CARDIAC DEPRESSANT FACTORS IN RENAL-DISEASE

Chronic (CRF) and acute renal failure (ARF) are accompanied by cardiac dysfunction, particularly if ARF is complicated by sepsis. Intermyoca rdiocytic fibrosis is described in CRF, but there is also evidence for functional cardiomyopathy. Acetate ion (present in the dialysate) and secondary hyperparathyroidism do not appear to be clinically relevant myocardial depressant factors in uremia. The role of carnitine defici ency is not clarified, because most of the data are evaluated in poorl y controlled study trials. Multiple effects of serum fractions and ult rafiltrates obtained from CRF and ARF patients during dialysis suggest the existence of myocardial depressant factor(s). Beneficial effects of continuous hemofiltration in multiorgan failure give evidence for t he pathogenetic role of this substance(s). One group of experiments su ggests a molecular weight between 500 and 5,000 d; other experiments s uggest activity at > 10,000 d. It is currently believed that myocardia l depressant substance is a water-soluble molecule weighing 10,000-30, 000 d. The data confirm the existence of ''specific cardiomyopathy'' c aused by a functional defect related to filterable toxins. There are d ifferent myocardial depressant factors in CRF, ARF, and sepsis.