Abstract
Progression of many glomerular diseases has been firmly tied to a loss of podocytes, followed by a deterioration of glomerular architectural stability eventuating in segmental, and ultimately global, sclerosis. Recent studies have begun to clarify the nature of the autonomous (disease-independent) aspects of this process, as well as to explore mechanistically the 'unreasonable effectiveness' of angiotensin blockade in slowing glomerular disease progression. Quantitative monitoring of podocyte loss (e.g., to assess therapy) remains a challenge.
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