Contribution of Genetic Background and Data Collection on Adverse Events of Anti-human Immunodeficiency Virus (HIV) Drugs (D:A:D) Clinical Risk Score to Chronic Kidney Disease in Swiss HIV-infected Persons With Normal Baseline Estimated Glomerular Filtration Rate.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
14 02 2020
Historique:
received: 18 01 2019
accepted: 01 04 2019
pubmed: 7 4 2019
medline: 7 1 2021
entrez: 7 4 2019
Statut: ppublish

Résumé

In human immunodeficiency virus (HIV), the relative contribution of genetic background, clinical risk factors, and antiretrovirals to chronic kidney disease (CKD) is unknown. We applied a case-control design and performed genome-wide genotyping in white Swiss HIV Cohort participants with normal baseline estimated glomerular filtration rate (eGFR >90 mL/minute/1.73 m2). Univariable and multivariable CKD odds ratios (ORs) were calculated based on the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) score, which summarizes clinical CKD risk factors, and a polygenic risk score that summarizes genetic information from 86 613 single-nucleotide polymorphisms. We included 743 cases with confirmed eGFR drop to <60 mL/minute/1.73 m2 (n = 144) or ≥25% eGFR drop to <90 mL/minute/1.73 m2 (n = 599), and 322 controls (eGFR drop <15%). Polygenic risk score and D:A:D score contributed to CKD. In multivariable analysis, CKD ORs were 2.13 (95% confidence interval [CI], 1.55-2.97) in participants in the fourth (most unfavorable) vs first (most favorable) genetic score quartile; 1.94 (95% CI, 1.37-2.65) in the fourth vs first D:A:D score quartile; and 2.98 (95% CI, 2.02-4.66), 1.70 (95% CI, 1.29-2.29), and 1.83 (95% CI, 1.45-2.40), per 5 years of exposure to atazanavir/ritonavir, lopinavir/ritonavir, and tenofovir disoproxil fumarate, respectively. Participants in the first genetic score quartile had no increased CKD risk, even if they were in the fourth D:A:D score quartile. Genetic score increased CKD risk similar to clinical D:A:D score and potentially nephrotoxic antiretrovirals. Irrespective of D:A:D score, individuals with the most favorable genetic background may be protected against CKD.

Sections du résumé

BACKGROUND
In human immunodeficiency virus (HIV), the relative contribution of genetic background, clinical risk factors, and antiretrovirals to chronic kidney disease (CKD) is unknown.
METHODS
We applied a case-control design and performed genome-wide genotyping in white Swiss HIV Cohort participants with normal baseline estimated glomerular filtration rate (eGFR >90 mL/minute/1.73 m2). Univariable and multivariable CKD odds ratios (ORs) were calculated based on the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) score, which summarizes clinical CKD risk factors, and a polygenic risk score that summarizes genetic information from 86 613 single-nucleotide polymorphisms.
RESULTS
We included 743 cases with confirmed eGFR drop to <60 mL/minute/1.73 m2 (n = 144) or ≥25% eGFR drop to <90 mL/minute/1.73 m2 (n = 599), and 322 controls (eGFR drop <15%). Polygenic risk score and D:A:D score contributed to CKD. In multivariable analysis, CKD ORs were 2.13 (95% confidence interval [CI], 1.55-2.97) in participants in the fourth (most unfavorable) vs first (most favorable) genetic score quartile; 1.94 (95% CI, 1.37-2.65) in the fourth vs first D:A:D score quartile; and 2.98 (95% CI, 2.02-4.66), 1.70 (95% CI, 1.29-2.29), and 1.83 (95% CI, 1.45-2.40), per 5 years of exposure to atazanavir/ritonavir, lopinavir/ritonavir, and tenofovir disoproxil fumarate, respectively. Participants in the first genetic score quartile had no increased CKD risk, even if they were in the fourth D:A:D score quartile.
CONCLUSIONS
Genetic score increased CKD risk similar to clinical D:A:D score and potentially nephrotoxic antiretrovirals. Irrespective of D:A:D score, individuals with the most favorable genetic background may be protected against CKD.

Identifiants

pubmed: 30953057
pii: 5429565
doi: 10.1093/cid/ciz280
doi:

Substances chimiques

Anti-HIV Agents 0
Pharmaceutical Preparations 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

890-897

Subventions

Organisme : Swiss National Science Foundation
ID : 177499
Pays : Switzerland

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

Auteurs

Léna G Dietrich (LG)

University Department of Medicine and Infectious Diseases Service, Kantonsspital Baselland, University of Basel, Bruderholz.

Catalina Barceló (C)

Division of Clinical Pharmacology, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Lausanne.

Christian W Thorball (CW)

Swiss Institute of Bioinformatics, Lausanne.
School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Switzerland.

Lene Ryom (L)

Center of Excellence for Health, Immunity and Infections, Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, Denmark.

Felix Burkhalter (F)

University Department of Medicine and Nephrology Service, Kantonsspital Baselland, University of Basel, Bruderholz.

Barbara Hasse (B)

Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich, Lugano.

Hansjakob Furrer (H)

Department of Infectious Diseases, Bern University Hospital, University of Bern, Lugano.

Maja Weisser (M)

Division of Infectious Diseases and Hospital Epidemiology, University Hospital Basel, Lugano.

Ana Steffen (A)

Division of Infectious Diseases, Kantonsspital St Gallen, Lugano.

Enos Bernasconi (E)

Division of Infectious Diseases, Ospedale Regionale, Lugano.

Matthias Cavassini (M)

Division of Infectious Diseases, Lausanne University Hospital.

Sophie de Seigneux (S)

Division of Nephrology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Switzerland.

Chantal Csajka (C)

Division of Clinical Pharmacology, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Lausanne.

Jacques Fellay (J)

Swiss Institute of Bioinformatics, Lausanne.
School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Switzerland.

Bruno Ledergerber (B)

Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich, Lugano.

Philip E Tarr (PE)

University Department of Medicine and Infectious Diseases Service, Kantonsspital Baselland, University of Basel, Bruderholz.

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