Vascular and glomerular manifestations of viral hepatitis B and C: a review

Abstract

Secondary vasculopathies have varied etiologies that include paraneoplastic processes (eg, migratory thrombophlebitis, urticarial vasculitis); direct invasion by tumors (eg, superior and inferior vena cava syndrome); metabolic diseases (eg, diabetes mellitus); and infections, among others. The infective causes of vasculitides could result from direct involvement of vessels by a vasculo-tropic agent (eg, mucor infection); adjacent inflammation nonspecifically affecting nearby vessels; or from infection-induced immune-mediated vasculitis. Viruses represent a major group in the development of the latter, and many human viruses have been reported to cause vasculitis. The vasculitic lesions secondary to hepatitis B and hepatitis C viruses largely fall within the spectrum of immune-mediated secondary vascular injury and are discussed in this review.