CRP and endothelial dysfunction: Flow-mediated dilation and nitroglycerin-mediated dilation were found to be impaired by mechanisms including endothelium-dependent vasodilation and decreased bioavailability of nitric oxide [4], and the endogenous inhibitor of nitric oxide synthase could be a potential biomarker of endothelial dysfunction along with C-reactive protein to predict all-cause and CV mortality in HD patients [25].