多瘤病毒感染：1、轻度动脉内膜炎；2、小管炎（程度？）3、一些肾小管上皮细胞中多瘤病毒感染，SV-40 stain

4、是否存在急性T细胞介导排斥反应5、类固醇推注，然后减量

 学习中，谢谢！

The above case also shows mild intimal arteritis (v1) in addition to BK virus infection.  BK virus infection also causes tubulitis, indistinguishable from acute T-cell-mediated rejection. But the endoarteritis is the strong evidence of acute T-cell-mediated rejection. I learned from consultation cases that some transplant pathologist takes the extent of tubulitis into consideration.  In their report, it states that " Interpretation of the tubulointerstitial nephritis in the setting of BK nephropathy is problematic.  The tubular epithelial cells with BK virus infection, which are highlighted by immunohistochemical stains for SV-40, only exist in some tubules.  However, the tubulitis is more diffuse, involving the tubules without positive BK virus stains. This raises the possibility of co-existing acute cellular rejection.  Clinical judgment and close follow up are suggested."

Can acute T-cell-mediated rejection co-exist with BK virus infection? The answer is YES. The problem is how to diagnose these conditions. If we only depend on arteritis to diagnose co-existing acute rejection, probably we underdiagnose the co-existing acute rejection.

There are protocols to treat BK virus infection with acute rejection. One of the protocols is that nephrologist will first bolus the patient with steroids and then do the reduction.  The above patient was treated in this way and improved. The following up biopsy demonstrated negative SV40 stain. But the tubulitis and glomerulitis persist. The creatinine went up again several weeks later. The nephrologist had to increase the immunosuppression.

I do not have much experience about this subject. I am still in the learning process. I welcome your input.

 谢谢frankbj老师的讲解和references. Based on your experience and/or references, how do you diagnose co-existing rejection?

 谢谢quhong 老师提供这么好的病例供大家学习!以下是我摘抄的：

Hirsch 等将BKN 的病理过程划分为3 期: (1) A 期:可见局灶性小管上皮细胞大T 抗原染色阳性,诸如病毒包涵体之类的细胞病理改变有限,无广泛的坏死和炎性浸润。此阶段不大可能出现明显的肾功能损害。(2) B 期:可见广泛的多灶性弥散性的细胞病理学改变,坏死伴有炎性反应,并出现了间质纤维化的初步征象。浸润的炎症细胞包括多形核细胞、单核细胞和浆细胞,分布方式多样。(3) C 期:可见肾间质纤维化、瘢痕甚至钙化。肾小管细胞变平、萎缩。但此时BKV 感染的细胞较前一期少见。一项大型序贯活检报告表明[ 3 ] ,有80 % BKN 患者会从A 期进展到B/ C 期,至少有30 %从B 期进展到C 期。B 期病例清除BKV 者少于10 % ,但A 期病例至少有30 %清除了BKV。因此,早期诊断和处理是十分必要的。