New levers for CKD blood pressure, and old assumptions tested

The edition in brief

A phase 2 crossover trial (Explore-CKD, 59 participants with uncontrolled hypertension, CKD and albuminuria already on a RAAS blocker and SGLT2 inhibitor) tested the novel aldosterone synthase inhibitor lorundrostat. It lowered automated office systolic blood pressure by 7.5 mmHg against placebo and reduced albuminuria by about 26–30%, with a small expected dip in eGFR; three participants stopped for adverse events including hyperkalaemia, acute kidney injury and retinal detachment. A commentary on the LIPS trial confirms that lanreotide did not slow measured GFR decline in autosomal dominant polycystic kidney disease, despite a signal on estimated GFR, supporting the KDIGO recommendation not to use somatostatin analogues to preserve kidney function. A secondary analysis of SODa-BIC, using win-ratio composite outcomes, upheld the trial's neutral result: sodium bicarbonate did not improve major adverse kidney events in critically ill patients with metabolic acidosis (win ratio 0.97), though effect varied by acute kidney injury and acidaemia severity. A clinic pearl: protect the CKD kidney from avoidable insults — NSAIDs, unnecessary contrast, un-adjusted renal drugs — and apply sick-day rules during acute illness. Finally, a meta-analysis of 17 trials (29,192 patients) found SGLT2 inhibitors in diabetic CKD improved HbA1c, weight and blood pressure but had neutral short-term effects on the surrogate markers eGFR and albuminuria, with more volume-depletion events. The practice point is not to be misled by flat surrogates: the large outcome trials show clear long-term cardiorenal protection, so SGLT2 inhibitors remain foundational in diabetic CKD and should not be stopped because albuminuria or eGFR appears unchanged.