Introduction:
Urinary calculi and renal cancer are significant urological conditions that may share overlapping etiologies. Despite common links to metabolic dysfunction and chronic inflammation, their co-occurrence and shared molecular mechanisms remain underexplored. This study aimed to evaluate clinical, biochemical, and molecular associations between these conditions.

Material and methods:
A cohort of 526 patients was analyzed for demographic data, clinical features, and laboratory markers. Molecular analyses were performed on key renal cancer–related genes: VHL, PBRM1, and MET. Structural models were generated using RCSB PDB data, and bioinformatics techniques were employed to assess protein expression and mutation frequency.

Results:
Obesity (OR = 2.1), hypertension (OR = 1.8), diabetes (OR = 1.7), and hypercalciuria (OR = 2.3) were all identified as significant risk factors (p < 0.05). Molecular analysis revealed frequent mutations in VHL (23.6%), PBRM1 (20.9%), and MET (18.6%). A pro-inflammatory environment was indicated by elevated oxidative stress markers (ROS, MDA) and inflammatory biomarkers (CRP, IL-6). Structural studies of VHL and MET proteins revealed conformational changes that may affect their biological activity.

Conclusions:
The co-occurrence of urinary calculi and renal cancer suggests a shared pathogenic mechanism involving chronic inflammation, metabolic dysfunction, and genetic alterations. These findings underscore the need for comprehensive clinical management and early genetic screening to reduce risk and improve outcomes.