Clinical Aspects of Cardiorenal Syndrome: Consequences of Therapy with the Renin-Angiotensin System Inhibitors

Abstract

The term “cardiorenal syndrome” has been introduced in an effort to describe problems of various kinds related to the simultaneous existence of heart and renal insufficiency. Synergism between two epidemiologic trends may support the construct of this syndrome, namely the population ageing and the epidemics of obesity and diabetes. Most studies indicate that the prevalence of anemia is increased in heart failure populations with co-morbid kidney disease, and therefore the term cardiorenal anemia syndrome has often been used. While rennin-angiotensin system inhibition improves morbidity and mortality in patients with congestive heart failure, it can further deteriorate renal function and increase incident anemia in patients with the cardiorenal syndrome. The mechanism is not yet fully understood, but angiotensin II, the active octapeptide of RAS, regulates intraglomerular filtration pressure and has been proven capable to both stimulate erythropoietin secretion and act as a direct growth factor on erythroid progenitors. Thus, RAS inhibition in patients with CRS may somehow diminish the beneficial effect anticipated from the studies in patients with CHF. Careful dose titration and frequent assessment of hemoglobin and hematocrit levels, estimated glomerular filtration rate, creatinine, sodium and potassium concentrations at the introduction of therapy is necessary to prevent this occurrence.