Heritability of renal function and inflammatory markers in adult male twins

Paolo Raggi, Shaoyong Su, Cristina Karohl, Emir Veledar, Enrique Rojas-Campos, Viola Vaccarino

Research output: Contribution to journalArticle

14 Citations (Scopus)

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. Study Design: 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. Conclusion: 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.

Original languageEnglish (US)
Pages (from-to)317-323
Number of pages7
JournalAmerican Journal of Nephrology
Volume32
Issue number4
DOIs
StatePublished - Oct 1 2010

Fingerprint

Glomerular Filtration Rate
Kidney
Inflammation
Interleukin-6 Receptors
P-Selectin
Tumor Necrosis Factor Receptors
Vietnam
Structural Models
Registries
Coronary Artery Disease
Diabetes Mellitus
Body Mass Index
Biomarkers
Smoking
Hypertension

Keywords

  • Heritability
  • Inflammation
  • Renal function

ASJC Scopus subject areas

  • Nephrology

Cite this

Raggi, P., Su, S., Karohl, C., Veledar, E., Rojas-Campos, E., & Vaccarino, V. (2010). Heritability of renal function and inflammatory markers in adult male twins. American Journal of Nephrology, 32(4), 317-323. https://doi.org/10.1159/000319449

Heritability of renal function and inflammatory markers in adult male twins. / Raggi, Paolo; Su, Shaoyong; Karohl, Cristina; Veledar, Emir; Rojas-Campos, Enrique; Vaccarino, Viola.

In: American Journal of Nephrology, Vol. 32, No. 4, 01.10.2010, p. 317-323.

Research output: Contribution to journalArticle

Raggi, P, Su, S, Karohl, C, Veledar, E, Rojas-Campos, E & Vaccarino, V 2010, 'Heritability of renal function and inflammatory markers in adult male twins', American Journal of Nephrology, vol. 32, no. 4, pp. 317-323. https://doi.org/10.1159/000319449
Raggi, Paolo ; Su, Shaoyong ; Karohl, Cristina ; Veledar, Emir ; Rojas-Campos, Enrique ; Vaccarino, Viola. / Heritability of renal function and inflammatory markers in adult male twins. In: American Journal of Nephrology. 2010 ; Vol. 32, No. 4. pp. 317-323.
@article{c9df905f39b04f40b8039c1d619a7369,
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. Study Design: 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. Conclusion: 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.",
keywords = "Heritability, Inflammation, Renal function",
author = "Paolo Raggi and Shaoyong Su and Cristina Karohl and Emir Veledar and Enrique Rojas-Campos and Viola Vaccarino",
year = "2010",
month = "10",
day = "1",
doi = "10.1159/000319449",
language = "English (US)",
volume = "32",
pages = "317--323",
journal = "American Journal of Nephrology",
issn = "0250-8095",
publisher = "S. Karger AG",
number = "4",

}

TY - JOUR

T1 - Heritability of renal function and inflammatory markers in adult male twins

AU - Raggi, Paolo

AU - Su, Shaoyong

AU - Karohl, Cristina

AU - Veledar, Emir

AU - Rojas-Campos, Enrique

AU - Vaccarino, Viola

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Background: Loss of renal function is accompanied by a progressive increase in markers of inflammation; it is unknown whether they share common genetic pathways. Study Design: 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. Conclusion: 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.

AB - Background: Loss of renal function is accompanied by a progressive increase in markers of inflammation; it is unknown whether they share common genetic pathways. Study Design: 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. Conclusion: 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.

KW - Heritability

KW - Inflammation

KW - Renal function

UR - http://www.scopus.com/inward/record.url?scp=77955646945&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77955646945&partnerID=8YFLogxK

U2 - 10.1159/000319449

DO - 10.1159/000319449

M3 - Article

C2 - 20720405

AN - SCOPUS:77955646945

VL - 32

SP - 317

EP - 323

JO - American Journal of Nephrology

JF - American Journal of Nephrology

SN - 0250-8095

IS - 4

ER -