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. 2014 Jun 19;89(9):907–914. doi: 10.1002/ajh.23762

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© 2014 The Authors American Journal of Hematology Published by Wiley Periodicals, Inc.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Proposed mechanisms of glomerulopathy in sickle cell disease. Multiple mechanisms may contribute to the pathogenesis of glomerular damage in sickle cell disease. These may occur due to changes in the renal vasculature, peritubular capillaries and the glomerulus. PG: prostaglandins; NO: nitric oxide; ANP: atrial natriuretic peptide; ROS: reactive oxygen species; sFLT-1: soluble fms-like tyrosine kinase-1; VEGF: vascular endothelial growth factor; ANG-II: angiotensin II; TGF-β: transforming growth factor-β; TNFα: tumor necrosis factor-α; ET-1: endothelin-1.