Transforming growth factor beta and progression of renal disease Phyllis August, Manikkam Suthanthiran  Kidney International  Volume 64, Pages S99-S104 (November 2003) DOI: 10.1046/j.1523-1755.64.s87.15.x Copyright © 2003 International Society of Nephrology Terms and Conditions

Figure 1 Differential level of expression of transforming growth factor beta 1 (TGF-β1) protein in African American ESRD patients and white ESRD patients. (A) The mean ± SEM TGF-β1 protein level was 207 ± 10ng/mL in African American ESRD patients (N = 52) and 137 ± 8ng/mL in white ESRD patients (N = 46). (B) The frequency distribution of TGF-β1 levels in the ESRD patients, distinguished by race. TGF-β1 values (96%) from African American ESRD patients were within 2 SD of the mean value, and the coefficient of skewness and the coefficient of kurtosis were 0.20 and 0.24, respectively; 93% of the TGF-β1 values from white ESRD patients were within 2 SD of the mean value, and the coefficient of skewness and the coefficient of kurtosis were 0.38 and 0.78, respectively. In view of the normal distribution of TGF-β1 values in the African American as well as white ESRD patients, Student t test was used to derive the P value shown. Kidney International 2003 64, S99-S104DOI: (10.1046/j.1523-1755.64.s87.15.x) Copyright © 2003 International Society of Nephrology Terms and Conditions

Figure 2 Transforming growth factor β1 (TGF-β1) mRNA steady state levels in hypertensives and normotensives. The mean ± SEM TGF-β1 mRNA/GAPDH mRNA ratios, calculated after quantification of mRNA levels in peripheral blood mononuclear cells (PBMC) were 3.35 ± 0.81 and 4.51 ± 0.69 in normotensives (N) and hypertensives (HT), respectively (P < 0.04, Mann-Whitney two-sample test). Kidney International 2003 64, S99-S104DOI: (10.1046/j.1523-1755.64.s87.15.x) Copyright © 2003 International Society of Nephrology Terms and Conditions

Figure 3 Hypothetical model of transforming growth factor beta 1 (TGF-β1) hyperexpression as a contributory factor for progressive renal insufficiency. In this hypothesis for the pathogenesis of progressive renal insufficiency, patients expressing high levels of TGF-β1 in response to renal injury are at an increased risk for progression. In this formulation, TGF-β1 expression is engendered by the primary insult (e.g., diabetes), and progressive renal insufficiency results from the heightened expression of TGF-β1. Abbreviations are: DM, diabetes mellitus; GN, glomerulonephritis; HT, hypertension; ESRD, end-stage renal disease. Kidney International 2003 64, S99-S104DOI: (10.1046/j.1523-1755.64.s87.15.x) Copyright © 2003 International Society of Nephrology Terms and Conditions