The high incidence of cardiac complications in endstage renal failure is not only related to the chronic pressure load of the left ventricle, although the proportion of patients with elevated blood pressure increases from 53 to 81% as reno-parenchymal disease progresses. Other factors as anemia, hyperparathyroidism, autonomic neuropathy and retention of electrolytes, metabolic products of toxins may cause damage to the heart. It is a matter of discussion whether uremia itself causes cardiomyopathy. Findings of a reduced Ca++-uptake during beta-adrenergic stimulation and a reduced reaction of (Na+, K+)-ATPase to digitalis suggest a basic change of myocardial membrane metabolism. Retention of an "endogenous digitalis" could help to explain some contradictory results.
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