Dysregulation of Interleukin 23 Receptor Expression in Kidney Allografts Associated with Composite OutcomeKuang-Chin Hsiao1,2, Wan-Ru Chao2,3, Jen-Pi Tsai4, Mei-Chin Wen5, Jong-Da Lian6, Wen-Chin Lee1, Jong-Yu Huang1, Shun-Chi Chang1 and Horng-Rong Chang2,6*
- *Corresponding Author:
- Horng-Rong Chang
Division of Nephrology, Department of Medicine
Chung Shan Medical University Hospital
Address: No. 110, Sec. 1, Jianguo N. Road South District
Taichung 40201, Taiwan
Tel: +886-4-24739595 extn. 32620
Fax: +886-4-24739220 extn. 32624
E-mail: [email protected]
Received Date: September 23, 2014; Accepted Date: November 17, 2014; Published Date: November 19, 2014
Citation: Hsiao KC, Chao WR, Tsai JP, Wen MC, Lian JD, et al. (2014) Dysregulation of Interleukin 23 Receptor Expression in Kidney Allografts Associated with Composite Outcome. J Cytol Histol S4:017. doi:10.4172/2157-7099.S4-017
Copyright: © 2014 Hsiao KC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.