Progression of diabetic kidney disease has slowed over the past 40 years by as much as 70–75%, thanks to a diversity of drug classes that have less effect on glucose and more on reducing cardiorenal risk.

With the advent of sodium-glucose co-transporter 2 (SGLT2) inhibitors and the novel nonsteroidal mineralocorticoid antagonist, finerenone, we now have three ‘pillars of therapy’ considering the renin–angiotensin system (RAS) inhibitors as already established treatment to slow diabetic kidney disease. Both renal and cardiovascular outcomes trials have provided solid evidence of the benefit by these agents to slow kidney disease progression and reduce heart failure hospitalizations. Using these agents together reduces the risk of hyperkalemia by finerenone and further reduces albuminuria in animal models. Trials are underway to also see if the glucagon-like peptide 1 receptor agonist, semaglutide, will also protect against diabetic kidney disease progression as seen in post hoc analyses of positive cardiovascular outcome trials. If positive, this would be the fourth pillar to support cardiorenal protection without fear of hypoglycemia.

Nephrologists now have three different agents neither of which has a major effect on blood pressure but both add to further reduce progression of diabetic nephropathy and hospitalization from heart failure.