By Sharma S Prabhakar
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Additional info for An update on glomerulopathies : clinical and treatment aspects
The overexpression of transforming growth factor β (TGFβ) or its downstream proteins, the ‘Smads’ lead to glomerulosclerosis in animal models. Activation of the renin-angiotensin system upregulates TGFβ, which is considered to cause further progression of the disease (Harris RC et al. 2006). Angiogenic factors, like platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) seem to play a role in disease progression. This is based upon the rat remnant kidney model (RK model) experimental studies of progressive glomerulosclerosis.
Glomerular tip lesion patients may develop reversible acute renal failure, at the times of initial presentation when the degree of proteinuria, edema, hypoalbuminemia are at their peak. This behaves like minimal change disease and this rarely happens in any other forms of FSGS. Patients with glomerular tip lesion FSGS tend to be older white males in comparison to younger black males predominance in collapsing variant FSGS. Distinguishing between primary and secondary FSGS is important, since secondary FSGS should not respond to immunosuppressive therapy.
Nephrol. 5, 469–479 (2009); published online 7 July 2009 Wehrmann M, Bohle A, Bogenschutz O, et al. Long-term prognosis of chronic idiopathic membranous glomerulonephritis: An analysis of 334 cases with particular regard to tubulointerstitial changes. Clin Nephrol 1989;3:67. 2 Focal Segmental Glomerulosclerosis Dawinder S. Sohal and Sharma S. Prabhakar Department of Medicine, Texas Tech University Health Sciences Center USA 1. Introduction Focal segmental glomerulosclerosis (FSGS) as the name implies is a histopathological pattern of lesions, where the “focal” refers to, involving minority of glomeruli and the “segmental” refers to, involving a portion of the glomerular capillary tuft caused by injury to podocytes (Fig 1A).