De novo papillary renal cell carcinoma in an allograft kidney : Evidence of donor origin
De novo papillary renal cell carcinoma in an allograft kidney : Evidence of donor origin
复制标题
同种异体移植肾中的新生乳头状肾细胞癌：供体来源的证据
DOI：
10.1111/j.1440-1827.2011.02714.x
复制
发表时间：
2011
期刊：
影响因子：
2.2
通讯作者：
et al
中科院分区：
文献类型：
--
作者：
Naruke Y;Ito M;Nakashima M;et al
在移植受者中，原发性恶性肿瘤的发生率增加已被认识到。肾细胞癌（RCC）占肾移植受者所有恶性肿瘤的4.6%，而一般人群中肾细胞癌占所有癌症的2%。根据辛辛那提移植肿瘤登记处的数据，在同种异体移植肾脏中发生RCC的病例较少（高达10%），而在肾移植受者中，近90%的RCC发生在原生肾脏。新生肾细胞癌被描述为与移植前存在的肿瘤相反。在同种异体移植肾中发生的新生肾细胞癌的病理特征尚未得到很好的描述。此外，仅在少数报道的RCC病例中进行了确定肿瘤起源的遗传学研究，无论是来自供体还是受体，尽管考虑到肿瘤传播的关联，这在临床上很重要。我们报告一例在肾移植后13年诊断为异体移植肾的新生乳头状肾细胞癌，遗传学证实为供体来源。一位49岁的日本男性在25岁时出现继发于病因不明的慢性肾小球肾炎的终末期肾脏疾病。患者无肾脏疾病家族史。经过5年的血液透析，他在29岁时接受了来自已故供者的肾移植。捐献者是一名死于脑出血的37岁日本男性。根据医疗记录，捐赠者的家族史或既往史均无重大疾病。免疫抑制治疗继续使用甲基强的松龙、环孢素和米佐利滨。患者出现慢性排斥反应，移植后7年类固醇治疗成功。此时，超声检查未发现同种异体移植肾的实性或囊性病变。移植物功能稳定，血清肌酸水平为1.1至1.3 mg/dL，尽管患者在极少数情况下表现出30 mg/dL的蛋白尿。然而，移植13年后，超声检查显示移植肾的下极有一个2.3厘米的孤立囊性病变。在接下来的7年里，囊肿的大小增加到4.0厘米，里面有轻微的血流，导致怀疑是恶性的。同种异体移植肾及原生肾均未见其他囊性病变。广泛的检查排除了任何原发或转移性病变。该患者在移植后20年，即2010年接受了同种异体肾的部分切除手术。在最近的评估中没有发现复发。移植物功能恢复，患者保持无透析状态。这个特殊的供者的对侧肾脏被移植给一名日本女性，在移植12年后由于慢性排斥而切除，没有出现实性或囊性病变。在切除的标本中，一个边界清晰的肿瘤位于肾皮质。肿瘤大小为4.0× 3.5× 3.5 cm。切口表面呈实心黄白色，有少量出血。未见坏死。组织学上，单眼囊肿密集充满小立方体细胞，嗜碱性细胞质稀少。立方细胞也排列在囊壁上（图1a）。肿瘤细胞形成乳头状和小管，在基底膜上排列成单层。细胞核小而均匀，染色质深染，呈细颗粒状。乳头状核常含有泡沫状巨噬细胞和含铁血黄素的巨噬细胞聚集。肿瘤周围肾实质…
An increased incidence of primary malignancies has been recognized in transplant recipients. Renal cell carcinomas (RCC) represent 4.6% of all malignancies in renal transplant recipients, whereas RCC constitutes 2% of all cancers in the general population. 1 According to the Cincinnati Transplant Tumor Registry, there are fewer instances of RCC that develop in the allograft kidneys (up to 10%), while nearly 90% of RCC in renal transplant recipients have been found in native kidneys. 1 De novo RCC has been described as the opposite of pre-existing tumors before transplantation. 1–3 Pathological characteristics of de novo RCC occurring in the allograft kidney have not been well described. Furthermore, genetic studies to determine the tumor origin, whether from the donor or the recipient, have been performed in only a few reported RCC cases, although it is clinically important considering the association of tumor transmission. We report a case of de novo papillary RCC developing in an allograft kidney diagnosed 13 years after renal transplantation, and which was genetically confirmed to be of donor origin. A 49-year-old Japanese male presented with end-stage renal disease secondary to chronic glomerulonephritis of unknown etiology when he was at the age of 25. The patient had no family history of renal disease. After 5 years of hemodialysis, he underwent renal transplantation at the age of 29 from a deceased donor. The donor was a 37-year-old Japanese male who died of cerebral hemorrhage. The donor had no significant medical illness in his family history or past history according to medical records. Immunosuppressive therapy was maintained with methylprednisolone, cyclosporine and mizoribine. The patient presented with an episode of chronic rejection that successfully treated by steroids 7 years after transplantation. At that point, ultrasonography showed no evidence of a solid or cystic lesion in the allograft kidney. Graft function had been stable with serum creatine level of 1.1 to 1.3 mg/dL, although the patient exhibited 30 mg/dL of proteinuria on rare occasions. However, 13 years after transplantation, ultrasonography revealed a 2.3 cm solitary cystic lesion in the lower pole of the allograft kidney. During the following 7 years, the cyst had increased in size to 4.0 cm with slight blood flow inside, which led to suspicion of malignancy. There was no other cystic lesion in the allograft kidney or native kidneys. An extensive workup ruled out any primary or metastatic lesion. The patient underwent a partial nephrectomy of the allograft kidney in 2010, 20 years after transplantation. No recurrence has been found on most recent evaluation. Graft function has resumed and the patient has maintained dialysis-free status. The contralateral kidney of this particular donor, which had been transplanted to a Japanese female and resected 12 years after transplantation due to chronic rejection, presented no solid or cystic lesion. In the resected specimen, a well-circumscribed tumor was located in the renal cortex. The tumor measured 4.0× 3.5× 3.5 cm in size. The cut surface was solid and yellowish-white with tiny hemorrhages. No necrosis was noted. Histologically, a unilocular cyst was densely filled with small cuboidal cells with scanty basophilic cytoplasm. The cuboidal cells also lined the cyst wall (Fig. 1a). The tumor cells formed papillae and tubules, arranged in a single layer on the basement membrane. The nuclei were small, uniform and had hyperchromatic chromatin with a finely granular pattern. The papillary cores frequently contained aggregates of foamy macrophages and hemosiderin laden macrophages. Kidney parenchyma around the tumor …