Expression Profiles of Claudin Gene Family Members in Patients With Recurrent Calcium Oxalate Kidney Stones

• Published in: Curēus (Palo Alto, CA) Vol. 16; no. 9; p. e70354
• Main Authors: Uysal, Umit, Sagir, Süleyman, Baris Mogul, Cansu, Caner, Vildan, Tuncay, O Levent
• Format: Journal Article
• Language: English
• Published: United States Cureus Inc 27.09.2024; Cureus
• Subjects: Biopsy; Disease; Family medical history; Genes; Kidney stones; Patients; Polymerase chain reaction; Urological surgery; Urology; United States > US; paracellular pathway; nephrolithiasis; recurrent kidney stones; calcium oxalate stone; claudins; claudin 1
• ISSN: 2168-8184; 2168-8184
• DOI: 10.7759/cureus.70354

In this study, we aimed to evaluate and compare the expression profiles of 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. 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. The urinary calcium, oxalate, and citrate levels of the patients included in the study, as well as those in the control group, were within normal ranges. They did not have proteinuria in their urine. The biochemical parameters were also within normal limits. Biopsy samples taken from the intact renal cortex parenchymal tissue were consistent. Total RNA was isolated from biopsy samples and expression profiles of target genes ( ) were determined by real-time polymerase chain reaction (PCR). It was determined that gene expression in patients with recurrent calcium oxalate kidney stones was approximately four times higher than in the control group; this difference was statistically significant (p<0.050). expression was also strongly positively correlated with (r=0.642), (r=0.753) and (r=0.651) Conclusions: We thought that overexpression might play a role in the pathogenesis of recurrent calcium oxalate stone formation. together with , , , and are also probably responsible for this pathogenesis.