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The enzyme renin is produced exclusively by juxtaglomerular cells in the kidney; until now, its only known substrate was angiotensinogen. B ékássy and colleagues showed that renin can cleave complement component C3 into C3a and C3b, thereby activating the alternative pathway. Renin cleaves C3 in the same place as the C3 convertase, and with similar activity. Renin-mediated complement activation was blocked by aliskiren, a renin inhibi tor approved for the treatment of hypertension. Békássy’s team then treated 3 patients who had dense deposit disease with aliskiren and showed that systemic C3 levels improved, suggesting less C3 cleavage.
Source: Kidney International - Category: Urology & Nephrology Tags: In This Issue Source Type: research