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Titolo:
Anaemia in end-stage renal disease: pathophysiological considerations
Autore:
Eckardt, KU;
Indirizzi:
Humboldt Univ, Charite, Dept Nephrol & Med Intens Care, D-13353 Berlin, Germany Humboldt Univ Berlin Germany D-13353 ntens Care, D-13353 Berlin, Germany
Titolo Testata:
NEPHROLOGY DIALYSIS TRANSPLANTATION
, volume: 16, anno: 2001, supplemento:, 7
pagine: 2 - 8
SICI:
0931-0509(2001)16:<2:AIERDP>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECOMBINANT-HUMAN-ERYTHROPOIETIN; HEMODIALYSIS-PATIENTS; NITRIC-OXIDE; CARDIOVASCULAR CONSEQUENCES; UREMIC ANEMIA; HEMOGLOBIN; MORTALITY; THERAPY; FAILURE; IMPACT;
Keywords:
anaemia; endothelial cell dysfunction; angiogenesis; hypoxia-inducible factor-1; nitric oxide; renal disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Eckardt, KU Humboldt Univ, Charite, Dept Nephrol & Med Intens Care, CampusVirchow Klinikum,Augustenberger Pl 1, D-13353 Berlin, Germany Humboldt Univ Campus Virchow Klinikum,Augustenberger Pl 1 Berlin Germany D-13353
Citazione:
K.U. Eckardt, "Anaemia in end-stage renal disease: pathophysiological considerations", NEPH DIAL T, 16, 2001, pp. 2-8

Abstract

Anaemia is a frequent complication of many diseases but the mechanisms that link reduced blood oxygen content to the long-term consequences of anaemia are incompletely understood. The maintenance of oxygen supply to the tissues during anaemia involves complex cardiovascular adaptations, including an increase in cardiac output, reduced peripheral resistance and increased oxygen extraction from haemoglobin (Hb). In addition, hypoxia-inducible factors are associated with the transcriptional activation of genes involved inadaptive mechanisms that increase oxygen delivery and provide alternative metabolic pathways. The complex pathophysiology of chronic kidney disease alters the adaptations to anaemia in uraemic patients. The increased cardiacOutput induced by anaemia is associated with left ventricular hypertrophy and cardiac disease in renal patients. Alterations in endothelial cell function, common in renal disease, may diminish endothelium-induced vasodilatation, increase the risk of atherosclerosis and impair angiogenesis. Many potential reasons for erythropoietin-induced hypertension in uraemic patients have been postulated, including increased blood viscosity as haematocrit rises, a reversal of hypoxic vasodilatation, increased blood volume that is not compensated by haemodialysis, ultrafiltration and impaired nitric oxide synthesis, preventing vascular relaxation in response to increased blood viscosity. In view of this impaired vascular reactivity, rapid increases in haematocrit should be avoided during epoetin treatment. As the interaction between anaemia and uraemia is very complex, it is not possible to derive the optimal Hb concentration for individual patients by using simple physiological or pathophysiological models and there is a need for good randomized controlled clinical trials to address this issue.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 12:13:59