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In an individual participant data meta-analysis of three randomized, double-blind, placebo-controlled trials including 14,574 adults with chronic kidney disease (mean age 63.7 years), finerenone versus placebo reduced the composite kidney outcome (kidney failure or sustained ≥57% decline in eGFR) by 24% (HR 0.76) and reduced kidney failure alone (HR 0.85). Finerenone also reduced the composite cardiovascular outcome (hospitalisation for heart failure or cardiovascular death; HR 0.80), heart failure hospitalisation (HR 0.78), cardiovascular death (HR 0.82), and all-cause death (HR 0.88), with treatment effects on kidney outcomes consistent across glycaemic status, CKD aetiology, baseline eGFR, albuminuria, and SGLT2 inhibitor use. Hyperkalaemia was more frequent with finerenone than placebo, although hyperkalaemia leading to hospitalisation was uncommon.

This review summarizes evidence that albuminuria, commonly measured by urinary albumin-to-creatinine ratio (present in nearly half of patients with heart failure), is an independent risk marker for incident heart failure and for worse outcomes in established heart failure even at low levels. It notes that routine UACR screening is not universally recommended in heart-failure guidelines, and that reductions in UACR with therapies (renin-angiotensin inhibitors, SGLT2 inhibitors, finerenone) are associated with lower risks of cardiovascular, heart failure, and chronic kidney disease outcomes, supporting albuminuria as a potential modifiable risk marker.

This random-effects meta-analysis pooled 29 observational studies (497,368 patients) comparing AMI-related cardiogenic shock (AMI-CS) versus acutely decompensated heart failure CS (ADHF-CS) and found AMI-CS patients were slightly older and had higher presenting LVEF but presented more fulminantly with higher odds of cardiac arrest (OR 2.03) and SCAI stage D/E shock (OR 1.50). AMI-CS had markedly greater use of temporary mechanical circulatory support (eg, any device OR 5.44) and higher short-term (in-hospital/30-day) mortality (OR 1.58); the authors note phenotype-defining variables were extractable in <1.1% of the pooled cohort.