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Chronic Kidney Disease and Diabetes · Journal article
Medical Sciences · September 9, 2026
Encouraging direction, but not yet definitive.
This narrative review synthesizes evidence that SGLT2 inhibitors reproducibly increase urinary citrate and may reduce calcium phosphate and, in some patients, uric acid supersaturation. Observational studies suggest fewer nephrolithiasis events among SGLT2 inhibitor users, but these findings rest on surrogate urinary endpoints and adverse-event data lacking standardized stone imaging and composition analysis. The clinical benefit for stone prevention remains unproven and phenotype-dependent; SGLT2 inhibitors should not be initiated for this indication alone.
Narrative review and evidence synthesis. Studies of patients with nephrolithiasis, type 2 diabetes, obesity, gout, chronic kidney disease, and other cardiometabolic disorders; 15 studies included. Intervention: SGLT2 inhibitors. Compared with: Control or comparator arms (standard care, placebo, or other agents in constituent studies).
SGLT2 inhibition is associated with reproducible increases in urinary citrate and variable effects on urine volume, urinary pH, and excretion of calcium, phosphate, and urate Short-term mechanistic studies suggest reductions in calcium phosphate supersaturation and in selected uric acid stone formers, uric acid supersaturation Effects on calcium oxalate supersaturation remain inconsistent
Observational studies and secondary analyses of randomised trials generally indicate fewer nephrolithiasis events among SGLT2 inhibitor users, but most outcomes were based on adverse-event reporting or administrative codes
For urologists and internists: SGLT2 inhibitors should not be prescribed solely to prevent kidney stones. In patients with established cardiovascular, renal, or metabolic indications for SGLT2 inhibition, potential benefits on urinary lithogenic factors may be an additional consideration, but stone recurrence prevention has not been demonstrated. Dedicated long-term randomized trials with stone-specific endpoints are needed before clinical recommendations can be made.
A rigorous narrative review of mechanistic and clinical evidence suggesting SGLT2 inhibitors may reduce nephrolithiasis risk, but based on short-term surrogate endpoints and observational data lacking standardized stone outcomes, requiring confirmation in dedicated randomized trials.
As stated by the source record.
Quoted from the source exactly as published.
For urologists and internists: SGLT2 inhibitors should not be prescribed solely to prevent kidney stones. In patients with established cardiovascular, renal, or metabolic indications for SGLT2 inhibition, potential benefits on urinary lithogenic factors may be an additional consideration, but stone recurrence prevention has not been demonstrated. Dedicated long-term randomized trials with stone-specific endpoints are needed before clinical recommendations can be made.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background: Nephrolithiasis frequently coexists with type 2 diabetes, obesity, gout, chronic kidney disease, and other cardiometabolic disorders. Sodium–glucose cotransporter 2 (SGLT2) inhibitors may influence stone formation through effects on glucosuria, natriuresis, urine volume, urinary citrate, pH, urate handling, and relative supersaturation. This review aimed to examine the current mechanistic, biochemical, and clinical evidence linking SGLT2 inhibition to nephrolithiasis, with particular attention to its relevance for urological practice. Methods: A clinically oriented narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar. The final search was performed on 1 July 2026. A total of 15 studies were included. Randomised trials, pooled and post hoc analyses, observational and comparative-effectiveness studies, meta-analyses, human mechanistic studies, and relevant experimental investigations were considered. Evidence was synthesised narratively according to biological mechanisms, urinary chemistry and relative supersaturation, randomised evidence, and observational clinical outcomes. Clinical stone events were analysed separately from surrogate urinary endpoints. Results: SGLT2 inhibition is associated with reproducible increases in urinary citrate and variable effects on urine volume, urinary pH, and the excretion of calcium, phosphate, and urate. Short-term mechanistic studies suggest reductions in calcium phosphate supersaturation and, in selected uric acid stone formers, uric acid supersaturation, whereas effects on calcium oxalate supersaturation remain inconsistent. Observational studies and secondary analyses of randomised trials generally indicate fewer nephrolithiasis events among SGLT2 inhibitor users; however, most outcomes were based on adverse-event reporting or administrative codes and lacked stone composition, standardised imaging, urinary phenotyping, and recurrence adjudication. Conclusions: SGLT2 inhibitors may favourably modify selected lithogenic pathways, but their effects appear phenotype-dependent and have not yet been shown to directly prevent stone recurrence. They should not be initiated solely for the prevention of nephrolithiasis. In patients with established cardiovascular, renal, or metabolic indications, their potential urinary effects may represent an additional benefit. Dedicated long-term randomised studies with stone-specific endpoints are required.
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