Background: Interleukin 23 (IL-23) and interleukin 23 receptor (IL-23R) play a role in the pathogenesis of multiple autoimmune processes and renal inflammation, but research has yet to clarify the histological association of IL-23/IL-23R and transplant kidney allografts.
Methods: Between July 2009 and August 2011, 31 renal transplant recipients who received sonography-guided kidney allograft biopsy were enrolled in this retrospective study. The patients were divided into two groups including group A (patients reaching composite outcome) and group B (patients not reaching composite outcome). The composite outcome was defined as serum creatinine (Scr) doubling and lower estimated glomerular filtration rate (eGFR). Specimens of 31 patients were examined by the immunohistochemical stain of IL-23 and IL-23R in allograft kidneys, and clinico-pathological associations were evaluated.
Results: Of the 31 patients, group A had 15 patients (48.3%) and group B had 16 patients (52.7%). Group A had significantly higher SCr, lower eGFR, and low serum albumin (p=0.024). Univariate analysis showed that group A was negatively associated with atrophic glomerular mesangial cell cytoplasmic IL-23R expression (p=0.044). The decreased expression of IL-23R could be due to higher acute antibody-mediated rejection with heavy proteinuria in our study. In other words, the more the glomerular damage due to antibody-mediated rejection, the less the expression of IL-23R in atrophic glomerular mesangial cell cytoplasma.
Conclusions: The patients with composite outcome may have decreased expression of IL-23R in atrophic glomerular mesangial cell cytoplasm.
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