SP205ENDOTHELIAL GLYCOCALYX DAMAGE AND RENAL DYSFUNCTION IN HIV PATIENTS RECEIVING COMBINED ANTIRETROVIRAL THERAPY

Abstract

Introduction and Aims: Both HIV infection and kidney diseases are associated with endothelial dysfunction and accelerated cardiovascular events. HIV patients receiving combined antiretroviral therapy (cART) may have endothelial dysfunction with subsequent hypertension and atherosclerosis. The aim of this study was to investigate endothelial damage in HIV patients receiving cART, through glycocalyx injury biomarkers. Methods: This is a cross-sectional study of HIV-infected patients recruited from public health centers in Fortaleza city, Northeast of Brazil between January and December 2015. Three groups of HIV patients were included: 1) those who never received cART, 2) HIV patients receiving cART containing tenofovir/lamivudine/efavirenz, and 3) zidovudine/lamivudine/efavirenz. Also, a group of 13 healthy subjects were included as a control group. Endothelial biomarkers were measured in specific serum samples aliquots by ELISA kits: ICAM-1 (ELISA set ab47349; Abcam, Cambridge, MA, USA). Syndecan-1 was measured as a biomarker of eGC injury (ELISA set ab47352; Abcam, Cambridge, MA, USA). Results: After exclusion criteria, a total of 66 HIV patients were included in this study. The mean age was 33.4 ± 8.9 years and 51 patients were male (77.3%). In the groups of HIV patients, 18 (27.3%) have never received cART, 27 (40.9%) received Tenofovir and 21 (31.8%) received zidovudine on cART. There was no significant difference between age, gender, body mass index and blood pressure in the groups. The majority of the patients (63.6%) had undetectable viral load and 12 patients (18.2%) had elevated viral load. Serum urea, creatinine and eGFR were similar in all groups No HIV patient had glomerular filtration rate less than 60 mL/ min/1.73 m2 and only two patients (3%) had microalbuminuria (albumin excretion rate greater than 30 mg/g-Cr). Regarding ICAM-1, no difference between the all groups was observed (p=0.757). However, all HIV patients had higher systemic syndecan-1 compared with healthy controls using Student's t test (71.8±25.4 vs 36.5±14.3 ng/mL, p<0.001). When we analyzed the different groups of HIV patients by the one-way analysis of variance, was observed that higher levels of syndecan-1 remains statistically significant only in group receiving cART/tenofovir (74.2±27.9 vs 36.5±14.3 ng/mL, p=0.001) and cART/zidovudine (76.7 ±24.8 vs 36.5±14.3 ng/mL, p=0.0006) showing that there is important endothelial dysfunction even in patients under specific treatment for HIV infection. No significant correlation between syndecan-1 and ICAM-1 (r=0.177, p=0.154) was observed. Conclusions: HIV patients in chronic use of cART present endothelial damage. In HIV patients with apparently no renal and cardiovascular disease it was observed elevated levels of syndecan-1, signaling subclinical endothelial injury. For the first time was demonstrated that syndecan-1 may be useful early biomarker to renal and endothelial dysfunction in HIV patients.