Pentraxin 3 as a novel bio-marker of inflammation and endothelial dysfunction in autosomal dominant polycystic kidney disease

Abstract

Cardiovascular disease (CVD) is the main cause of mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Prior to hypertension early vascular changes and inflammation have been reported. We aimed to investigate long pentraxin 3 (PTX-3), which has been recently described as a biomarker of inflammation, and its relation with endothelial dysfunction in early ADPKD patients. Twenty-five ADPKD patients without hypertension and 25 healthy controls were studied cross-sectionally. Hypertension was diagnosed with ambulatory blood pressure monitoring. Plasma concentrations of PTX-3 and proteinuria levels were obtained from each participant. Endothelial dysfunction was assessed using ischemia-induced forearm flow-mediated vasodilation (FMD). PTX-3 levels were higher in ADPKD patients compared to healthy controls (4.2 [1.2-10.1] vs. 1.4 [0.4-3.1] ng/ml, p < 0.001). Additionally, C-reactive protein (CRP) and proteinuria levels were higher in ADPKD patients than in healthy subjects. In the whole cohort, PTX-3 correlated negatively with FMD (r: -0.58, p < 0.001) and positively with proteinuria (r: 0.56, p < 0.001) and uric acid (r: 0.57, p < 0.001). In all subjects, FMD was independently predicted by PTX-3, but not by uric acid, CRP or proteinuria. PTX-3 may be a better biomarker of inflammation than CRP to predict endothelial dysfunction in normotensive ADPKD patients with well-preserved kidney function. Hence, inflammation which is demonstrated by PTX-3 may potentially be used to predict future CVD in this population.