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Large clinical trials have demonstrated profound benefits of aldosterone inhibition by spironolactone in patients with heart failure (impaired left ventricle function <40%) and with eplerenone in patients with myocardial infarction.1 The key enzyme in aldosterone production is aldosterone synthase (CYP11B2). CYP11B2 is predominantly expressed in the adrenal gland but is also expressed in the cardiovascular system. Angiotensin (Ang) II is the major stimulus for CYP11B2-related aldosterone synthesis. Preclinical and clinical studies have shown that Ang II inhibition is pivotal to the treatment of heart failure and ischemic heart disease. The previous belief was that inhibition of Ang II should be sufficient to block aldosterone production; however, aldosterone levels can be elevated although Ang II production is inhibited or its action is blocked. This state of affairs is called the aldosterone breakthrough phenomenon; its mechanisms are unclear.2 Indeed, additional inhibition of the mineralocorticoid receptor (MR) reduces proteinuria in Ang-converting enzyme inhibitor–treated patients with early diabetic nephropathy.3 …

Cardiac Benefits of Mineralocorticoid Receptor Inhibition in Renal Failure