Apolipoprotein E genotypes as predictors of high-risk groups for developing hyperlipidemia in kidney transplant recipients undergoing sirolimus treatment

Daniel Maluf, Valeria Mas, Kellie J. Archer, Kenneth Yanek, Anne King, Andrea Ferreira-Gonzalez, Robert A. Fisher, Marc Posner

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background. Hypercholesterolemia (HCHL) and hypertriglyceridemia (HTRG) have emerged as the most significant metabolic consequences of therapy with sirolimus. Lipid status can be exacerbated by a variety of factors in the posttransplant setting, including genetic factors. Apoliprotein E (Apo E) polymorphism is an established genetic risk factor for hyperlipidemia. We studied the association between Apo E gene polymorphisms and lipids after kidney transplantation in patients undergoing sirolimus treatment. Methods. We studied 98 kidney transplant patients (KTP) with stable renal allograft undergoing sirolimus treatment: 39 with HCHL and HTRG within 90 days postsirolimus treatment (PST) and 59 without hyperlipidemia PST. Apo E genotyping was performed using INNO-LiPA-ApoE. Results. The cholesterol and the triglyceride values between the groups were 323.3±71.6 vs. 180.9±31.2 mg/dL (P<0.001) and 318.9±97.2 vs. 159.7±38.7 mg/dL (P<0.001). There was a significant difference in the genotype distribution of the hyperlipidemia and normal groups (P=0.009) with the percentages in each group as follows: E2/2 and E3/2: 12.8 vs. 5.1%; E3/3: 69.2% vs. 86.4%; and E4/3 and E4/4: 18.0% vs. 8.5%. We observed a higher number of patients with the genotype E3/3 in the group without hyperlipidemia PST (P=0.039). E3/2 and E4/4 genotype frequencies were higher in patients with hyperlipidemia PST. LDL levels in the hyperlipidemia PST group was statistical significant higher (P<0.001) and we observed an association between Apo E allelic distribution and LDL (P=0.005). Conclusions. Genetic factors, as Apo E genotypes, could allow the early identification of patients who are at a high risk for developing hyperlipidemia PST.

Original languageEnglish (US)
Pages (from-to)1705-1711
Number of pages7
JournalTransplantation
Volume80
Issue number12
DOIs
StatePublished - Dec 1 2005
Externally publishedYes

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Apolipoproteins E
Sirolimus
Hyperlipidemias
Genotype
Kidney
Therapeutics
Hypertriglyceridemia
Hypercholesterolemia
Lipids
Transplant Recipients
Normal Distribution
Kidney Transplantation
Allografts
Triglycerides
Cholesterol
Transplants

All Science Journal Classification (ASJC) codes

  • Transplantation
  • Immunology

Cite this

Apolipoprotein E genotypes as predictors of high-risk groups for developing hyperlipidemia in kidney transplant recipients undergoing sirolimus treatment. / Maluf, Daniel; Mas, Valeria; Archer, Kellie J.; Yanek, Kenneth; King, Anne; Ferreira-Gonzalez, Andrea; Fisher, Robert A.; Posner, Marc.

In: Transplantation, Vol. 80, No. 12, 01.12.2005, p. 1705-1711.

Research output: Contribution to journalArticle

Maluf, Daniel ; Mas, Valeria ; Archer, Kellie J. ; Yanek, Kenneth ; King, Anne ; Ferreira-Gonzalez, Andrea ; Fisher, Robert A. ; Posner, Marc. / Apolipoprotein E genotypes as predictors of high-risk groups for developing hyperlipidemia in kidney transplant recipients undergoing sirolimus treatment. In: Transplantation. 2005 ; Vol. 80, No. 12. pp. 1705-1711.
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abstract = "Background. Hypercholesterolemia (HCHL) and hypertriglyceridemia (HTRG) have emerged as the most significant metabolic consequences of therapy with sirolimus. Lipid status can be exacerbated by a variety of factors in the posttransplant setting, including genetic factors. Apoliprotein E (Apo E) polymorphism is an established genetic risk factor for hyperlipidemia. We studied the association between Apo E gene polymorphisms and lipids after kidney transplantation in patients undergoing sirolimus treatment. Methods. We studied 98 kidney transplant patients (KTP) with stable renal allograft undergoing sirolimus treatment: 39 with HCHL and HTRG within 90 days postsirolimus treatment (PST) and 59 without hyperlipidemia PST. Apo E genotyping was performed using INNO-LiPA-ApoE. Results. The cholesterol and the triglyceride values between the groups were 323.3±71.6 vs. 180.9±31.2 mg/dL (P<0.001) and 318.9±97.2 vs. 159.7±38.7 mg/dL (P<0.001). There was a significant difference in the genotype distribution of the hyperlipidemia and normal groups (P=0.009) with the percentages in each group as follows: E2/2 and E3/2: 12.8 vs. 5.1{\%}; E3/3: 69.2{\%} vs. 86.4{\%}; and E4/3 and E4/4: 18.0{\%} vs. 8.5{\%}. We observed a higher number of patients with the genotype E3/3 in the group without hyperlipidemia PST (P=0.039). E3/2 and E4/4 genotype frequencies were higher in patients with hyperlipidemia PST. LDL levels in the hyperlipidemia PST group was statistical significant higher (P<0.001) and we observed an association between Apo E allelic distribution and LDL (P=0.005). Conclusions. Genetic factors, as Apo E genotypes, could allow the early identification of patients who are at a high risk for developing hyperlipidemia PST.",
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T1 - Apolipoprotein E genotypes as predictors of high-risk groups for developing hyperlipidemia in kidney transplant recipients undergoing sirolimus treatment

AU - Maluf, Daniel

AU - Mas, Valeria

AU - Archer, Kellie J.

AU - Yanek, Kenneth

AU - King, Anne

AU - Ferreira-Gonzalez, Andrea

AU - Fisher, Robert A.

AU - Posner, Marc

PY - 2005/12/1

Y1 - 2005/12/1

N2 - Background. Hypercholesterolemia (HCHL) and hypertriglyceridemia (HTRG) have emerged as the most significant metabolic consequences of therapy with sirolimus. Lipid status can be exacerbated by a variety of factors in the posttransplant setting, including genetic factors. Apoliprotein E (Apo E) polymorphism is an established genetic risk factor for hyperlipidemia. We studied the association between Apo E gene polymorphisms and lipids after kidney transplantation in patients undergoing sirolimus treatment. Methods. We studied 98 kidney transplant patients (KTP) with stable renal allograft undergoing sirolimus treatment: 39 with HCHL and HTRG within 90 days postsirolimus treatment (PST) and 59 without hyperlipidemia PST. Apo E genotyping was performed using INNO-LiPA-ApoE. Results. The cholesterol and the triglyceride values between the groups were 323.3±71.6 vs. 180.9±31.2 mg/dL (P<0.001) and 318.9±97.2 vs. 159.7±38.7 mg/dL (P<0.001). There was a significant difference in the genotype distribution of the hyperlipidemia and normal groups (P=0.009) with the percentages in each group as follows: E2/2 and E3/2: 12.8 vs. 5.1%; E3/3: 69.2% vs. 86.4%; and E4/3 and E4/4: 18.0% vs. 8.5%. We observed a higher number of patients with the genotype E3/3 in the group without hyperlipidemia PST (P=0.039). E3/2 and E4/4 genotype frequencies were higher in patients with hyperlipidemia PST. LDL levels in the hyperlipidemia PST group was statistical significant higher (P<0.001) and we observed an association between Apo E allelic distribution and LDL (P=0.005). Conclusions. Genetic factors, as Apo E genotypes, could allow the early identification of patients who are at a high risk for developing hyperlipidemia PST.

AB - Background. Hypercholesterolemia (HCHL) and hypertriglyceridemia (HTRG) have emerged as the most significant metabolic consequences of therapy with sirolimus. Lipid status can be exacerbated by a variety of factors in the posttransplant setting, including genetic factors. Apoliprotein E (Apo E) polymorphism is an established genetic risk factor for hyperlipidemia. We studied the association between Apo E gene polymorphisms and lipids after kidney transplantation in patients undergoing sirolimus treatment. Methods. We studied 98 kidney transplant patients (KTP) with stable renal allograft undergoing sirolimus treatment: 39 with HCHL and HTRG within 90 days postsirolimus treatment (PST) and 59 without hyperlipidemia PST. Apo E genotyping was performed using INNO-LiPA-ApoE. Results. The cholesterol and the triglyceride values between the groups were 323.3±71.6 vs. 180.9±31.2 mg/dL (P<0.001) and 318.9±97.2 vs. 159.7±38.7 mg/dL (P<0.001). There was a significant difference in the genotype distribution of the hyperlipidemia and normal groups (P=0.009) with the percentages in each group as follows: E2/2 and E3/2: 12.8 vs. 5.1%; E3/3: 69.2% vs. 86.4%; and E4/3 and E4/4: 18.0% vs. 8.5%. We observed a higher number of patients with the genotype E3/3 in the group without hyperlipidemia PST (P=0.039). E3/2 and E4/4 genotype frequencies were higher in patients with hyperlipidemia PST. LDL levels in the hyperlipidemia PST group was statistical significant higher (P<0.001) and we observed an association between Apo E allelic distribution and LDL (P=0.005). Conclusions. Genetic factors, as Apo E genotypes, could allow the early identification of patients who are at a high risk for developing hyperlipidemia PST.

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