Abstract
Anaemia appears to play an important role in left ventricular (LV) enlargement in chronic kidney disease patients. The objective of this study was to evaluate LV echocardiography changes during anaemia correction with recombinant human erythropoietin (rHu-Epo) in chronic haemodialysis patients (HD pts) with signs of anaemia and LV hypertrophy (LVH). The study included 20 HD pts aged 39,6 +/- 5,3 yrs, with the same condition of HD treatment, anaemia and echocardiographically LVH verified. At the beginning of the rHu-Epo treatment haemoglobin (Hb) level was < 90 g/L and the target Hb level was 110 g/L. Echocardiography was performed at the beginning (baseline) and after six months of rHu-Epo treatment. LVH was defined as LV mass index >100 g/m2 in women and >131 g/m2 in men. We observed significant reduction of LV mass index (LVMI) (mean 26,4%, p=0.008), as well as LV volumen. There was a significant negative correlation between Hb level and LVMI with predictive LVMI reduction of 2,317 g/m2 for each 1g/L rising of mean Hb level. The results of the study confirm the importance of early anaemia correction in haemodialysis patients aimed to improve LV parameters.
Highlights
Cardiovascular complications are the leading couse of mortality in the end stage renal disease and are responsible for about 50% of total mortality rate of uraemic patients treated by dialysis [1,2]
Anaemia presents a proven factor related to cardial abnormalities within these group of patients [5,6]. It is mostly mediated by the lack of erythropoietin, a hormone produced by type I fibroblasts of peritubular interstitium and epithelial cells of proxymal tubuls, which is the key regulator of erythropoiesis
Efficient correction of anaemia led to significant reduction of left ventricular (LV) mass index in these patients (p=0.008), achieving normal values in few patients (Table 2)
Summary
Cardiovascular complications are the leading couse of mortality in the end stage renal disease and are responsible for about 50% of total mortality rate of uraemic patients treated by dialysis [1,2]. Anaemia presents a proven factor related to cardial abnormalities within these group of patients [5,6]. It is mostly mediated by the lack of erythropoietin , a hormone produced by type I fibroblasts of peritubular interstitium and epithelial cells of proxymal tubuls, which is the key regulator of erythropoiesis. Lower oxygen delivery leads to local vasodilatation, which significantly increases ventricular preload and cardiac output, as an compansatory mechanism of reduced capacity for oxygen transport. The increment of cardiac output aimed to satisfy metabolic needs has significant impact to LV geometry
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