Eight patients with diffuse livedo reticularis and cerebrovascular lesions (Sneddon's syndrome) are reported. The disorder was inherited by autosomal dominant transmission in 3 cases. Multiple occlusions in medium-sized arteries were demonstrated by cerebral and hand arteriograms. Digital artery biopsies showed intimal hyperplasia in 7 cases and recanalized thrombosis in one case. Our findings are compared with an extensive review of the literature. Differential diagnosis with other vascular disorders, especially cerebral thromboangiitis obliterans and the corticomeningeal angiomatosis of Divry and Van Bogaert is considered. We conclude that Sneddon's syndrome is a new genetic and progressive arteriopathy, occlusive and noninflammatory, involving medium-sized vessels. The pathogenesis has yet to be elucidated.

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IgA nephropathy is a common form of glomerulonephritis, classically manifested by asymptomatic hematuria. Although the exact pathophysiologic mechanism is still unknown, renal damage has been related to mesangial deposition of IgA-containing immune complexes. In recent years, some lung diseases have been associated with IgA nephropathy, including pulmonary hemorrhage and sarcoidosis. We report a patient with idiopathic bronchiolitis obliterans who developed a rapidly progressive glomerulonephritis due to IgA deposits. Extensive deposits of IgA were also found in the lungs, thus suggesting a pathogenetic role for IgA in tissue injury at both organ levels. To our knowledge this association has not been previously described in the literature.