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心血管手術後產生之急性腎衰竭與游離血紅素之關係

Relationship between Acute Kidney Injury and Free Hemoglobin Following Cardiac Surgery

摘要


急性腎衰竭是心血管手術後常見的併發症,一旦病人術後產生急性腎衰竭,其死亡率明顯增加,即使肌酸酐(creatinine)上升的程度很微小,也會使死亡率上升。了解心血管手術後急性腎衰竭的危險因子很重要,在術前針對這些病人積極預防急性腎衰竭,以及早期辨別出原因,可以改善術後病人的存活率。心血管手術後的游離血紅素可能會增加,以往認為尿液的游離血紅素(free hemoglobin)在腎臟會形成血鐵質沉著(hemosiderosis)及圓柱沉渣(cast)阻塞腎小管來損害腎功能,愈來愈多的証據顯示,血漿游離血紅素會減少血液一氧化氮(nitric oxide, NO),使內皮細胞調控血流的功能受到損傷,因而影響腎臟灌流,導致腎臟損傷。而游離血紅素的來源,除了體外循環(cardiopulmonary bypass)外,也可能與輸注的儲存紅血球有關。體外循環是心血管手術的特點,除了會增加游離血紅素外,也有其他因素使體外循環更容易產生腎衰竭。許多新的生物標記(biomarker)在心血管術後的研究與發展,提供早期辨認術後的腎臟損傷。了解這些機轉與新的研究,讓我們更能掌握病人的狀況與維護病人腎臟功能。

並列摘要


Acute kidney injury is common complication following cardiac surgery. Even if small increase in serum creatinine, post operative mortality siginificantly increase. It is important to recognize the risk factor of acute kidney injury following cardiac surgery. To prevent before operation and identify the cause of acute kidney injury after operation can improve patient survival. Free hemoglobin can increase after cardiac surgery. Urine free hemoglobin can cause hemosiderosis and cast formation to damage the kidney. Growing evidence revealed plasma free hemoglobin reduce nitric oxide bioavailability and therefore interfere endothelium mediated vasodilatation and subsequently impair kidney perfusion. Besides cardiopulmonary bypass, the source of free hemoglobin may be from transfusion of storage red blood cells. Cardiopulmonary bypass can also worsen kidney function by other pathogenesis. Recently, several studies about novel biomarkers for acute kidney injury following cardiac surgery have also been proposed. After we understand the pathogenesis and new development of biomarkers, we can do our best to protect patient's kidney function.

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