#5867 EFFECT OF SGLT2I ON URIC ACID AND GLUCOSE URINARY FRACTIONAL EXCRETION IN PATIENTS WITH CHRONIC KIDNEY DISEASE AND TYPE 2 DIABETES MELLITUS

Abstract

Abstract Background and Aims Sodium-glucose cotranspoter type 2 inhibitors (SGLT2i) have demonstrated broad benefits beyond glycemic control, including hypouricemic effects. However, this fact has not been completely validated in chronic kidney disease (CKD). The mechanism by which SGLT2i produces an increase in uric acid elimination is not fully understood and appears to be mediated in part by increased glucose in the renal tubule, which would compete in reabsorption with uric acid through GLUTb transporter. The aim of this study is to analyse the effect of SGLT2i on uric acid and glucose urinary fractional excretion (FE) in type 2 diabetes mellitus (T2DM) + CKD patients. Method Retrospective observational single-center study conducted between January18 and December 22 in T2DM-CKD patients on SGLT2i. Subjects on renal replacement therapy, treatment with GLP1 analogues and those for whom we did not have uricosuria prior to the start of iSGLT2 were excluded. Urinary uric acid and glucose FE were analysed at baseline and during follow-up of up to 24 months, with 3, 6 and 12 months cut-offs. Data are described as mean and standard deviation (SD). Statistical analysis was performed using STATA v14 with statistics for paired samples. Results 82 patients were included in the study, with a mean follow-up of 1.2 years. During follow-up, 23 patients left the study (arGLP1 initiation (n = 9), adverse reactions (n = 4), exitus (n = 2) and loss to follow-up (n = 8). 78.1% were male, mean age 72.7 years (SD 8.5), and main co-morbidities were: obesity 76.8%, arterial hypertension 95%, hyperuricemia 75.6% and congestive heart failure 25.6%. Distribution according SGLT2i drug was: 65.6% dapagliflozin, 25% canagliflozin and 9.4% empagliflozin. eGFR decreased immediately after initiation of SGLT2i with ulterior stabilization as described elsewhere (Table 1). We observed a significant increase on urinary uric acid FE that remain stable along the follow-up: basal 7.4%, 3 months 9.4% (p < 0.001). However, serum uric acid levels did not show significant differences along the study. Urinary glucose FE increase remained stable along the whole observation period in spite of no significant differences from a clinical point of view on % of glycosylated haemoglobin (Table 1). Conclusion Despite decreased GFR, T2DM-CKD patients exhibited significant urinary uric acid and glucose FE increase after starting SGLT2i. This increase remained stable for at least 2 years. However, we did not observe significant reductions on uricemia in these patients, implying that increase on urinary uric acid excretion is not enough in this setting to obtain significant modifications on uricemia.