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Serum Lipoprotein (a) Levels in Patients with Chronic Renal Failure – Evolution after Renal Transplantation and Relationship with Other Parameters of Lipoprotein Metabolism: A Prospective Study

 

作者: A. Segarra,   P. Chacón,   M. Martin,   M. Vilardell,   J. Vila,   M. Cotrina,   J. Fort,   A. Olmos,   L.L. Piera,  

 

期刊: Nephron  (Karger Available online 1995)
卷期: Volume 69, issue 1  

页码: 9-13

 

ISSN:1660-8151

 

年代: 1995

 

DOI:10.1159/000188353

 

出版商: S. Karger AG

 

关键词: Chronic renal failure;Lipoprotein (a);Lipoproteins;Renal transplantation

 

数据来源: Karger

 

摘要:

In order to analyze the relationship between lipoprotein (a) [Lp (a)] and other lipoproteins during chronic renal failure and once renal function is restored after kidney transplantation, we determined the serum levels of total lipoprotein, high-density lipoprotein, low-density lipoprotein, and very-low-density lipoprotein cholesterols, total and very-low-density lipoprotein triglycerides, apohpoproteins A-I, B, C-II, C-III, and E, and E, and Lp (a) in 30 patients with chronic renal failure before and 12 months after renal transplantation. During the 1st year after transplantation, all patients were treated only with ciclosporin and prednisone and had serum creatinine levels < 1.6 mg/dl (140 μmol/l) and proteinuria < 500 mg/day. No patients had chronic hepatic disease. To determine reference values we studied a control group of 60 healthy volunteers. Before renal transplantation, the study group showed higher concentrations of triglycerides, very-low-density triglycerides, very-low density lipoprotein cholesterol, apohpoproteins, C-II and C-III, and Lp(a) than the control group. There was no correlation between Lp(a) and any of the studied variables. After renal transplantation, the serum levels of total lipoprotein, high-density lipoprotein, and low-density lipoprotein and apohpoproteins A-I and B increased significantly. Apohpoproteins C-II and C-III and Lp(a) decreased and normalized. After these changes had taken place, there was no relationship between Lp(a) and other parameters of lipoprotein metabolism. We conclude that the increase in Lp(a) during the chronic renal failure phase is basically related to the loss of renal function and does not depend on the resultant alterations which are produced in other lipoprotein variables

 

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