Anaemia: Cardiovascular adaptations and maladaptive responses in chronic kidney disease

Abstract

Without intervention, premature cardiovascular disease is virtually certain in progressive chronic kidney disease (CKD). Whatever age the patient, the cardiovascular system in uraemia is senescent and poorly suited to dealing with supraphysiological haemodynamic demands. Anaemia and hypertension are the principal haemodynamic risk factors that can be treated. Many observational studies have shown that anaemia is a risk factor for haemodynamic overload, maladaptive left ventricular growth, left ventricular failure and death. The justification for normal target haemoglobin (Hb) in patients with CKD is still debated. Observational studies of left ventricular size, quality of life, functional status, hospital admission, and survival support higher Hb concentrations (≥ 12 g/dl). Intervention trials to date suggest that a physiological approach to anaemia management benefits quality of life, and possibly left ventricular hypertrophy and dilatation. Obviously, avoiding anaemia is the only way to minimize time-averaged, anaemia-related haemodynamic load. Whether this strategy, involving efficient surveillance, early detection, early intervention, and high Hb targets that are independent of the phase of CKD, actually reduces cardiac failure or death remains to be seen.