title: Heritability of renal function and inflammatory markers in adult male twins.
abstract: BACKGROUND
  Loss of renal function is accompanied by a progressive increase in markers of inflammation; it is unknown whether they share common genetic pathways.
  
  
  METHODS
  We evaluated the shared heritability of estimated glomerular filtration rate (eGFR) and markers of inflammation and endothelial activation in 524 twin males from the Vietnam Era Twin Registry; 9 twins were excluded due to incomplete or incorrect data. Models were adjusted for age, race, body mass index, smoking, hypertension, diabetes mellitus, prior coronary artery disease and intercurrent medications.
  
  
  RESULTS
  The mean eGFR was 89 ± 13 ml/min/1.73 m² (range 35-146); eGFR, intracellular adhesion molecule (ICAM) and TNF-α receptor (TNF-αR) were moderately heritable (all ∼50%), while IL-6 receptor (IL-6R) and P-selectin were highly heritable (68 and 76%, respectively). IL-6R and TNF-αR showed a significant inverse association with eGFR (p = 0.04 and p < 0.0001) while the association with ICAM and P-selectin was direct (p = 0.001 and p = 0.06). Bivariate structural equation models showed that the association between eGFR and biomarkers was due to unique environmental factors and there were no shared genetic pathways.
  
  
  CONCLUSIONS
  We found no shared genetic pathways between renal function and inflammation. Thus, increased inflammation represents a response to declining renal function rather than being a mechanism contributing to renal deterioration.
authors: Department of Medicine, Emory University, Atlanta, GA, USA. praggi@emory.edu
authors: Paolo
authors: P
authors: Raggi
authors: Shaoyong
authors: S
authors: Su
authors: Cristina
authors: C
authors: Karohl
authors: Emir
authors: E
authors: Veledar
authors: Enrique
authors: E
authors: Rojas-Campos
authors: Viola
authors: V
authors: Vaccarino
mesh_terms: D015415:Biomarkers / Q000097:blood*; D004777:Environment; D005919:Glomerular Filtration Rate / Q000235:genetics*; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000235:genetics*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000235:genetics; D007668:Kidney / Q000378:metabolism / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D008962:Models, Theoretical; D019007:P-Selectin / Q000097:blood / Q000235:genetics; D019947:Receptors, Interleukin-6 / Q000097:blood / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood / Q000235:genetics; D014427:Twins
chemical_list: D015415:Biomarkers; D019007:P-Selectin; D019947:Receptors, Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D018799:Intercellular Adhesion Molecule-1