Rabbit Anti-Human CD4 monoclonal antibody, clone TU1599

Objectives A risk score for long-term prediction of chronic kidney disease (CKD) in people living with HIV (PLHIV) has been developed using data from the D:A:D cohort. We assessed the performance of the D:A:D risk score in a cohort of PLHIV in West Africa. Methods Data from PLHIV starting antiretroviral treatment in four clinics in Burkina Faso, Cote d'Ivoire and Togo participating in the IeDEA West Africa collaboration were analysed. CKD was defined as two consecutive estimated glomerular filtration rates (eGFRs) of <= 60 mL/min/1.73 m(2). The D:A:D score (short version) was calculated using age, gender, nadir CD4 and baseline eGFR and was categorized into low, medium, and high-risk groups. Results In 14 930 participants (70% female, median age = 38 years; median nadir CD4 count = 183 cells/mu L) followed for a median duration of 5.7 years, 660 (4.4%) progressed to CKD, with an incidence [95% confidence interval (CI)] of 7.8 (7.2-8.4) per 1000 person-years (PY). CKD incidence rates were 2.4 (2.0-2.8), 8.1 (6.8-9.6) and, 30.9 (28.0-34.1) per 1000 PY in the low-, medium- and high-risk groups, respectively. In the high-risk group, 14.7% (95% CI: 13.3; 16.3) had progressed to CKD at 5 years. Discrimination was good [C-statistics = 0.81 (0.79-0.83)]. In all, 79.4% of people who progressed to CKD were classified in the medium- to high-risk group at baseline (sensitivity) and 66.5% of people classified in the low risk group at baseline did not progress to CKD (specificity). Conclusions These findings confirm the validity of the D:A:D score in identifying individuals at risk of developing CKD who could benefit from enhanced kidney monitoring in West African HIV clinics.

Background: Persons living with HIV (PLWH) are at an increased risk of myocardial dysfunction and metabolic disturbances represent one of several potential contributing factors. Adiponectin is an adipokine that enhances insulin sensitivity with potential cardioprotective effects. We therefore investigated the relationship between myocardial fibrosis, adiponectin, and related metabolic parameters to better understand the pathophysiologic mechanisms of myocardial injury in PLWH. Methods: This is a prospective, cross-sectional study of PLWH without known cardiovascular disease (n = 87) and 28 healthy matched controls. Diffuse myocardial fibrosis and epicardial adipose tissue (EAT) were evaluated using cardiac magnetic resonance imaging and cardiac computed tomography. Results: Myocardial fibrosis was increased in PLWH and was correlated with adiponectin (r = 0.26, P = 0.004) and EAT (r = -0.42, P < 0.0001). Myocardial fibrosis was not associated with smoking pack years or CD4/CD8 ratio. In multivariate analysis that included body mass index, HIV status (P = 0.04), female sex (P < 0.0001), higher adiponectin (P = 0.046) and lower EAT (P = 0.01) were independently associated with myocardial fibrosis. Conclusion: We describe a novel association between serum adiponectin and subclinical intramyocardial fibrosis, as well as a significant inverse relationship between intramyocardial fibrosis and EAT. Adiponectin may represent a target for preventing myocardial injury in the future; however, our findings reflect the complexity of the metabolic interactions of adiponectin and epicardial adipose as factors associated with the myocardial architecture.