| 초록 |
Progression of chronic kidney disease can be ameliorated or stabilized by different interventions. Experimental data and limited clinical data suggest existing sclerosis could even be reversed. Most data suggest that current therapy, especially renin- angiotensin system inhibition alone, is not sufficient to initiate and maintain long-term regression of glomerular structural injury. Additional mechanisms that involve matrix remodeling, capillary reorganization, and podocyte reconstitution, and the role of parietal epithelial cells, may also contribute to remodeling. Importantly, tubulointerstitial fibrosis may also contribute to increased susceptibility of glomeruli to injury, and thus enhance ongoing progressive kidney scarring. Thus, a multipronged strategy including novel anti-inflammatory and antifibrotic molecules and amelioration and protection against tubulointerstitial fibrosis, should be considered to potentiate regression of glomerulosclerosis. |