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

Citation
A. Segarra et al., 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, Nephron, 69(1), 1995, pp. 9-13
Citations number
25
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00282766
Volume
69
Issue
1
Year of publication
1995
Pages
9 - 13
Database
ISI
SICI code
0028-2766(1995)69:1<9:S(LIPW>2.0.ZU;2-P
Abstract
In order to analyze the relationship between lipoprotein (a) [Lp (a)] and other lipoproteins during chronic renal failure and once renal fun ction is restored after kidney transplantation, we determined the seru m levels of total lipoprotein, high-density lipoprotein, low-density l ipoprotein, and very-low-density lipoprotein cholesterols, total and v ery-low-density lipoprotein triglycerides, apolipoproteins A-I, B, C-I I, C-III, and E, and E, and Lp (a) in 30 patients with chronic renal f ailure before and 12 months after renal transplantation. During the is t year after transplantation, all patients were treated only with cicl osporin and prednisone and had serum creatinine levels < 1.6 mg/dl (14 0 mu mol/l) and proteinuria < 500 mg/day. No patients had chronic hepa tic disease. To determine reference values we studied a control group of 60 healthy volunteers. Before renal transplantation, the study grou p showed higher concentrations of triglycerides, very-low-density trig lycerides, very-low density lipoprotein cholesterol, apolipoproteins, C-II and C-III, and Lp(a) than the control group. There was no correla tion between Lp(a) and any of the studied variables. After renal trans plantation, the serum levels of total lipoprotein, high-density lipopr otein, and low-density lipoprotein and apolipoproteins A-I and B incre ased significantly. Apolipoproteins C-II and C-III and Lp(a) decreased and normalized. After these changes had taken place, there was no rel ationship between Lp(a) and other parameters of lipoprotein metabolism . We conclude that the increase in Lp(a) during the chronic renal fail ure phase is basically related to the loss of renal function and does not depend on the resultant alterations which are produced in other li poprotein variables.