Abstract
ObjectiveTo explore the expression of Glycogen synthase kinase 3 beta (GSK-3β) in renal allograft tissue and its significance in the pathogenesis of chronic allograft dysfunction.MethodsRenal allograft biopsy was performed in all of the renal allograft recipients with proteinuria or increased serum creatinine level who came into our hospital from January 2007 to December 2009. Among them 28 cases was diagnosed as chronic allograft dysfunction based on pahtological observation, including 21 males with a mean age of 45 ± 10 years old and 7 females with a mean age of 42 ± 9 years old. The time from kidney transplantation to biopsy were 1-9 (3.5) years. Their serum creatinine level were 206 ± 122 umol/L. Immunohistochemical assay and computer-assisted genuine color image analysis system (imagepro-plus 6.0) were used to detect the expression of GSK-3β in the renal allografts of 28 cases of recipients with chronic allograft dysfunction. Mean area and mean integrated optical density of GSK-3β expression were calculated. The relationship between expression level of GSK-3β and either the grade of inflammatory cell infiltration or interstitial fibrosis/tubular atrophy in renal allograft was analyzed. Five specimens of healthy renal tissue were used as controls.ResultsThe expression level of the GSK-3β was significantly increased in the renal allograft tissue of recipients with chronic allograft dysfunction, compared to normal renal tissues, and GSK-3β expression became stronger along with the increasing of the grade of either inflammatory cell infiltration or interstitial fibrosis/tubular atrophy in renal allograft tissue.ConclusionThere might be a positive correlation between either inflammatory cell infiltration or interstitial fibrosis/tubular atrophy and high GSK-3β expression in renal allograft tissue.Virtual slidesThe virtual slide(s) for this article can be found here:http://www.diagnosticpathology.diagnomx.eu/vs/9924478946162998.
Highlights
Kidney transplantation is the optimal renal replacement therapy for the patients with end stage renal disease (ESRD)
Researches have proved that chronic inflammatory was the key pathogenic course of nephron loss in various of kidney disease, including chronic renal allograft dysfunction
We mainly detected the expression of Glycogen synthase kinase 3 beta (GSK-3b) in the tissue of renal allograft, and analyzed the relationship between the expression of GSK-3b and inflammatory cell infiltration in renal interstitium, interstitial fibrosis and tubule atrophy
Summary
Kidney transplantation is the optimal renal replacement therapy for the patients with end stage renal disease (ESRD). As the application of more new effective immunodepressants and the development of transplant technique, the incidence of acute rejection is obviously decreasing in the early stage post transplantation, but the long term survival of renal allografts is still a challenge of infiltration in the renal tissue. Researches have proved that chronic inflammatory was the key pathogenic course of nephron loss in various of kidney disease, including chronic renal allograft dysfunction. Researches discovered that GSK-3b mediated chronic inflammatory related to deterioration of renal allograft function, but the mechanism has not been fully interpreted. We mainly detected the expression of GSK-3b in the tissue of renal allograft, and analyzed the relationship between the expression of GSK-3b and inflammatory cell infiltration in renal interstitium, interstitial fibrosis and tubule atrophy. The role of GSK-3b in chronic allograft dysfunction was discussed
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