ERYTHROPOIETIN SYNTESIS IN PATIENTS WITH CHRONIC HEART FAILURE DEPENDING ON COMORBID PATHOLOGY

Abstract

Introduction. Decreased production of erythropoietin by the kidneys plays crucial role in the development of anemia in patients with chronic heart failure, especially on the background of comorbid diabetes mellitus type 2. In diabetic patients due to early damage of the kidney vessels and following erythropoietin deficiency anemia develops much earlier than clinically significant decrease of glomerular filtration rate. The aim of the study was to find out possible dependence of changes in the erythropoietinsynthesizing function of the kidneys on the degree of severity of anemic hypoxia in elderly and senile patients with chronic heart failure, including those with comorbid type 2 diabetes mellitus. Materials and methods. 120 patients with chronic heart failure of ischemic origin, type 2 diabetes mellitus and mild and moderate anemia were examined. Control group comprised 12 people with chronic heart failure without comorbid pathology. The examined groups were comparable in terms of gender and age, differing in the presence of comorbid diabetes mellitus and degree of severity of anemic syndrome. The level of erythropoietin in blood serum was determined by standard enzymelinked immunosorbent assay. Results. Type 2 diabetes mellitus in patients with chronic heart failure results in a significant decrease in erythropoietin production by 25 % compared to the control group (p<0,05). Comorbid to heart failure anemia leads to an increase in the level of erythropoietin by 74,4 % (р<0,05), and in the case of chronic heart failure and type 2 diabetes mellitus on the background of concomitant anemia – only by 39,5 % (р<0,05). As the severity of anemia in patients with chronic heart failure without diabetes progresses, the severity of the compensatory response of the kidneys to chronic anemic hypoxia is significantly higher than in patients with heart failure and comorbid type 2 diabetes. Conclusions. Diabetic nephropathy in patients with chronic heart failure and comorbid anemia leads to a significant deterioration of the erythropoietin-synthesizing function of the kidneys, complicating the course of both main and comorbid diseases.