Abstract
ObjectivePrevious evidence suggested that sodium–glucose cotransporter 2 inhibitor (SGLT2i)-mediated urinary glucose excretion (UGE) appeared to be reduced with a decrease in glomerular filtration rate. Thus, we conducted a systematic review and meta‐analysis to compare SGLT2i-mediated UGE among individuals with different levels of renal function.MethodsWe conducted systematic searches in PubMed, Medline, Embase, Cochrane Central Register of Controlled Trials, and ClinicalTrial.gov from inception to May 2021. Clinical studies of SGLT2i with reports of UGE changes in predefined different levels of renal function were included. The results were expressed as pooled effect sizes with 95% confidence interval (CI). A random-effects model was used to calculate the pooled effect sizes.ResultsIn total, eight eligible studies were included. Significant differences were observed in the post-treatment UGE level among subgroups stratified by renal function (P <0.001 for subgroup difference), which were gradually decreased along with the severity of impaired renal function. Consistently, changes in UGE before and after SGLT2i treatment were also decreased along with the severity of impaired renal function [67.52 g/day (95%CI: 55.58 to 79.47 g/day) for individuals with normal renal function, 52.41 g/day (95%CI: 38.83 to 65.99 g/day) for individuals with mild renal function impairment, 35.11 g/day (95%CI: 19.79 to 50.43 g/day) for individuals with moderate renal function impairment, and 13.53 g/day (95%CI: 7.20 to 19.86 g/day) for individuals with severe renal function impairment; P <0.001 for subgroup differences].ConclusionsSGLT2i-mediated UGE was renal function dependent, which was decreased with the extent of renal function impairment.
Highlights
Sodium–glucose cotransporter 2 inhibitors (SGLT2i) are widely used for the treatment of type 2 diabetes mellitus (T2DM) [1, 2]
SGLT2i-mediated urinary glucose excretion (UGE) was renal function dependent, which was decreased with the extent of renal function impairment
Combined with the available evidence from clinical trials, we found that, with SGLT2i use, there was a significant difference in the absolute value of post-treatment UGE among patients with different levels of renal function
Summary
Sodium–glucose cotransporter 2 inhibitors (SGLT2i) are widely used for the treatment of type 2 diabetes mellitus (T2DM) [1, 2]. SGLT2i increases urinary glucose excretion (UGE) by blocking the reabsorption of glucose in the renal proximal tubule [3]. SGLT2i-mediated glycosuria is associated with improved glycemic control and reduced levels of glycosylated hemoglobin (HbA1c) [4]. Since SGLT2i exerted their effects in the kidneys, it was advised to make specific dose adjustments based on renal function when giving a prescription [5]. Studies have shown that the glucose-lowering effect of SGLT2i was dependent on glomerular filtration [6]. Compared to patients with normal renal function or mild chronic kidney disease (CKD), the hypoglycemic efficacy of SGLT2i was reduced in patients with moderate CKD [7]
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