APOPROTEIN AND LIPID PROFILES AFTER RENAL -TRANSPLANTATION

Citation
A. Segarra et al., APOPROTEIN AND LIPID PROFILES AFTER RENAL -TRANSPLANTATION, Nefrologia, 15(2), 1995, pp. 163-170
Citations number
NO
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
02116995
Volume
15
Issue
2
Year of publication
1995
Pages
163 - 170
Database
ISI
SICI code
0211-6995(1995)15:2<163:AALPAR>2.0.ZU;2-I
Abstract
In order to examine the effects of renal transplantation on serum lipo protein concentrations in patients with chronic renal failure (CRF) tr eated with hemodialysis, we prospectively measured the serum concentra tions of lipids and apoproteins AI, B, CII, CIII and E in a sample of 50 non-diabetic patients (36 male, 14 female, age 44 +/- 11) with end- stage renal failure before and after successful renal transplantations . All patients were given cyclosporin-A and prednisone as the only tre atment, and during the first year following transplant they had normal renal function (serum creatinine < 1,5 mg/dL/140 mu mol/L) and protei nuria < 500 mg/day. They did not suffer from hepatic disease, hypothyr oidism or cholestasis. Reference values were obtained from a control g roup of 60 healthy volunteers whose age, sex and body mass index match ed those of the study group. Befores renal transplant the study group showed an increase in serum triglycerides, VLDL triglycerides and VLDL cholesterol and a decrease in HDL cholesterol. In 90 % of the study g roup we observed an increase in apo CIII, CII, CIII/CII ratio and a de crease in apo AI. After renal transplantation serum concentrations of total, LDL, HDL-cholesterol, apo B and apo A1 increased significantly. Before renal transplantation, characteristic apolipoprotein disturban ces were observed which were common to most patients; These alteration s seem to be interrelated and determined by renal failure. After the r ecovery of renal function, serum concentrations of lipids and apolipop roteins changed remarkably as did the relationship between lipids and apoproteins. In this phase, the apoprotein pattern suggests that hyper lipidemia may be due to a combination of an increase in hepatic synthe sis of apo B/VLDL and one or more defects in the catabolism of apo B10 0-rich lipoproteins. We wish to point out that, in contras pre-transpl ant hyperlipidemia, it is unlikely that a single factor can account fo r the different apoprotein patterns observed in these patients after r enal transplant.