical analyses were made by the Chi-square test and one-way analysis of variance (ANOVA).Results There was no difference significantly for urea-creatinine levels between groups. Pathologically, there was serious tubular necrosis and fibrosis in group 3 and there was significantly decreasing for tubular necrosis and fibrosis in group 4(p<0.005). Also, there was significantly increasing for NO and MDA levels; decreasing for GSH levels in group 3 compared the other groups(p<0.005).Conclusıon We can say that montelukast prevent kidney damage with antioxidant effect, independently of NO.
Highlights
Chronic kidney diseases, which lead to end-stage kidney failure, are associated with changes in kidney structure and fibrosis regardless of the underlying cause
There was no significant difference for urea-creatinine levels between groups (Table-1)
ureteral obstruction (UUO) induced a significant increase in the tissue Nitric oxide (NO) levels that have been prevented by montelukast sodium (ML) (Table-2)
Summary
Chronic kidney diseases, which lead to end-stage kidney failure, are associated with changes in kidney structure and fibrosis regardless of the underlying cause. The acute phase of obstructed kidney in unilateral ureteral obstruction (UUO) is characterized by dramatic changes in glomerular filtration rate, renal blood flow, and interstitial edema [2, 3]. Such an obstruction might be observed after benign prostatic hyperplasia; renal, ureteral, or bladder calculi; urethral stricture; and neoplasm of the bladder, prostate, or urethra [1]. The injuries are characterized by tubular dilatation or atrophy, inflammatory infiltration of leucocytes, fibroblast activation, proliferation, increase in matrix proteins, and progressive interstitial fibrosis with the loss of renal parenchyma. Unilateral ureteral obstruction (UUO) is an experimental rat model of renal injury that imitates the process of obstructive nephropathy in an accelerated manner[1]
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