Effects of sodium-glucose co-transporter 2 (SGLT2) inhibition on renal function and albuminuria in patients with type 2 diabetes: a systematic review and meta-analysis

PeerJ. 2017 Jun 27:5:e3405. doi: 10.7717/peerj.3405. eCollection 2017.

Abstract

Aim: To evaluate the effects of sodium-glucose co-transporter 2 (SGLT2) inhibition on renal function and albuminuria in patients with type 2 diabetes.

Methods: We conducted systematic searches of PubMed, Embase and Cochrane Central Register of Controlled Trials up to June 2016 and included randomized controlled trials of SGLT2 inhibitors in adult type 2 diabetic patients reporting estimated glomerular filtration rate (eGFR) and/or urine albumin/creatinine ratio (ACR) changes. Data were synthesized using the random-effects model.

Results: Forty-seven studies with 22,843 participants were included. SGLT2 inhibition was not associated with a significant change in eGFR in general (weighted mean difference (WMD), -0.33 ml/min per 1.73 m2, 95% CI [-0.90 to 0.23]) or in patients with chronic kidney disease (CKD) (WMD -0.78 ml/min per 1.73 m2, 95% CI [-2.52 to 0.97]). SGLT2 inhibition was associated with eGFR reduction in short-term trials (WMD -0.98 ml/min per 1.73 m2, 95% CI [-1.42 to -0.54]), and with eGFR preservation in long-term trials (WMD 2.01 ml/min per 1.73 m2, 95% CI [0.86 to 3.16]). Urine ACR reduction after SGLT2 inhibition was not statistically significant in type 2 diabetic patients in general (WMD -7.24 mg/g, 95% CI [-15.54 to 1.06]), but was significant in patients with CKD (WMD -107.35 mg/g, 95% CI [-192.53 to -22.18]).

Conclusions: SGLT2 inhibition was not associated with significant changes in eGFR in patients with type 2 diabetes, likely resulting from a mixture of an initial reduction of eGFR and long-term renal function preservation. SGLT2 inhibition was associated with statistically significant albuminuria reduction in type 2 diabetic patients with CKD.

Keywords: Albuminuria; Diabetic nephropathy; Glomerular filtration rate; Meta-analysis; SGLT2 inhibitor.

Grants and funding

This work was supported by the Key Project of the Chinese National Program for Fundamental Research and Development (973 Program 2012CB517803 to LC), the Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences (2016-I2M-2-004 to LC), the National Natural Science Foundation, China (81170674 and 81470937 to LC), and Xiehe Scholar Fund to LC. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.