Affiliation:
1. Department of Urology, Mardin Training and Research Hospital
2. Department of Medical Biology, School of Medicine, Pamukkale University
3. Department of Medical Genetics, School of Medicine, Pamukkale University
4. Department of Urology, School of Medicine, Pamukkale University
Abstract
Abstract
OBJECTİVES: It is thought that genetic variations observed in members of the Claudin (CLDN) gene family may be responsible for the pathogenesis of recurrent kidney stone disease. In this study, we aimed to evaluate and compare the expression profiles of CLDN gene family members responsible for the mechanism of stone formation in patients with recurrent calcium oxalate stones and in a control group without a history of renal stones.
METHODS: Nineteen patients with recurrent calcium oxalate renal calculi who underwent percutaneous nephrolithotomy and 21 control patients without renal calculi who underwent surgery for other reasons were included in the study. Biopsy samples were taken from the intact renal parenchymal tissue consistent with computerized tomography images of all individuals. Total RNA was isolated from biopsy samples and expression profiles of target genes (Claudin 1-4, 7, 8, 10, 14, 16, 18, 19) were determined by real-time PCR(Polymerase Chain Reaction).
RESULTS: It was determined that CLDN1 gene expression in patients with recurrent calcium oxalate kidney stones was approximately 4 times higher than in the control group, this difference was significant (p<0.050). CLDN1 expression was also strongly positively correlated with CLDN4 (r=0.642), CLDN7 (r=0.753) and CLDN14 (r=0.651)
CONCLUSIONS: We thought that CLDN1 overexpression might play a role in the pathogenesis of recurrent calcium oxalate stone formation. CLDN1 together with CLDN2, CLDN4, CLDN7, and CLDN14 are also probably responsible for this pathogenesis. More studies are needed on CLDN gene family members responsible for the pathogenesis of recurrent calcium oxalate kidney stones
Publisher
Research Square Platform LLC