Cardiac depressant factors in renal disease.

Abstract

Chronic (CRF) and acute renal failure (ARF) are accompanied by cardiac dysfunction, particularly if ARF is complicated by sepsis. Intermyocardiocytic 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 deficiency is not clarified, because most of the data are evaluated in poorly controlled study trials. Multiple effects of serum fractions and ultrafiltrates 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 the pathogenetic role of this substance(s). One group of experiments suggests a molecular weight between 500 and 5,000 d; other experiments suggest activity at > 10,000 d. It is currently believed that myocardial depressant substance is a water-soluble molecule weighing 10,000-30,000 d. The data confirm the existence of "specific cardiomyopathy" caused by a functional defect related to filterable toxins. There are different myocardial depressant factors in CRF, ARF, and sepsis.