Ultrasonographic Evaluation of Resistive Index and Renal Artery Stenosis in Patients with Anti-Phospholipid Syndrome: Two Distinct Mechanisms?

Abstract

Renal involvement in anti-phospholipid syndrome (APS) is still relatively unknown and probably underestimated. The described lesions consist of renal artery stenosis (RAS), venous renal thrombosis and glomerular lesions. The resistive index (RI) of intra-renal arteries, expression of the degree of vascular resistance, has been analyzed in different nephropathies and observed to be associated with functional parameters and some histologic features. In contrast, there are no studies on patients with APS. We evaluated the presence of a pathologic RI and RAS in a cohort of patients with APS. The study protocol included ultrasonographic assessment to measure the RI (RIs >0.7 were considered pathologic) and to determine the presence of RAS. We enrolled 36 patients with APS, 13 with primary APS and 23 with the form associated with systemic lupus erythematosus (SLE, secondary APS). As controls, we enrolled 10 anti-phospholipid antibody carriers, 10 patients with SLE without renal involvement and 14 age- and sex-matched healthy patients. A pathologic RI was identified in five patients with APS (13.9%) and in none of the anti-phospholipid antibody carriers (p = 0.00007). Four of the five (80%) patients with a pathologic RI had secondary APS. Three patients, all with primary APS, had RAS. The almost exclusive association of a pathologic RI with secondary APS and of RAS with primary APS suggests the involvement of two pathogenic pathways in the development of these different manifestations. The hypercoagulability status driven by APS could play a central role in the determination of RAS in patients with primary APS, whereas the activation of mTORC (mammalian target of rapamycin complex) pathways could be the pathogenic mechanism inducing development of a pathologic RI.