Two asymptomatic teenage females with proteinuria, hematuria, and persistent hypocomplementemia are presented. Renal biopsy studies revealed membranous glomerulopathy. During follow-up periods of 4.0 and 4.5 years, the clinical courses and sequential monitoring of immunologic studies failed to demonstrate lupus erythematosus or other systemic disorders. Serum complement levels were consistent with activation of the alternate complement pathway in the first patient and the classic pathway in the second. In both cases further depression in serum complement levels occurred during intervals of greater urinary protein excretion. These findings suggest that the complement system may play a more important role in the pathogenesis of idiopathic membranous glomerulopathy than realized previously.