Lewis rats rendered cirrhotic by the administration of carbon tetrachloride developed mesangial and glomerular capillary wall deposits of immunoglobulins (especially IgA) and complement. These rats also had circulating immune complexes and markedly elevated serum IgA concentrations. The model suggests that defective hepatic sequestration of circulating IgA polymers and immune complexes may be responsible for the glomerular deposits. A similar mechanism may account for the high incidence of glomerulonephritis in patients with alcoholic cirrhosis.