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慢性腎臟病貧血的病生理機轉

Pathophysiological Mechanism of Anemia in Chronic Kidney Disease

摘要


紅血球生成(erythropoiesis)牽涉到:一、紅血球生成素(erythropoietin, EPO)促進的紅血球前驅細胞的分化與成熟;二、鐵質平衡(iron homeostasis)促進的網狀紅血球(reticulocyte)成熟。在慢性腎病患者中,EPO的製造受到腎臟間質纖維化(kidneyfibrosis)影響,EPO生成細胞(renal EPO-producingcell)製造EPO能力下降。前者的病生理機轉,與血管周細胞(pericyte)轉變為肌纖維母細胞(myofibroblast)相關的基因調控、缺氧誘導因子(hypoxia-induciblefactor, HIF)有關。後者,鐵質平衡中,慢性腎病將促使功能性缺鐵;鐵質平衡亦受鐵調節素(hepcidin)、HIF偵測調控。

並列摘要


Erythropoiesis involves: (1) differentiation and maturation of red blood cell precursors, promoted by erythropoietin (EPO); (2) reticulocyte maturation, induced by iron homeostasis. In patients with chronic kidney disease, the EPO producing cells gain some phenotype change and the ability of EPO producing is decreased during the process of renal fibrosis. The physiology of the former is related to the gene regulation and hypoxia-inducible factors associated with the transformation of pericytes into myofibroblasts. In the latter, iron homeostasis, chronic kidney disease will promote functional iron deficiency; homeostasis is also regulated by hepcidin and hypoxia-inducible factors.

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