Dapagliflozin may confer renal protection
Sodium-glucose transport protein 2 (SGLT2) inhibitors exert a putative epigenetic regulation of the protecting cardiovascular effect, reports a study, adding that dapagliflozin may protect the kidneys by preserving renal vasodilating capacity.
To determine whether dapagliflozin modulated systemic and renal vascular function and structure and induced epigenetic modification, 40 hypertensive patients with type 2 diabetes were randomized to 4-week treatment with dapagliflozin 10 mg or hydrochlorothiazide (HCT) 12.5 mg.
The investigators performed routine analyses and measured the following at baseline and after treatment: plasma renin activity, aldosterone, catecholamine and 24-hour urinary electrolyte levels; flow-mediated dilation (FMD) of the brachial artery; carotid-femoral pulse-wave velocity (PWV); augmentation index; and resistive index and dynamic renal resistive index (DRIN).
Circulating miRNAs (miRs) associated with heart failure (miR30e-5p, miR199a-3p), endothelial dysfunction (miR27b and miR200b) and renal function (miR130b-3p, miR21-5p) were evaluated and compared with the treatment effects.
Dapagliflozin and HCT slightly reduced blood pressure. Dapagliflozin also lowered fasting glucose and increased 24-hour diuresis, glycosuria and osmolar clearance (p-all<0.001), without affecting sodium excretion and glomerular filtration rate. Treatment with dapagliflozin also led to a significant increase in magnesium levels (p=0.02).
Both dapagliflozin and HCT did not modify FMD or PWV. While DRIN did not change in the dapagliflozin group, it increased in the HCT group (p-interaction=0.047). The two treatments also resulted in variations in the expression of some miRs, but only dapagliflozin significantly upregulated miR30e-5p and downregulated miR199a-3p.