Immuno-pathological studies in IgA nephropathy : The role of virus for etiological and progressive factors

我们已经报道，小鼠静脉注射柯萨奇病毒后，可引起类似IgA肾病的系膜增生性肾小球肾炎。另一方面，病毒感染宿主细胞的能力取决于适当细胞受体的存在。近年来，腺病毒和柯萨奇病毒有一个共同的受体，该受体被鉴定为柯萨奇病毒和腺病毒共同的受体CAR，CAR的分布可能影响病毒性肾炎的病理生理过程。结果如下：1）在小鼠或大鼠的几乎所有器官中检测到CAR的表达。2）在消化系统内脏器官如消化道和肝脏中检测到更强的CAR信息。3）在肾脏中也检测到CAR信息，特别是在肾皮质部分。4）在肾病综合征模型中，结论：柯萨奇病毒可能是肾脏疾病的始动因素，在各种肾小球肾炎或肾病综合征患者中，所述疾病可能受到病毒感染的高度影响，并且病毒感染可能导致肾脏疾病的急性加重或复发。

We have been reporting that the mice injected coxsackievirus intravenously affect the mesangial proliferative glomerulonephritis similar to IgA-nephropathy. On the other hand, the ability of viruses to infect host cells is dependent on the presence of an appropriate cellular receptor. Recently, adenoviruses and coxsackievirus share one common receptor, and the receptor has been identified as a common coxsackievirus and adenovirus receptor ; CAR.The distribution of CAR may influence the pathophysiology of virus induced glomerulonephritis.Therefore, we examined the expression of CAR in various organs of adult rat and mouse. The results were as follows ;1) The expression of CAR was detected in almost all organs of mouse or rat.2) CAR messages were detected stronger in the digestive-system internal organs, such as digestive tract and liver.3) CAR messages were also detected in the kidney, especially in the renal-cortex part.4) In the model of nephrotic syndrome, the expression of CAR messages in rat kidneys was enhanced during the early stages of the illness.In conclusion, the above results indicate that coxsackievirus may serve as the initiated factors of renal disease.Furthermore, in patients involved various glomerulonephritis or nephrotic syndrome, the disease may be highly influenced by viral infections and the viral infections may cause the acute aggravation of the renal disease or relapse.