Clinical history
A 73-year-old man, who had previously presented with angina and interstitial pneumonia, developed left lower back pain and attended our hospital. Peri–pelvic extravasation of urine was observed with magnetic resonance imaging. Contrast–enhanced computed tomography confirmed a left renal pelvic tumor. The patient’s tumor marker serum levels, such as those for carcinoembryonic antigen, carbohydrate antigen 19–9, and squamous cell carcinoma, were within the normal range. No malignant cells were identified in the patient’s urine cytology. A left nephroureterectomy was subsequently performed with a clinical diagnosis of left pelvic renal cancer.
Left nephroureterectomy specimens were obtained that were originally prepared from 10% buffered formalin–fixed, paraffin–embedded tissue according to our routine hospital procedure. A histopathological examination was performed using hematoxylin and eosin staining. Immunohistochemistry was conducted using an autoimmunostainer (Leica BOND–III system: Leica Biosystems, Newcastle, UK). The antibodies we employed are listed in Table 1.
Pathologic findings
There was a well–circumscribed exophytic lesion in the renal pelvis that measured 42 x 25 mm. The cut surface of the tumor showed a whitish mass with a partially myxoid change (Fig. 1A). Microscope observations revealed that the tumor was mainly located in the renal pelvic mucosa (Fig. 1B). The tumor exhibited two distinct morphological components. The tumor surface comprised a noninvasive urothelial carcinoma, which included a high-grade papillary urothelial carcinoma and a carcinoma in situ (CIS) (Fig. 1C and 1D). Whereas the invasive urothelial carcinoma was composed of cells that were dyscohesive, lacked cell adhesion and were set in a loose myxoid stroma (Fig. 1D and 1E). The transition of CIS and the invasive urothelial carcinoma was seen (Fig. 1D). The invasive tumor cells had an eccentrically placed nucleus and abundant amphophilic to eosinophilic cytoplasm and exhibited a striking morphologic overlap with plasma cells (Fig. 1F). A plasmacytoid urothelial carcinoma was diagnosed based on the morphology findings.
Immunohistochemically, the noninvasive urothelial carcinoma was positive for cytokeratin and E–cadherin, whereas it was negative for vimentin (Fig. 2A–C). CD138 and CD38, which are immunohistochemical markers for plasma cells, showed opposite immunostaining, and this noninvasive urothelial carcinoma was positive for CD138 and negative for CD38 (Fig. 2D and 2E). These cells were also negative for ZEB1 (Fig. 2F). On the other hand, the component of the plasmacytoid urothelial carcinoma was immunoreactive for cytokeratin, suggesting that these findings indicated the characteristics of an epithelium (Fig. 2A). However, E–cadherin was negative, and vimentin, CD138 and CD38 were positive for this component (Fig. 2B–E). In addition, ZEB1 expression was diffuse positive for this component (Fig. 2F). In summary, as shown in Table 2, the immunohistochemical determination of an invasive plasmacytoid urothelial carcinoma was characterized by E-cadherin negative, CD38 positive, and ZEB1 positive cells, unlike a noninvasive urothelial carcinoma.