Key result
Spironolactone shows no benefit over chlorthalidone for reducing left ventricular mass in nondiabetic CKD.
Why the study?
It was unknown whether spironolactone's reductions in left ventricular mass and arterial stiffness in early-stage CKD were due to BP reduction or specific vascular and myocardial effects.
Does spironolactone reduce left ventricular mass compared to chlorthalidone in patients with nondiabetic stage 2 and 3 CKD?
RCT (n=154)
Open-label, blinded end point
randomized
Yes
Does spironolactone reduce left ventricular mass compared to chlorthalidone in patients with nondiabetic stage 2 and 3 CKD?
Spironolactone was not superior to chlorthalidone in reducing left ventricular mass, blood pressure, or arterial stiffness in patients with nondiabetic CKD.
Spironolactone is not superior to chlorthalidone for LV mass regression in nondiabetic CKD and increases hyperkalemia; challenges MRA preference and supports thiazide-like diuretics as alternative.
Background and objectives In a randomized double-blind, placebo-controlled trial, treatment with spironolactone in early-stage CKD reduced left ventricular mass and arterial stiffness compared with placebo. It is not known if these effects were due to BP reduction or specific vascular and myocardial effects of spironolactone. Design, setting, participants, & measurements A prospective, randomized, open-label, blinded end point study conducted in four UK centers (Birmingham, Cambridge, Edinburgh, and London) comparing spironolactone 25 mg to chlorthalidone 25 mg once daily for 40 weeks in 154 participants with nondiabetic stage 2 and 3 CKD (eGFR 30–89 ml/min per 1.73 m 2 ). The primary end point was change in left ventricular mass on cardiac magnetic resonance imaging. Participants were on treatment with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker and had controlled BP (target ≤130/80 mm Hg). Results There was no significant difference in left ventricular mass regression; at week 40, the adjusted mean difference for spironolactone compared with chlorthalidone was −3.8 g (95% confidence interval, −8.1 to 0.5 g, P =0.08). Office and 24-hour ambulatory BPs fell in response to both drugs with no significant differences between treatment. Pulse wave velocity was not significantly different between groups; at week 40, the adjusted mean difference for spironolactone compared with chlorthalidone was 0.04 m/s (−0.4 m/s, 0.5 m/s, P =0.90). Hyperkalemia (defined ≥5.4 mEq/L) occurred more frequently with spironolactone (12 versus two participants, adjusted relative risk was 5.5, 95% confidence interval, 1.4 to 22.1, P =0.02), but there were no patients with severe hyperkalemia (defined ≥6.5 mEq/L). A decline in eGFR >30% occurred in eight participants treated with chlorthalidone compared with two participants with spironolactone (adjusted relative risk was 0.2, 95% confidence interval, 0.05 to 1.1, P =0.07). Conclusions Spironolactone was not superior to chlorthalidone in reducing left ventricular mass, BP, or arterial stiffness in nondiabetic CKD.
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Edwards et al. (2021) conducted an RCT in Nondiabetic stage 2 and 3 chronic kidney disease (n=154). Spironolactone vs. Chlorthalidone 25 mg once daily was evaluated on Change in left ventricular mass on cardiac magnetic resonance imaging (adjusted mean difference -3.8 g, 95% CI -8.1 to 0.5, p=0.08). Spironolactone was not superior to chlorthalidone in reducing left ventricular mass in nondiabetic CKD (adjusted mean difference -3.8 g; 95% CI -8.1 to 0.5; P=0.08).
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