Progression and potential regression of glomerulosclerosis

Abstract

All the data I have discussed today demonstrate that regression of biopsy-proven glomerulosclerosis can be achieved in various experimental settings, including those germane to human disease in which moderate glomerulosclerosis, proteinuria, and hypertension frequently are present at the time of diagnosis. Limited data show the feasibility of regression of injury in human diabetic nephropathy. The potential importance of the renin-angiotensin system in the spectrum of injuries leading to mesangial matrix accumulation and sclerosis is underscored by the effectiveness of therapies that aim to inhibit its manifold actions, including induction of PAI-1. Understanding of interactions of the RAS and aldosterone with PAI-1, and of the dynamic control of cell proliferation, apoptosis, and regeneration is now evolving. Ongoing studies will establish which of these recent provocative findings from animal models are relevant to human diseases and might lead to optimal therapies to forestall progression, and perhaps even induce regression, of sclerosis.