Levine D M, Gordon B R
Rogosin Institute, New York, NY 10021, USA.
Am J Kidney Dis. 1995 Jul;26(1):162-9. doi: 10.1016/0272-6386(95)90170-1.
Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for vascular disease and a potential link between coagulation, lipoproteins, and the development of atherosclerosis. Its role in the vascular complications of patients with chronic renal disease is unclear. We review methodologic issues involved in measuring Lp(a), particularly as they relate to studies of patients with chronic renal disease. The accurate measurement of Lp(a) is difficult because all the commercially available assays are sensitive to apolipoprotein(a) isoform size, Lp(a) behaves like an acute phase reactant, and levels vary markedly among ethnic groups. The results of 12 studies that included data on median Lp(a) levels in controls and patients receiving renal replacement therapy were analyzed. Although there was variation among studies, most found elevated levels of Lp(a) in patients receiving hemodialysis (range of medians, 9.0 to 38.4 mg/dL) compared with controls (range of medians, 4.7 to 19.7 mg/dL). With the exception of one study, Lp(a) levels also were elevated in patients receiving continuous ambulatory peritoneal dialysis compared with controls and patients receiving hemodialysis. In one study, an elevated Lp(a) level in patients receiving hemodialysis correlated with subsequent development of vascular events. A separate study associated the occurrence of vascular access occlusion with Lp(a) level. Following renal transplantation, Lp(a) levels decreased in all four studies, which included data before and after transplantation. Although variability in results were seen, Lp(a) levels appear to be elevated in patients receiving renal replacement therapy. Renal transplantation at least partially reverses this effect. The variability in results is probably related to methodologic difficulties in measuring Lp(a) and failure to segregate ethnic groups in study design and analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
脂蛋白(a)[Lp(a)]是一种由基因决定的血管疾病危险因素，也是凝血、脂蛋白与动脉粥样硬化发展之间的潜在联系。其在慢性肾病患者血管并发症中的作用尚不清楚。我们回顾了测量Lp(a)所涉及的方法学问题，尤其是与慢性肾病患者研究相关的问题。准确测量Lp(a)很困难，因为所有市售检测方法都对载脂蛋白(a)异构体大小敏感，Lp(a)表现得像一种急性期反应物，且不同种族群体中的水平差异显著。分析了12项研究的结果，这些研究包含了对照组和接受肾脏替代治疗患者的Lp(a)中位数水平数据。尽管研究之间存在差异，但大多数研究发现，与对照组（中位数范围为4.7至19.7mg/dL）相比，接受血液透析的患者Lp(a)水平升高（中位数范围为9.0至38.4mg/dL）。除一项研究外，与对照组和接受血液透析的患者相比，接受持续性非卧床腹膜透析的患者Lp(a)水平也升高。在一项研究中，接受血液透析患者的Lp(a)水平升高与随后血管事件的发生相关。另一项研究将血管通路闭塞的发生与Lp(a)水平相关联。在所有四项包含移植前后数据的研究中，肾移植后Lp(a)水平均下降。尽管结果存在差异，但接受肾脏替代治疗的患者Lp(a)水平似乎升高。肾移植至少部分逆转了这种效应。结果的差异可能与测量Lp(a)的方法学困难以及在研究设计和分析中未对种族群体进行区分有关。（摘要截选至250字）
