The Uricosuric Effect of SGLT2 Inhibitors Is Maintained in the Long Term in Patients with Chronic Kidney Disease and Type 2 Diabetes Mellitus.
Paula Sánchez-BrialesMaría Marques VidasPaula López-SánchezMaría Victoria López-IllázquezLucía Martín-TestillanoAylin Vedat-AliJose M PortolésPublished in: Journal of clinical medicine (2024)
(1) Background: Sodium-glucose co-transporter 2 inhibitors (SGLT2is) increase uric acid excretion. The intensity of uricosuria is linked to glycosuria. (2) Methods: We aim to analyze the effect of SGLT2 inhibitors on urinary fractional excretion (FE) of uric acid and glucose in patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) in a single-center retrospective study with patients with T2DM and CKD who started on treatment with SGLT2is. Patients on renal replacement therapy or with glucagon-like peptide-1 (GLP1) analogs were excluded. Subgroup analysis was performed according to the estimated glomerular filtration rate (eGFR), the SGLT2i molecule, the main comorbidities, and concomitant treatment. As a secondary objective, the study analyzed the effect of SGLT2 inhibitors on uricemia levels. (3) Results: Seventy-three patients were analyzed, with a mean follow-up of 1.2 years. Uric acid and glucose FE significantly increased after the initiation of SGLT2is. This increase remained stable during the follow-up without differences among eGFR groups. No significant reduction in uricemia was observed. However, a trend towards a decrease was observed. (4) Conclusion: The use of SGLT2is in patients with CKD and T2DM is associated with an increase in uric acid FE, which maintains stability irrespective of glomerular filtration loss at least during 24 months of follow-up.
Keyphrases
- uric acid
- chronic kidney disease
- end stage renal disease
- metabolic syndrome
- small cell lung cancer
- peritoneal dialysis
- newly diagnosed
- epidermal growth factor receptor
- prognostic factors
- blood pressure
- patient reported outcomes
- randomized controlled trial
- combination therapy
- blood glucose
- cardiovascular risk factors
- molecular docking
- endothelial cells
- replacement therapy
- patient reported