Mineralocorticoid receptor blockade quiesces parietal epithelial cell activation.

Rapid podocyte loss activates adjacent parietal epithelial cells, triggering aberrant proliferation and migration, leading to crescents or pseudocrescents and eventual glomerulosclerosis. In this issue, Lazareth, Lenoir, and colleagues demonstrate that genetic and pharmacologic mineralocorticoid receptor inhibition in activated parietal epithelial cells blunts albuminuria, aberrant parietal epithelial cell activation and migration, extracapillary proliferation, and eventual glomerulosclerosis, thereby highlighting the potential use of mineralocorticoid receptor antagonists in the therapeutic strategy for glomerulonephritis and focal segmental glomerulosclerosis with parietal epithelial cell activation.