Interstitial fibrosis: tubular hypothesis versus glomerular hypothesis Erik I. Christensen, Pierre J. Verroust  Kidney International  Volume 74, Issue 10, Pages 1233-1236 (November 2008) DOI: 10.1038/ki.2008.421 Copyright © 2008 International Society of Nephrology Terms and Conditions

Figure 1 A highly simplified scheme of the two proposed mechanisms leading to progressive nephron degeneration. On the left, the increased ultrafiltered protein load triggers inflammatory and fibrogenic processes, destroying the tubule. Tubule cells and monocyte macrophages contribute to the fibrotic process. Autocrine loops may be formed. On the right, denuded basement membrane adheres to parietal epithelial cells, creating glomerular crescents that encroach on the glomerulotubular junction, leading to aglomerular tubules and atubular glomeruli. Abbreviations: C3aR, C3a receptor; TGF, transforming growth factor; TNF, tumor necrosis factor. (Adapted from refs. 5, 6.) Kidney International 2008 74, 1233-1236DOI: (10.1038/ki.2008.421) Copyright © 2008 International Society of Nephrology Terms and Conditions