J Hypertens 2021 Jan 11. Epub 2021 Jan 11.
Department of Nephrology, Hippokration Hospital, Aristotle University of Thessaloniki, Greece IIS-Fundacion Jimenez Diaz, School of Medicine, University Autonoma of Madrid, FRIAT and REDINREN, Madrid, Spain Department of Renal Medicine, University Hospitals Birmingham, Edgbaston, Birmingham, UK Service de Nephrologie-HTA, dialyses, transplantation rénale, CHRU de Tours-Hospital Bretonneau, Tours, France Institute of Clinical Pharmacology and Toxicology, Charité-Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany CNR-Institute of Clinical Physiology, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio Calabria Università Milano-Bicocca, Milan and Policlinico di Monza, Monza, Italy Division of Nephrology, Wuerzburg University Clinic, Würzburg, Germany.
Chronic kidney disease (CKD) is a major issue of public health. Hypertension control and use of renin--angiotensin system (RAS) blockers are the cornerstones of treatment for CKD of any cause. However, even under optimal RAS blockade, many individuals will progress towards more advanced CKD. Within the past few years, evidence from cardiovascular outcome trials with sodium--glucose co-transporter-2 (SGLT-2) inhibitors clearly suggested that these agents substantially delay CKD progression in patients with diabetes mellitus on top of standard-of-care treatment. The Canagliflozin-and-Renal-Events-in-Diabetes-with-Established-Nephropathy-Clinical-Evaluation (CREDENCE) study, showed that canagliflozin substantially reduced the risk of doubling of SCr, end-stage kidney disease (ESKD), or death from renal or cardiovascular causes in 4401 patients with diabetic CKD compared with placebo (hazard ratio 0.70; 95% CI 0.59-0.82). Recently, the Study-to-Evaluate-the-Effect-of-Dapagliflozin-on-Renal-Outcomes-and-Cardiovascular-Mortality-in-Patients-With-Chronic-Kidney-Disease (DAPA-CKD), including 2510 patients with diabetic and 1803 with nondiabetic CKD, also showed an impressive reduction in the risk of ≥50% decline in eGFR, ESKD, or death from renal or cardiovascular causes (HR 0.61; 95% CI 0.51-0.72). The benefit was similar for patients with diabetic and nondiabetic CKD, including patients with glomerulonephritides. Following this conclusive evidence, relevant guidelines should accommodate their recommendations to implement treatment with SGLT-2 inhibitors for patients with diabetic and nondiabetic CKD.