title: Apolipoprotein E genotypes as predictors of high-risk groups for developing hyperlipidemia in kidney transplant recipients undergoing sirolimus treatment.
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.
authors.affiliation: Division of Transplantation, Department of Surgery, Virginia Commonwealth University, Richmond, VA 23298-0248, USA. dgmaluf@vcu.edu
authors.forename: Daniel G
authors.initials: DG
authors.lastname: Maluf
authors.forename: Valeria R
authors.initials: VR
authors.lastname: Mas
authors.forename: Kellie J
authors.initials: KJ
authors.lastname: Archer
authors.forename: Kenneth
authors.initials: K
authors.lastname: Yanek
authors.forename: Anne
authors.initials: A
authors.lastname: King
authors.forename: Andrea
authors.initials: A
authors.lastname: Ferreira-Gonzalez
authors.forename: Robert A
authors.initials: RA
authors.lastname: Fisher
authors.forename: Marc
authors.initials: M
authors.lastname: Posner
mesh_terms: D000328:Adult; D000368:Aged; D001057:Apolipoproteins E / Q000235:genetics*; D002784:Cholesterol / Q000097:blood; D003404:Creatinine / Q000097:blood; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D006949:Hyperlipidemias / Q000139:chemically induced / Q000453:epidemiology* / Q000235:genetics; D007166:Immunosuppressive Agents / Q000009:adverse effects; D016030:Kidney Transplantation / Q000276:immunology / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D020123:Sirolimus / Q000009:adverse effects*; D014280:Triglycerides / Q000097:blood; D014768:Virginia
chemical_list: D001057:Apolipoproteins E; D007166:Immunosuppressive Agents; D008077:Lipoproteins, LDL; D014280:Triglycerides; D002784:Cholesterol; D003404:Creatinine; D020123:Sirolimus