Volume 69, Issue 12, Pages 2131-2147 (June 2006) The podocyte's response to injury: Role in proteinuria and glomerulosclerosis  S.J. Shankland  Kidney International  Volume 69, Issue 12, Pages 2131-2147 (June 2006) DOI: 10.1038/sj.ki.5000410 Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 1 Podocyte response to injury. Podocytes are injured by immune- and non-immune-mediated disease, resulting in damage to the glomerular filtration barrier. This typically results in proteinuria and effacement. The fate of the podocyte then depends on several factors, such as reparative mechanisms. If these are present, and/or the initial injury is halted, there may be resolution. However, if injury persists, and/or there are inadequate repair mechanisms presents, proteinuria persists, with the development of glomerulosclerosis, leading to reduced renal function. Kidney International 2006 69, 2131-2147DOI: (10.1038/sj.ki.5000410) Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 2 Factors governning podocyte number. Total podocyte (podo) number is a balance between proliferation and loss. Podocyte number is reduced by either a decrease in proliferation owing to lack of DNA synthesis, DNA damage or hypertrophy, and/or an in crease in podocyte loss owing to detachment and apoptosis. Kidney International 2006 69, 2131-2147DOI: (10.1038/sj.ki.5000410) Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 3 Injurious effects of angiotensin II on podocytes. The numerous deleterious actions of angiotensin II (AT) and its receptor are shown, providing the rationale for the use of angiotensin-converting enzyme Inhibitors and angiotensin receptor blockers in patients with proteinuria. Kidney International 2006 69, 2131-2147DOI: (10.1038/sj.ki.5000410) Copyright © 2006 International Society of Nephrology Terms and Conditions