A novel role of renin inhibitor in the complement cascade.

Aberrant regulation of an alternative pathway of the complement system could be a therapeutic target of C3 glomerulopathy, including dense deposit disease. In the current issue, Békássy and colleagues provide data on enzymatic conversion of C3 by renin in vitro and on the efficacy of a direct renin inhibitor, aliskiren, on systemic and renal complement activation in patients with dense deposit disease.