Abstract
Evidence is reviewed that indicates that an immune deficiency state may underlie patients with immune complex nephritis. Studies in several laboratories provide data that show defective immune function in patients with nephritis at the following loci: defective immunoglobulin production, impaired monocyte Fc and C3b receptor function, diminished complement biosynthesis, and decreased mesangial cell colony-stimulating factor-1 biosynthesis. Aberrant monocyte function may be an important common denominator. The validation of this hypothesis has important implications for therapeutic strategies.