Abstract
Aim The renoprotective effect of sodium-glucose cotransporter 2 inhibitors is thought to be due, at least in part, to a decrease in blood pressure. The aim of this study was to determine the renal effects of these inhibitors in low blood pressure patients and the dependence of such effect on blood pressure management status. Methods The subjects of this retrospective study were 740 patients with type 2 diabetes mellitus and chronic kidney disease who had been managed at the clinical facilities of the Kanagawa Physicians Association. Data on blood pressure management status and urinary albumin-creatinine ratio were analyzed before and after treatment. Results Changes in the logarithmic value of urinary albumin-creatinine ratio in 327 patients with blood pressure < 130/80 mmHg at the initiation of treatment and in 413 patients with BP above 130/80 mmHg were −0.13 ± 1.05 and −0.24 ± 0.97, respectively. However, there was no significant difference between the two groups by analysis of covariance models after adjustment of the logarithmic value of urinary albumin-creatinine ratio at initiation of treatment. Changes in the logarithmic value of urinary albumin-creatinine ratio in patients with mean blood pressure of <102 mmHg (n = 537) and those with ≥102 mmHg (n = 203) at the time of the survey were −0.25 ± 1.02 and −0.03 ± 0.97, respectively, and the difference was significant in analysis of covariance models even after adjustment for the logarithmic value of urinary albumin-creatinine ratio at initiation of treatment (p < 0.001). Conclusion Our results confirmed that blood pressure management status after treatment with SGLT2 inhibitors influences the extent of change in urinary albumin-creatinine ratio. Stricter blood pressure management is needed to allow the renoprotective effects of sodium-glucose cotransporter 2 inhibitors.
Highlights
Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are new oral glucose-lowering agents, which act by increasing urine glucose excretion through inhibition of SGLT2 present in the renal proximal tubules
The inclusion criteria of this study were as follows: type 2 diabetes mellitus (T2DM) patients (1) aged more than 20 years, (2) who commenced treatment with SGLT2i for the first time at least 4 months before the current study, and (3) who had chronic kidney disease (CKD) as defined by the K/DOQI clinical practice guidelines for CKD [4]. These guidelines include >3 months of diagnosis of CKD that was based on one of the following criteria: (i) positivity for markers of kidney damage (albuminuria (ACR > 30 mg/gCr), urine sediment abnormalities, electrolyte and other abnormalities associated with tubular disorders, abnormalities detected by histology, and structural abnormalities detected by imaging), (ii) history of kidney transplantation, or (iii) low glomerular filtration rate (GFR)
Our study showed no significant improvement in albumin-creatinine ratio (ACR) in patients of the mean arterial pressure (MAP) ≥ 102 group after treatment with SGLT2i
Summary
Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are new oral glucose-lowering agents, which act by increasing urine glucose excretion through inhibition of SGLT2 present in the renal proximal tubules. The associated loss of calories through the huge amount of urinary glucose excretion leads to body weight (BW) loss In addition to their direct effects on blood glucose level, SGLT2i have other indirect beneficial effects, such as lowering blood pressure (BP) and improving. Our group reported previously that SGLT2i reduce the urinary albumin-creatinine ratio (ACR; mg/gCr) in Japanese T2DM patients with chronic kidney disease (CKD) [3]. This mechanism of this effect was not completely understood and presumed to be indirectly related to a decrease in BP. The aim of the present retrospective study was to investigate these two issues in adult patients with diabetic nephropathy treated with SGLT2i
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