 He was the first to show that C3 nephritic factor is an autoantibody that activates the alternative complement pathway, a finding that suggested the potential of B cell or complement C5 depletion as adjunct therapies in certain forms of kidney inflammation.He was also the first to identify the antigen targeted by autoantibodies in patients with systemic vasculitis, which formed the basis for a routinely used diagnostic assay.He was the first to show that polycystin-1, one of two gene products mutated in patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD), is required for the structural integrity of blood vessels, indicating that the early onset of high blood pressure and presence of vascular aneurysms in ADPKD is caused by a primary defect in vascular polycystin-1.