Diastolic blood pressure was increased in these white HIV-infected patients compared with the general population, but there was no difference in the prevalence of hypertension. However, the duration of combination antiretroviral therapy predicted hypertension independently.

Hypertension is associated with cardiovascular disease in the human immunodeficiency virus (HIV)-infected population. The authors aimed to test the hypothesis whether advanced immunosuppression with low nadir CD4 lymphocyte cell count is a predictor of sustained hypertension in HIV-infected individuals. In a longitudinal study of an HIV cohort of 434 patients (43AE11 years, 72% men, 71% Caucasians), standardized blood pressure was measured in duplicate during 3 clinical visits both at baseline and after 3.4AE0.8 years. The lowest CD4 cell count in the individual history was recorded as nadir CD4. Both nadir CD4 cell count <50 cells ⁄ lL and duration of antiretroviral therapy (ART) were associated with sustained hypertension, and the highest proportion of hypertensive patients was observed in those who had both nadir CD4 cell count <50 cells ⁄ lL and prolonged ART duration. Nadir CD4 cellcount <50 cells ⁄ lL was an independent predictor of hypertension (adjusted odds ratio [OR], 2.48; 95% confidence interval [CI], 1.27-4.83), as was ART duration (adjusted OR, 1.13; 95% CI, 1.03-1.24). The predictive power of ART duration was more pronounced in patients with nadir CD4 cell count <50 cells ⁄ lL. Delaying ART initiation until a state of advanced immunosuppression might add to and even fuel the cardiovascular risk associated with ART. J Clin Hypertens (Greenwich). 2013; 15:101-106 Ó2012 Wiley Periodicals, Inc.

Background. The survival of human immunodeficiency virus (HIV)-infected patients has increased significantly since the introduction of combination antiretroviral therapy, leading to the development of important long-term complications including cardiovascular disease (CVD) and renal disease. Microalbuminuria, an indicator of glomerular injury, is associated with an increased risk of progressive renal deterioration, CVD and mortality. However, the prevalence of microalbuminuria has barely been investigated in HIV-infected individuals.Methods. Based on three prospective urine samples in an unselected nonhypertensive, nondiabetic HIV-positive cohort (n = 495), we analysed the prevalence of microalbuminuria and compared the Caucasian share with that of a nonhypertensive, nondiabetic population-based control group (n = 2091). Significant predictors for microalbuminuria were analysed within the HIV-positive cohort.Results. The prevalence of microalbuminuria was 8.7% in the HIV-infected cohort, which is three to five times higher than that in the general population. HIV-infected patients with microalbuminuria were older, and had higher blood pressure, longer duration of HIV infection, higher serum beta 2-microglobulin, higher serum creatinine and a reduced glomerular filtration rate of ≤90 mL/min, compared with those with normal albumin excretion. In multivariate analysis, systolic blood pressure, serum beta 2-microglobulin and duration of HIV infection were found to be independent predictors of microalbuminuria.Conclusions. Our findings indicate that in addition to haemodynamic effects, inflammatory activity may be implicated as a cause of the development of microalbuminuria. With respect to the increasing risk of developing CVD or renal diseases and mortality, the high prevalence of microalbuminuria in HIV-infected individuals warrants special attention.

ObjectivesThe aim of the study was to test the hypothesis that microbial translocation, quantified by levels of lipopolysaccharide (LPS) and subsequent monocyte activation [soluble (sCD14)], is associated with hypertension in HIV-infected individuals. MethodsIn this exploratory substudy, 42 patients were recruited from a larger, longitudinal HIV-infected cohort study on blood pressure. LPS and sCD14 levels were measured retrospectively at the time of nadir CD4 cell count, selecting untreated HIV-infected patients with both advanced immunodeficiency and preserved immunocompetence at the time of nadir. Patients with later sustained hypertension (n = 16) or normotension (n = 26) throughout the study were identified. LPS was analysed using the Limulus Amebocyte Lysate colorimetric assay (Lonza, Walkersville, MD) and sCD14 using an enzyme-linked immunosorbent assay (ELISA). Nonparametric statistical tests were applied. ResultsIn the HIV-infected patients [median (interquartile range) age 42 (32-46) years; 79% male and 81% Caucasian], LPS and sCD14 levels were both negatively correlated with nadir CD4 cell count. Plasma levels of LPS (P < 0.001) and sCD14 (P = 0.024) were elevated in patients with later hypertension compared with patients with normotension. There was a stepwise increase in the number of patients with hypertension across tertiles of LPS (P = 0.001) and sCD14 (P = 0.007). Both LPS and sCD14 were independent predictors of elevated blood pressure after adjustment for age and gender. For each 10-unit increase in LPS (range 66-272 pg/ml), the increment in mean blood pressure in the first period of blood pressure recording was 0.86 (95% confidence interval 0.31-1.41) mmHg (P = 0.003). ConclusionsAs LPS and sCD14 were both independently associated with elevated blood pressure, microbial translocation may be linked to the development of hypertension.Keywords: HIV infection, hypertension, lipopolysaccharide, nadir CD4 cell count, soluble CD14. Accepted 5 December 2012 IntroductionNon-AIDS-related morbidities such as hypertension, cardiovascular disease (CVD), malignancy, and renal, liver and bone diseases have emerged as increasing clinical problems in HIV-infected patients [1]. In fact, non-AIDS-related mortality today exceeds AIDS-related mortality in populations with access to antiretroviral therapy (ART) [2]. A premature ageing process has been suggested to occur in HIV-infected individuals for which several contributing factors have been proposed, including viral replication, drug toxicity, lifestyle factors, and persistent immune Primary HIV infection is characterized by massive T-cell depletion in the gastrointestinal mucosa with subsequent enhanced translocation of bacterial products such as lipopolysaccharide (LPS) and flagellin from the intestinal lumen into the systemic circulation [3,4]. LPS is a potent inducer of immune response and inflammation through the innate immune system. Soluble CD14 (sCD14) is a marker of monocyte activation and is shed from monocytes upon LPS stimulation [5]. Microbial tr...