Systemic sclerosis (SSc) is an autoimmune disease characterized by endothelial dysfunction, inflammation and fibrosis of skin and internal organs. An imbalance of pro-angiogenic factors and angiogenesis inhibitors has been implicated in the progression of vascular damage and fibrosis. In SSc, scleroderma renal crisis, isolated reduced glomerular filtration rate (GFR) and abnormal renal vascular resistance indices were observed. The subclinical renal vasculopathy is most frequent and it is characterized by increased renal resistive index (RRI) and reduction of parenchymal thickness with impaired function. Inflammation may lead to glomerulosclerosis, vascular damage and fibrosis. The interleukin-33/suppression of tumorigenicity 2 (IL-33/ST2) axis plays an important role in the diabetic nephropathy. The persistence of inflammation activates the production of pro-fibrotic cytokines. Failure to resolve inflammation may be linked to a reduced production of pro-resolving mediators. Resolution of inflammatory response is now considered a biosynthetically active process governed by specialized pro-resolving mediators. These chemically distinct families include lipoxins, resolvins, protectins and maresins that are biosynthesized from essential fatty acids. In SSc, there are no data about pathogenetic mechanisms of renal damage from angiogenesis to the resolution of inflammation. Primary objective of this study is to evaluate the intrarenal arterial stiffness by renal Doppler (renal resistive index) and to correlate it with renal ultrasound parameters (parenchymal thickness). Secondary objective is to evaluate the role of angiogenesis, inflammation and resolution of inflammation on SSc nephropathy. In SSc patients, serum levels of vascular endothelial growth factor, endostatin, IL-33, sST2, lipoxin A, resolvin D1 and maresin 1 will be evaluated. The identification and actions of pro-resolving mediators, conjugates in tissue regeneration, could offer new therapeutic horizons.
