Elevated level of renal xanthine oxidase mRNA transcription after nephropathogenic infectious bronchitis virus infection in growing layers

Lin, Huayuan; Huang, Qiqi; Guo, Xiaoquan; Liu, Ping; Liu, Weilian; Zou, Yuelong; Zhu, Shuliang; Deng, Guangfu; Kuang, Jun; Zhang, Caiying; Cao, Huabin; Hu, Guoliang

Uric acid is as an end product of endogenous or dietary purines generated by XOD in chickens. In the present study, a significant increase in the serum concentration of UA was observed in the infected group relative to the control group at 15 dpi (p ＜ 0.01). These findings were positively correlated with the increase of serum XOD activity at 15 dpi. Ejaz et al. [10] revealed that long-standing hyperuricemia could result in UA crystal deposition in intrarenal tissues and tubulointerstitial injury. A previous study showed that NIBV triggers UA salt precipitation by invading the tubule cell to initiate kidney tissue damage, and that the accumulation of UA salt could block the ureter [33] . Therefore, the increase in UA generation induced by the hyperactivity of XOD and damage of the kidney caused by NIBV might be the major reason for chicken hyperuricemia.