BACKGROUND: Vascular endothelial growth factor (VEGF) expression influences tubular repair and promotes angiogenesis. The aim of the present study was to determine the relation of VEGF expression and cortical vascularity with renal pathological changes and clinical parameters in allograft biopsies. MATERIALS AND METHODS: Sections from 50 renal allograft biopsies were evaluated by streptavidine-biotin immunohistochemistry by primary antibodies against VEGF and CD34. Cortical tubulointersititial (TI) VEGF expression was scored by light microscopic examination considering intensity and density. Glomerular expression was scored as 0: no staining; 1: faint staining in less than 50% of glomeruli; 2: moderate to strong staining in more than 50% of glomeruli. We determined the number of vessels per cortical high power field (Nves) highlighted by CD34 staining. The clinical and pathological features were retrieved from patient files. RESULTS: Nves was decreased with interstitial fibrosis (IF): 56.3 +/- 3.7; 53.3 +/- 9.8, 46.6 +/- 10.5, 36.75 +/- 1.89 for cases with no IF to mild, moderate, and severe forms, respectively (P << .000). There was increased TI VEGF expression: 1.86 +/- 2.12, 5.8 +/- 3.1, 5.85 +/- 4.4, 10.25 +/- 2.06, respectively (P = .004). The NVes values were not different for cases with high and low to negative VEGF expression scores. There was a negative correlation between Nves values and creatinine at the time of biopsy and time from transplantation to biopsy (r = -.325, P = .024 and r = -.294, P = .038, respectively). Nves and VEGF scores were not different when acute rejection scores or cyclosporine toxicity were considered (P > .05), while Nves were significantly different for chronic allograft nephropathy scores (P = .05). CONCLUSIONS: Chronic renal changes seemed to be associated with decreased cortical vascularity in renal allografts, while the TI VEGF expression was increased. In contrast Nves was not increased with VEGF expression in this series. It seems that along with VEGF, other factors are required for protection against vascular reduction. The aging of the allograft is also a negative influence on cortical vascularity.
BACKGROUND:Vascular endothelial growth factor (VEGF) expression influences tubular repair and promotes angiogenesis. The aim of the present study was to determine the relation of VEGF expression and cortical vascularity with renal pathological changes and clinical parameters in allograft biopsies. MATERIALS AND METHODS: Sections from 50 renal allograft biopsies were evaluated by streptavidine-biotin immunohistochemistry by primary antibodies against VEGF and CD34. Cortical tubulointersititial (TI) VEGF expression was scored by light microscopic examination considering intensity and density. Glomerular expression was scored as 0: no staining; 1: faint staining in less than 50% of glomeruli; 2: moderate to strong staining in more than 50% of glomeruli. We determined the number of vessels per cortical high power field (Nves) highlighted by CD34 staining. The clinical and pathological features were retrieved from patient files. RESULTS: Nves was decreased with interstitial fibrosis (IF): 56.3 +/- 3.7; 53.3 +/- 9.8, 46.6 +/- 10.5, 36.75 +/- 1.89 for cases with no IF to mild, moderate, and severe forms, respectively (P << .000). There was increased TI VEGF expression: 1.86 +/- 2.12, 5.8 +/- 3.1, 5.85 +/- 4.4, 10.25 +/- 2.06, respectively (P = .004). The NVes values were not different for cases with high and low to negative VEGF expression scores. There was a negative correlation between Nves values and creatinine at the time of biopsy and time from transplantation to biopsy (r = -.325, P = .024 and r = -.294, P = .038, respectively). Nves and VEGF scores were not different when acute rejection scores or cyclosporinetoxicity were considered (P > .05), while Nves were significantly different for chronic allograft nephropathy scores (P = .05). CONCLUSIONS: Chronic renal changes seemed to be associated with decreased cortical vascularity in renal allografts, while the TI VEGF expression was increased. In contrast Nves was not increased with VEGF expression in this series. It seems that along with VEGF, other factors are required for protection against vascular reduction. The aging of the allograft is also a negative influence on cortical vascularity.