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Relationship between changes in uric acid levels and renal function during 12 months of treatment with luseogliflozin
Takuma Izutsu1,2, Hiroyuki Ito2, Suzuko Matsumoto2
1Department of Diabetes and Endocrinology, Iwate Prefectural Central Hospital, Iwate Prefectural Central Hospital, 1-4-1 Ueda, Moriokasi, Iwate 020-0066 Japan.
Background:
Sodium-glucose cotransporter-2 (SGLT2) inhibitors can effectively improve blood glucose levels in patients with type 2 diabetes, reduce the risk of cardiovascular disease and heart failure, and prevent chronic kidney disease. Although they reduce uric acid (UA) levels, few studies have investigated the relationship between UA reduction and renal function. We evaluated the degree of reduction in UA levels, various metabolic parameters, and renal function in patients with type 2 diabetes mellitus treated with luseogliflozin in order to develop a better renal protection strategy.
Methods:
This retrospective study analyzed 353 patients with type 2 diabetes who were newly treated with luseogliflozin. Patients were divided into two groups based on baseline UA levels, namely, the low group (< 6.0 mg/dL) and high group (≥ 6.0 mg/dL), with 74 patients in each group. Changes in metabolic parameters including glycated hemoglobin (HbA1c), UA levels, and estimated glomerular filtration rate (eGFR) were monitored over 12 months.
Results:
Both groups showed significant reductions in UA and HbA1c at 12 months. eGFR decreased significantly in the low group (- 3.1 ± 0.9 mL/min/1.73 m2, p = 0.002), whereas no significant change was observed in the high group (- 0.8 ± 1.3 mL/min/1.73 m2, p = 0.667). UA reduction was greater in the high group (- 1.0 ± 0.2 mg/dL vs. - 0.3 ± 0.1 mg/dL, p < 0.001). UA changes were significantly correlated with eGFR changes (p = 0.008) but not with HbA1c changes.
Conclusion:
Changes in eGFR after luseogliflozin administration were significantly correlated with baseline eGFR, uACR, and changes in uric acid levels (Δ uric acid). The change in uric acid levels following SGLT2 inhibitor treatment was associated with metabolic parameters such as blood pressure and albuminuria, suggesting that it may function as a surrogate marker reflecting renal metabolic processes.
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