Management of urinary stones by experts in stone disease (ESD 2026)

The prevalence of urinary stones range between 1 and 14% in different countries around the world. Men account for approximately 67% of cases, but the gender gap is narrowing over time. A study conducted in the Russian Federation showed that 22.2% of subjects interviewed with a questionnaire reported a history of urolithiasis. Stone formation begins with the urinary crystallization of less soluble solutes contained in urine (calcium oxalate and/or calcium phosphate, uric acid, struvite, and cystine), which often depends on urinary pH values. The most common calcium oxalate stones can grow on calcium phosphate plaques (Randall's plaque) that emerge on the surface of the papilla or on calcium oxalate plugs that form in the collecting ducts due to excessive concentrations of calcium or oxalate. Randall's plaques form due to a proinflammatory process initiated by local macrophages with activation of fibroblasts, matrix modeling, and interstitial calcium phosphate deposition. The inhibitory effect of crystallization and crystal aggregation was studied in vitro demonstrating a reduction in the nucleation inhibition index and in aggregation inhibition index in renal stone formers compared to healthy controls (2.15% vs 6.15% and 34.15% vs 62.15%, respectively). Urolithiasis is a cluster of metabolic phenotypes interacting through urinary supersaturation. The metabolic work-up consists in the identification of high-risk patients requiring full metabolic profiling by basic metabolic panel, two 24-hour urine collections, stone analysis (when available), and software assessment of Relative Supersaturation (RSS) for calcium oxalate, calcium phosphate and uric acid. The endpoint of therapy is to reduce RSS not just to achieve "normal" lab values. The most active agents used for the prevention of calcium oxalate stones are phytate, potassium citrate, and magnesium. Phytate stands as the most potent inhibitor of both calcium oxalate and calcium phosphate crystallization exerting its therapeutic effect without modifying urinary pH. It is the ideal inhibitor of calcium oxalate crystallization, particularly in cases of severe hypercalciuria, because it does not increase the risk of secondary calcium phosphate crystallization. Potassium citrate has a weaker direct inhibitory potential at the concentrations achieved in standard clinical practice and tends to increase urinary pH, posing a risk of inducing calcium phosphate precipitation. Magnesium does not affect urinary pH, but its inhibitory effect of calcium oxalate crystallization is negligible at conventional clinical doses [...].