1 Department of Nephrology 2 Department of Cardiology Soroka Medical Center and Faculty of Health Sciences Ben-Gurion University Beer-Sheva, Israel Email: hausmann{at}bgumail.bgu.ac.il
Sir,
We appreciate the comments of Azar et al. and Fenwick et al. Azar et al. emphasize that the use of aldactone is safe in a specific group of patients with severe congestive heart failure despite a certain degree of renal failure, provided they are treated by peritoneal dialysis. Hyperkalaemia has recently been reported in an aldactone-treated patient with chronic renal failure. This patient was not a dialysis patient [1]. The fact that hypokalaemia is not uncommon in peritoneal dialysis patients reflects the efficiency of dialysate potassium disposal in these patients [2]. This contrasts with the higher prevalence of hyperkalaemia in haemodialysis patients [3].
Our patient differs from the 15 patients mentioned in the comment of Azar et al., by the fact that peritoneal dialysis has been initiated in our patient for the treatment of end-stage renal disease whereas peritoneal dialysis in their patients improves the management of severe congestive heart failure. The number of peritoneal dialysis patients with decreased left ventricular function as exemplified by our patient is likely to be greater than the number of patients with congestive heart failure treated by peritoneal dialysis [4].
Our patient also differs from Azar's patients in that he has not been treated with ACE inhibitors. ACE inhibition has also been part of the treatment in the RALES study as mentioned in the comment of Fenwick [5]. This is important because angiotensin II and aldosterone are both known for their independent stimulatory effect on cardiac fibrogenesis [6,7]. We agree with Fenwick et al., that a combination therapy with aldosterone and an ACE inhibitor is likely to be more effective in cardiac fibrosis [8].
Revascularization has probably contributed to the improved cardiac function in our patient. Since the publication of our report, a follow-up echocardiographic examination of the patient 2 years after initiation of aldactone therapy disclosed a further improvement in his left ventricular systolic function. This late effect is unlikely to be attributed to revascularization but to the long-term effect of aldactone.
The question whether the beneficial effect of aldactone in congestive heart failure is due to its diuretic effect concerns the very basis of the RALES study. The experimental study of Bauersachs et al., mentioned by Fenwick et al., does in fact not support the RALES study which raised the possibility that saluresis is not required for its beneficial clinical effect [9,10]. Thus, we do not agree with the conclusion of Fenwick et al., that renal function is necessary to attain an effect of aldactone and that it is unjustified to extrapolate the potential benefits seen in RALES to patients with advanced renal disease. On the contrary, we believe that peritoneal dialysis patients provide an appropriate clinical model to test this hypothesis, as the renal effects of aldactone are excluded.
References