SCF ASON treatment increases renal injury.

<p>(A) Whole kidney sample analysis of SCF expression by ELISA did not show any significant difference in SCF levels between NSON (□) and ASON (▪) treated animals (<i>P</i> = 0.09, non significant). Data are expressed as mean±SEM. (B) Digital image analysis of SCF immunostainings per hpf of the corticomedullary region demonstrated significantly less staining on tissue sections from ASON treated animals (▪) compared to controls (□) at day 1 after ischemia (*<i>P</i> = 0.003). Data are expressed as mean±SEM. (C) and (D) Representative SCF immunostainings of ischemic kidney sections used for image analysis of NSON (c) and ASON (d) treated animals; original magnification: 40×. (E) Tubular damage was scored in a semi-quantitative fashion. The degree of injury one day after ischemia was significantly increased in ASON treated animals (▪) compared to NSON controls (□) (*<i>P</i> = 0.005). Data are expressed as mean±SEM. (F) and (G) Renal function was determined by measurement of (f) plasma urea and (g) creatinine values. ASON treatment (▪) resulted in significantly elevated plasma urea (*<i>P</i> = 0.0047) and creatinine (*<i>P</i> = 0.001) compared to NSON controls (□) at day one after ischemia. Data are expressed as mean±SEM. (H) Representative PAS-D stainings illustrating tubular injury as scored in (E). Kidneys from sham operated animals after NSON and ASON treatment show no histologic signs of tubular injury. In contrast, at day 1 after ischemia most tubules in the corticomedullary area appear dilated with loss of the brush border or display denudation of the tubular basement membrane. In NSON-treated animals, more undamaged tubules were present compared to ASON-treated animals.