Soluble CD163 predicts incident chronic lung, kidney and liver disease in HIV infection
Ditte M Kirkegaard-Klitbo1, Niels Mejer, Troels B Knudsen
1aDepartment of Infectious Diseases, Hvidovre Hospital bDepartment of Infectious Diseases, Rigshospitalet cDepartment of Pulmonary and Infectious Diseases, Hillerød Hospital, University of Copenhagen, Copenhagen dDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus eDepartment of Molecular Medicine, University of Southern Denmark, Odense fDepartment of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Objective:
To examine if monocyte and macrophage activity may be on the mechanistic pathway to non-AIDS comorbidity by investigating the associations between plasma-soluble CD163 (sCD163) and incident non-AIDS comorbidities in well treated HIV-infected individuals.
Design:
Prospective single-center cohort study.
Methods:
Plasma sCD163 was quantified by ELISA technique at study entry in 2004/2005, and non-AIDS comorbidity was identified by International Classification of Disease Tenth revision diagnosis codes and registry linkage in 2015. Associations between sCD163 and incident comorbidity was examined using multivariable Cox proportional hazards models adjusted for pertinent covariates.
Results:
In HIV-1-infected individuals (n = 799), the highest quartile of plasma sCD163 was associated with incident chronic lung disease [adjusted hazard ratio (aHR), 3.2; 95% confidence interval (CI): 1.34; 7.46] and incident chronic kidney disease (aHR, 10.94; 95% CI: 2.32; 51.35), when compared with lowest quartiles. Further, (every 1 mg) increase in plasma sCD163 was positively correlated with incident liver disease (aHR, 1.12; 95% CI: 1.05; 1.19). The sCD163 level was not associated with incident cancer, cardiovascular disease or diabetes mellitus.
Conclusion:
sCD163 was independently associated with incident chronic kidney disease, chronic lung disease and liver disease in treated HIV-1-infected individuals, suggesting that monocyte/macrophage activation may be involved in the pathogenesis of non-AIDS comorbidity and a potential target for therapeutic intervention.
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