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      Sialyl Lewis X and Anti-P-Selectin Antibody Attenuate Lipopolysaccharide-Induced Acute Renal Failure in Rabbits

      , , ,
      Nephron
      S. Karger AG

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          Abstract

          Background/Aim: Acute renal failure (ARF) is one of the common problems associated with sepsis or multiple organ dysfunction syndrome (MODS). We have investigated the effects of inhibiting selectin-mediated cell adhesion on lipopolysaccharide-induced ARF in rabbits, using sialyl Lewis X oligosaccharide and PB1.3, an anti-human P-selectin monoclonal antibody, as inhibitors. Methods: ARF was induced by intravenous administration of lipopolysaccharide (0.3 mg/kg, i.v. bolus injection) to New Zealand White rabbits. Induction of ARF was characterized by increases in blood urea nitrogen (BUN), creatinine, and the number of polymorphonuclear leukocytes infiltrating glomeruli, and by fibrin deposition in glomeruli, and tubular dilatation in the kidney. Sialyl Lewis X oligosaccharide (14 mg/kg, i.v. bolus injection immediately before lipopolysaccharide administration and 9 mg/kg/h, i.v. infusion) or PB1.3 (5 mg/kg, i.v. bolus injection before lipopolysaccharide administration), anti-P-selectin antibody, were treated. Results: Treatment with sialyl Lewis X oligosaccharide inhibited the increases in BUN, creatinine, and the number of infiltrating polymorphonuclear leukocytes, and attenuated histopathological impairments. Similarly, treatment with PB1.3 prevented some of the characteristics associated with lipopolysaccharide-induced ARF, not but the increase in creatinine. Conclusion: These results suggest that selectin inhibitors, including sialyl Lewis X oligosaccharide and PB1.3, may provide clinical benefits in the prevention of ARF associated with sepsis and MODS. To our knowledge, this is the first report that P-selectin is directly involved in lipopolysaccharide-induced ARF in rabbits.

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          Adhesion molecules and urinary tumor necrosis factor-alpha in idiopathic membranous glomerulonephritis.

          Adhesion molecules are required in several physiological processes, but their altered function/expression is associated with the pathogenesis of inflammatory diseases. In the present study on idiopathic membranous glomerulonephritis (MGN) the expression of adhesion molecules (ICAM-1, VCAM-1, PECAM-1, E-selectin, LFA-1, Mac-1) was analyzed in different cellular compartments of the kidney using an indirect immunoperoxidase technique and monoclonal antibodies. Relationships between the expression of these molecules and the clinical and morphological activity of the disease and the urinary excretion of tumor necrosis factor alpha (TNF-alpha) were studied in 20 patients. The results were compared with the findings in ten normal kidneys and urinary TNF-alpha in 17 healthy subjects. The expression of adhesion molecules in glomeruli and tubules was unchanged apart from a diminished expression of VCAM-1 (P = 0.014) in glomerular parietal epithelial cells and PECAM-1 in glomerular endothelial cells (P < 0.01). Interstitial peritubular capillaries expressed significantly (P = 0.009) more E-selectin compared with the controls. The interstitial compartment had a highly increased number of cells expressing ICAM-1 in MGN (32.4 +/- 4.6 cells/high power field) compared with the controls (9.4 +/- 1.2; P < 0.001). Also, cells expressing VCAM-1 (10.2 +/- 1.6 vs. 2.8 +/- 1.9; P = 0.005). PECAM-1 (25.9 +/- 5.3 vs. 7.4 +/- 2.1; P = 0.006), and LFA-1 (20.4 +/- 3.6 vs. 8.3 +/- 1.5; P = 0.041) were increased in the interstitium. Proteinuria correlated particularly with the expression of E-selectin in peritubular capillaries (r = 0.63, P = 0.004). The number of LFA-1 expressing inflammatory cells in the interstitium correlated with peritubular capillary E-selectin (r = 0.8, P < 0.001) and interstitial ICAM-1 (r = 0.61, P = 0.009) expression, but histological alterations did not correlate with the expression of adhesion molecules. Tumor necrosis factor-alpha excretion was significantly increased in MGN (41 +/- 8 pg/mg creatinine) compared with the controls (13 +/- 2; P = 0.001), and in particular, it correlated with the interstitial expression of LFA-1 (r = 0.71, P = 0.002). This study suggests that active MGN leads not only to proteinuria but also to increased urinary TNF-alpha excretion. These may serve as triggers for the up-regulation of adhesion molecules in the peritubular capillaries and interstitial cells thus enhancing the development of the interstitial injury.
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            Author and article information

            Journal
            Nephron
            Nephron
            S. Karger AG
            1660-8151
            2235-3186
            July 1 2001
            2001
            March 21 2001
            : 87
            : 4
            : 352-360
            Article
            10.1159/000045942
            fba74905-37ab-4ff4-af60-529e6fbaa623
            © 2001

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