Author: Lin, Huayuan; Huang, Qiqi; Guo, Xiaoquan; Liu, Ping; Liu, Weilian; Zou, Yuelong; Zhu, Shuliang; Deng, Guangfu; Kuang, Jun; Zhang, Caiying; Cao, Huabin; Hu, Guoliang
Title: Elevated level of renal xanthine oxidase mRNA transcription after nephropathogenic infectious bronchitis virus infection in growing layers Document date: 2015_12_17
ID: t8547tse_27
Snippet: 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.....
Document: 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.
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