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

Michael J. Hausmann1 and Noah Liel-Cohen2

1 Department of Nephrology 2 Department of Cardiology, Soroka Medical Center and, Faculty of Health, Ben-Gurion University, Beer-Sheva, Israel Email: hausmann{at}bgumail.bgu.ac.il

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 (Kt/V 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, ß-blockers and digoxin were not part of his treatment. The plasma aldosterone level was 75 pg/ml. 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 meq/l in the pre-treatment period and did not exceed 5.5 meq/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 fibrosis as his glucose levels varied between 150 and 250 mg%.

Systemic aldosterone excess has been shown to cause cardiac hypertrophy and fibrosis independent of cardiac failure or hypertension. Several studies have demonstrated that dialysis patients have aldosterone levels manifold higher than normal controls [4]. Although in the presented diabetic patient systemic aldosterone level remains within normal limits, other non-diabetic patients may indeed be exposed to much higher aldosterone levels, which would further justify aldactone therapy.

The hazard of hyperkalaemia remains of a major concern, though, in dialysis patients treated by aldactone. Serious hyperkalaemia has not been a significant complication of aldactone therapy in the RALE study. In dialysis patients with increased aldosterone levels, extra-renal disposal of potassium supposedly compensates for the lost capacity of renal potassium excretion. In addition, other potassium regulatory hormones like insulin and catecholamines contribute to potassium homeostasis. These hormones will not be affected by aldactone therapy and the tendency in dialysis patients to hyperkalaemia is not necessarily more prominent following aldactone therapy [5]. The danger of hyperkalaemia is further reduced in peritoneal dialysis patients in whom the aldosterone-independent disposal of potassium into dialysate is continuous and daily. This can explain why no hyperkalaemia has been detected in our patient throughout the period of observation.

Echocardiographic examination of our patient demonstrates improved systolic and diastolic function of the left ventricle. This may be attributed in part to aldactone therapy and in part to the successful PTCA performed prior to initiation of aldactone treatment. Favourable cardiac effects of aldactone in patients with left ventricular dysfunction have been demonstrated in a few studies using echocardiography to measure left ventricular ejection fraction and mass [6]. In our patient, fractional shortening was included in echocardiographic evaluation as it has been shown to be an independent parameter associated with mortality in dialysis patients [7].

In conclusion, this report demonstrates that aldactone therapy is feasible in selected peritoneal dialysis patients. As cardiovascular morbidity has a high prevalence in dialysis patients, aldactone therapy may improve cardiac mortality in this group of patients.

References

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