Pathophysiology of cardiovascular damage in the early renal population.

Abstract

In renal disease, mechanisms available to compensate for the reduced haemoglobin levels associated with anaemia include increased oxygen extraction from peripheral tissues and, primarily, increased blood flow and changes in blood flow distribution. Haemodynamic changes induced by anaemia include decreases in blood viscosity, peripheral vascular resistance and oxygen delivery, and an increase in sympathetic activity. The overall effect of anaemia is a chronic increase in cardiac output and cardiac work. Under normal conditions, the increased cardiac work and blood flow associated with anaemia results in adaptive left ventricular hypertrophy (LVH)/remodelling and adaptive arterial hypertrophy/remodelling. However, under uraemic conditions these changes lead to maladaptive hypertrophy and arteriosclerosis. In end-stage renal disease (ESRD) patients, increases in both left ventricular end-diastolic volume and mass are related to decreases in haemoglobin. Therefore, LVH progresses in parallel with changes in haemoglobin level and is associated with decreased survival in ESRD patients receiving renal replacement therapy. In conclusion, anaemia is a contributory factor to LVH in renal disease and cardiovascular damage starts at an early stage. Therefore, early intervention to treat anaemia in these patients can prevent or delay this damage.