title: Anaemia, renal insufficiency and cardiovascular outcome.
abstract: Cellular models of cardiac hypertrophy and cardiac failure suggest that haemodynamic stresses lead to increased rates of cardiac myocyte apoptosis and fibrosis. Over the last 15 years, it has been become evident that the dramatically amplified exposure of patients with renal insufficiency to haemodynamic stress leads to maladaptive vascular and ventricular adaptations. Anaemia and hypertension are remediable haemodynamic stresses consistently associated with left ventricular enlargement in observational studies. Observational studies and clinical trials have shown consistently that treating the established, typically severe, anaemia of end-stage renal disease (ESRD) improves outcome. It has become clear that late intervention to normalize haemoglobin in patients with ESRD and cardiomyopathy achieves little. There is considerable observational evidence to suggest that intervention in haemodynamic risk factors, such as anaemia and hypertension, should coincide with their onset, which is typically years before renal replacement therapy. The optimum target haemoglobin, and timing of intervention, remain areas of intense speculation and research effort.
authors.affiliation: Department of Nephrology, Salford Royal Hospitals NHS Trust, Hope Hospital, Stott Lane, Salford M6 8HD, UK.
authors.forename: J
authors.initials: J
authors.lastname: Hegarty
authors.forename: R N
authors.initials: RN
authors.lastname: Foley
mesh_terms: D000740:Anemia / Q000209:etiology / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology*; D002319:Cardiovascular System / Q000503:physiopathology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology* / Q000628:therapy*; D017202:Myocardial Ischemia / Q000150:complications / Q000503:physiopathology; D006435:Renal Dialysis