Aldactone therapy in a peritoneal dialysis patient with decreased left ventricular function

Sir, Since the publication by Pitt et al. [1] of the randomized aldactone evaluation study (RALES) in 1999, patients with congestive heart failure are commonly treated with low dose aldactone to counteract the cardiac effects of aldosterone. The study excluded patients with a serum creatinine level of )2.5 mg%. While aldactone treatment in chronic renal failure patients is not recommended, it may be safe in dialysis patients. We present a peritoneal dialysis patient with congestive heart failure that is treated with aldactone without significant side effects. A 73-year-old patient with end-stage kidney disease due to diabetic nephropathy was treated by cycling peritoneal dialysis. Dialysis was adequate (KtuV 2.27) and he was in a good general condition. A year and a half after initiation of dialysis he presented with multiple premature ventricular beats. The patient was referred for further cardiac evaluation. Echocardiographic evaluation disclosed normal left ventricle size with symmetric hypertrophy and moderately decreased systolic left ventricular function (ejection fraction 32%). Elevated left ventricular diastolic filling pressure reflected a significant degree of diastolic dysfunction. At coronary angiography, three-vessel disease was diagnosed and relieved in two sessions by angioplasty and stenting. The patient’s treatment was complemented by aldactone 25 mg daily. ACE inhibitors, b-blockers and digoxin were not part of his treatment. The plasma aldosterone level was 75 pguml. The serum potassium level was monitored weekly for 1 month and then monthly for 10 months. The serum potassium level did not exceed 5.1 mequ l in the pre-treatment period and did not exceed 5.5 mequ l during the period of observation while treated with aldactone. A total of 34 meq potassium was disposed daily via dialysate and 18 meq via urinary output. The patient developed gynecomasty attributed to aldactone; malignancy was excluded by mammography. Echocardiography was repeated 10 months after aldactone treatment had been initiated. The ejection fraction had increased from 32 to 46%, with no change in left ventricular diameter and hypertrophy. Although impaired diastolic relaxation was still apparent, left ventricular filling pressure was normalized reflecting improved diastolic function. Efficacy of aldactone in reducing the mortality of patients with congestive heart failure has been demonstrated in patients with normal renal function. This case demonstrates that aldactone therapy in peritoneal dialysis patients can be safe and may contribute to improved cardiac function. As cardiovascular mortality is high in dialysis patients, this patient group should be considered for aldactone therapy to improve their survival. Aldactone’s favourable effect on cardiovascular mortality has been attributed to cardiac more than renal effects. Therefore, aldactone therapy is expected to benefit dialysis patients. Cardiac fibrosis is promoted by aldosterone and successfully suppressed by aldactone. Local cardiac aldosterone production is increased in congestive heart failure [2]. Furthermore, high glucose concentration in medium amplifies aldosterone-induced hypertrophy of cardiomyocytes [3]. The presented case may therefore be more prone to cardiac