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Port–Site recurrence following Laparoscopic Radical Nephrectomy for Chromophobe Renal Cell Carcinoma

Port-site metastasis following laparoscopic radical nephrectomy is being increasingly recognized as a complication following laparoscopic surgery, especially when correct surgical principles are violated. All previously reported cases have been of either the clear cell or papillary variant of renal cell carcinoma. Herein we report a case of chromophobe renal cell carcinoma with port-site recurrence 10 months after laparoscopic radical nephrectomy.

Authors: Javali, Tarun; Dogra, Premnath; Singh, Prabhjot
Corresponding Author: Javali, Tarun

 

Introduction
Port-site metastasis following laparoscopic radical nephrectomy is being increasingly recognized as a complication following laparoscopic surgery, especially when correct surgical principles are violated. All previously reported cases have been of either the clear cell or papillary variant of renal cell carcinoma. Herein we report a case of chromophobe renal cell carcinoma with port-site recurrence 10 months after laparoscopic radical nephrectomy.

Case History
A 44 year old lady presented with a 6 month history of left flank pain and hematuria. Computed tomography revealed a 12×5×5 cms heterogeneous enhancing left renal upper pole mass. [Fig.1]. There was no evidence of lymph node enlargement or liver metastasis, and no tumor thrombus. The CT scan also revealed a multiloculated right adnexal cyst of size 6×4×4 cms. The patient underwent laparoscopic transperitoneal left radical nephrectomy and right oophorectomy. Additional ports were placed for the oophorectomy. The radical nephrectomy was performed first because it was deemed to be more technically challenging than the oophorectomy. Both the specimens were entrapped separately in retrieval bags and removed through a Pfannensteil incision. The specimen was not morcellated.
Histopathology revealed a chromophobe renal cell carcinoma. On immunohistochemical analysis, the tumor was positive for cytokeratin and negative for CD10 and vimentin. There was no evidence of any capsular breach. The tumor had reached the renal sinus but had not infiltrated it. Histopathology of the right oophorectomy specimen showed an endometrial cyst.
The patient was reviewed on a three monthly basis with a chest x-ray, liver and kidney function tests and a full blood count. No abdominal imaging was done at this time. Ten months after surgery, the patient presented with pain and swelling at one of the port sites. Examination revealed a hard subcutaneous nodule of size 2×1.5 cm at the 12mm working port site above and medial to the left anterior superior iliac spine [Fig 2]. The surgical incision site for specimen removal had no evidence of recurrence. The patient had already had fine needle aspiration cytology (F.N.A.C.) performed, which was reported as showing ‘malignant cells suspicious for renal cell carcinoma’. A contrast enhanced CT scan of her abdomen revealed an irregular enhancing subcutaneous soft tissue lesion in left anterior abdominal wall measuring 1.8 cms, thought likely to be a metastasis. The liver and right kidney were normal and there were no retroperitoneal nodes or masses. Positron emission tomography-computed tomography (PET-CT) revealed increased 18-fluro deoxy glucose (18FDG) uptake in the soft tissue density lesion in left lower abdominal wall [Fig 3]. The patient underwent wide local excision of the port-site nodule. Histology revealed chromophobe renal cell carcinoma with the same histomorphology as the primary tumour [Fig 4,5].
At one year post excision of the port-site nodule, patient is well, and has had no recurrences, either local or systemic.

Discussion
Factors which have been implicated in port-site recurrence include natural tumor factors, local wound factors, immune response and laparoscopic related factors such as direct wound contamination, either instrument contamination or during specimen extraction, specimen morcellation, use of specimen retrieval bags and pneumoperitoneum pressure [1,2]. Poorly differentiated transitional cell carcinomas have accounted for most of the cases of port site recurrence in laparoscopic uro-oncologic case series [1,2,3]. Only a few cases of port site recurrence following laparoscopic nephrectomy for renal cell carcinoma have been reported [4,5,6,7,8,9,10]. In all of these cases the histopathology was clear cell carcinoma. Russo et al reported a case of papillary renal cell carcinoma with port site metastasis following laparoscopic partial nephrectomy [11]. To the best of our knowledge this the first case of chromophobe renal cell carcinoma with port site recurrence. In the present case the tumor was organ confined (pT2) and well differentiated. Most studies report more favorable prognosis for chromophobe compared to conventional renal cell carcinoma. This goes against the commonly held notion that adverse tumor biology or aggressive nature of the tumor is the most important causative factor in port site recurrence [1]. Greco et al have further elaborated on the factors that accelerate the development of port-site metastasis [12]. These conditions include performing laparoscopic surgery in the presence of ascites, lack of trocar fixation to prevent dislodgement and gas leakage around the trocars, inadequate laparoscopic equipment and technique and tumour boundary violation. Factors which have deemed to reduce the incidence of port-site metastases include use of a bag for specimen retrieval, placement of drainage before desufflation, povidone-iodine irrigation of instruments, trocars and port-site wounds and suturing trocar wounds ≥10mm in size.
In the present case, all possible precautions were taken during the course of surgery, including changing the instruments, once the radical nephrectomy was over. A probable etiologic factor in this case may have been the prolonged operating time as laparoscopic nephrectomy was followed by laparoscopic oophorectomy and the gynaecologists also used the left sided 12mm working port. Microleakage around ports (“chimney effect”) has been postulated to play a role in port site metastasis [13]. Ports used by the main operating surgeon have been proved to have more contamination by tumor cells than either those used by the assistants or the camera port [14]. It is a matter of conjecture that whether performing the oophorectomy first followed by radical nephrectomy could have altered the result.
We wish to highlight two main points through this case report. Firstly, that tumor histology may not be predictive of port site recurrence. Chromophobe renal cell carcinoma is biologically a tumor of low malignant potential. Metastasis of chromophobe tumour constitute less than 1% of all metastatic renal cell carcinoma [15]. Advanced pathological T stage, tumor necrosis and sarcomatoid change have been purported to predict an aggressive phenotype of chromophobe renal cell carcinoma [16]. However none of these features were present in this case. Hence following laparoscopic radical nephrectomy patients need to be carefully examined at each visit with particular attention to the port sites. This should be done regardless of the grade, stage or histology of the tumor.
The second point we wish to highlight is that PET-CT could be a useful adjunct in diagnosing port-site recurrence in equivocal cases. This may be especially relevant in patients who return within a short span of time following laparoscopic radical nephrectomy, wherein induration due to surgical factors at scar site may be confused vis-a vis port site recurrence.

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Fig. 1 – CT KUB (Kidney-ureter-bladder) showing left upper pole tumor.

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Fig. 2 – Port-site nodule

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Fig. 3 – PET-CT showing port-site metastasis

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Fig. 4 – Hematoxylin and Eosin staining of excised port-site specimen. Sheets of cells with round to oval nuclei and perinuclear halo with prominent cell membranes.

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Fig. 5 – Immunohistochemistry. Negative for CD10 and vimentin.

References
1. Rassweiler J, Tsivian A, Kumar AV, Lymberakis C, Schulze M, Seeman O, et al. Oncological safety of laparoscopic surgery for urological malignancy: experience with more than 1,000 operations. J Urol 2003; 169:2072–5.
2. Tsivian A, Sidi AA. Port site metastases in urological laparoscopic surgery. J Urol 2003; 169:1213–8.
3. Micali S, Celia A, Bove P, et al: Tumor seeding in urological laparoscopy: an international survey. J Urol 2004; 171: 2151–4.
4. Fentie DD, Barret PH, and Taranger LA: Metastatic renal cell carcinoma after laparoscopic radical nephrectomy: long term follow-up. J Endourol 2000; 14: 407–11.
5. Landman J, and Clayman R: Re: port site tumor recurrences of renal cell carcinoma after videolaparoscopic radical nephrectomy (letter). J Urol 2001; 166: 629–30..
6. Castilho LN, Fugita OEH, Mitre AI, et al: Port site tumor recurrences of renal cell carcinoma after videolaparoscopic radical nephrectomy. J Urol 2001; 165: 519.
7. Chen YT, Yang SSD, Hsieh CH, et al: Hand port-site metastasis of renal-cell carcinoma following hand-assisted laparoscopic radical nephrectomy: case report. J Endourol 2003; 17: 771–4.
8. Iwamura M, Tsumura H, Matsuda D, et al: Port site recurrence of renal cell carcinoma following retroperitoneoscopic radical nephrectomy with manual extraction without using entrapment sac or wound protector. J Urol 2004; 171: 1234–5.
9. Dhobada S, Patankar S, Fais F, et al: Port-site metastasis after laparoscopic radical nephrectomy for renal-cell carcinoma: case report. J Endourol 2006; 20: 119–22.
10. Goyal R., Sing P., Mandhani A. et al. Port-site metastatis of renal cell carcinoma after laparoscopic transperitoneal radical nephrectomy. Ind J of Urol 2006; 22:150-1.
11. Masterson TA, Russo P. A case of port-site recurrence and loco-regional metastasis after laparoscopic partial nephrectomy. Nature Reviews Urology 2008; 5:345-9.
12. Greco F, Wagner S, Reichelt O, Inferrera A, Lupo A, Hoda MR, Hamza A, Fornara P
Huge port-site metastasis after laparoscopic partial nephrectomy: a case report. Eur Urol 2009; 56:737-39.
13. Curet MJ: Port site metastases. Am J Surg 2004; 187: 705-12.
14. Ramirez PT, Wolf JK, and Levenback C: Laparoscopic port-site metastases: etiology and prevention. Gynecol Oncol 2003; 91: 179–89.
15. Choueiri TK, Plantade A, Elson P et al. Efficacy of sunitinib and sorafenib in metastatic papillary and chromophobe renal cell carcinoma. J Clin Oncol 2008; 26:127-31.
16. Amin MB, Paner GP, Alvarado-Cabrero I et al. Chromophobe renal cell carcinoma: histomorphologic characteristics and evaluation of conventional pathologic prognostic parameters in 145 cases. Am J Surg Pathol 2008; 32:1822-34.

 

Date added to bjui.org: 05/12/2012

DOI: 10.1002/BJUIw-2012-035-web

 

Eosinophilic Variant of Chromophobe Renal Cell Carcinoma with Tubulocystic Features: A Case Report

Cells with eosinophilic granular or oncocytic cytoplasm are a hallmark of benign renal oncocytoma, but they can be seen in other renal tumors. We report an unusual case of a large renal tumor with medium-sized oncocytic cells that were arranged in sheets and tubulocystic growth patterns. With histological, immunohistochemical and ultrastructural studies, a diagnosis of eosinophilic variant of chromophobe renal cell carcinoma (ChRCC) with tubulocystic features was made. The eosinophilic granular cytoplasm that was visible on the H&E sections corresponded to the abundant microvesicles packing the cytoplasm. Since the prognosis of ChRCC is regarded as more favorable than other subtypes of renal cell carcinomas (RCC), an accurate identification of this tumor has significant clinical implications. However, there is no current literature describing renal tumor similar to our case. Here we discuss the histologic features of this unique neoplasm at light and electron microscopic levels, the immunohistochemical profile, and differential diagnosis from its mimickers, including oncocytoma, clear cell RCC with granular cytoplasm and tubulocystic carcinoma of the kidney.

Authors: Yin, Ming ; Falls, Randall
Corresponding Author: Yin, Ming

 

Introduction
Chromophobe renal cell carcinoma (ChRCC) accounts for approximately 5% of all renal cell carcinomas (RCC).(1), (2), (3) Even though ChRCC is typically associated with a better prognosis than the other RCC subtypes; aggressive behavior has been seen in some cases.(2), (4) ChRCC is characterized by large pale cells with marked cell membranes resembling “plant cells”. However, accurate diagnosis of ChRCC can be challenging at times, especially when the tumor is purely composed of granular eosinophilic (oncocytic) cells. Histopathological studies on the eosinophilic variant of ChRCC have not been fully described in the literature, but this is possibly due to the fact that the histological findings of this variant of ChRCC are similar to those of oncocytoma. Histochemical and immunohistochemical stains may be helpful in some situations; however, so far, no markers can reliably distinguish between oncocytoma and ChRCC, particularly the eosinophilic variant.(5) We describe the histopathologic, immunohistochemical and ultrastructural findings of an eosinophilic variant of ChRCC with tubulocystic features, with emphasis on its problematic differential diagnosis from those conditions which mimic it.

Case Report
A 63-year-old female presented with a large left renal mass that was discovered during a work-up for abdominal pain of unknown duration. Computerized tomography of the abdomen revealed an exophytic, rounded mass arising from the upper pole of the left kidney with distortion of the renal collecting system. The patient subsequently underwent a left radical nephrectomy. The kidney specimen measured 16.8 x 10.0 x 6.8 cm and weighed 610 grams. On sectioning, the kidney showed a well-circumscribed tumor that measured 12.0 x 6.8 x 5.7 cm and occupied the upper pole, compressing the renal pelvis and calyceal system. The cut surface of the mass was homogeneously tan-pink in color with focal brown areas suggestive of old hemorrhage; no tumor necrosis or central scar was seen (Figure 1). No lymph nodes were noted.

Histologic examination showed the mass to be composed of medium-sized polygonal cells, which displayed two architectural patterns. The majority of tumor cells were arranged in sheets or wide trabeculae (Figure 2). In adjacent areas, one could appreciate a tubulocystic growth pattern (Figure 3). The tumor cells had abundant granular eosinophilic cytoplasm with relatively well-defined cellular borders (Figure 4). There was mild to moderate nuclear pleomorphism, with an occasional thin-rim perinuclear halo. No sarcomatoid transformation was seen. The immunohistochemical stains showed diffuse immunoreactivity for pancytokeratin (AE1/3), cytokeratin 7, Ber-EP4, and CD117 (Figure 5). The stains with antibodies against RCC marker, CD10 and vimentin were negative. There was also cytoplasmic positive staining with Hale’s colloidal iron. Electron microscopy showed that abundant microvesicles, admixed with mitochondria, were distributed diffusely throughout the cytoplasm (Figure 6). On higher power, the microvesicles were bound by smooth single membranes, measuring 200 – 500 nm in diameter, and packing the spaces between mitochondria (Figure 7). A small number of lysosomes, lipid vacuoles and glycogen granules were noted in the cytoplasm, where the Golgi apparatus and the rough endoplasmic reticulum were poorly developed. Nuclei were rounded with irregular folded nuclear membrane and heterochromatin.

Discussion
When renal tumor cells show distinctive granular eosinophilic cytoplasm, the main diagnostic challenge is to separate an eosinophilic variant of ChRCC from the benign renal oncocytoma. Grossly, 33% of large oncocytomas may have a central stellate scar, which was not visible in the current tumor. Histologically, oncocytoma usually has tumor cells with inconspicuous cell borders arranged in nests or acini in a hypocellular hyalinized stroma, features that were not seen in this tumor either. Nuclear membrane irregularity and coarse chromatin are noted in this case, while oncocytomas usually have cells showing bland, uniform nuclei with smooth nuclear membranes. Hale’s colloidal iron stain showed diffuse cytoplasmic positivity in our case, whereas oncocytoma often displays focal positive staining confined to the luminal borders. Immunohistochemical stains performed on the current tumor showed that the cells were positive for cytokeratin 7, Ber-EP4, and CD117; and negative for RCC marker, CD10 and vimentin; a staining profile favoring a ChRCC. However, there is no established panel of immunohistochemical stains that can differentiate ChRCC from oncocytoma with certainty. This could, in part, be explained by the fact that these two tumors may share a common cell of origin in the distal nephron, namely intercalated cells of the collecting ducts.(5), (6) Electron microscopic analysis is considered the only definitive method to consistently distinguish these two entities.(7) The granular appearance of the cytoplasm on light microscopy corresponds to the ultrastructural finding of abundant microvesicles and scattered mitochondria in the cytoplasm of a majority of tumor cells, which is considered diagnostic for ChRCC.(7) In contrast; it is known that oncocytoma is characterized by the packing of the cytoplasm by mitochondria with paucity of microvesicles and other cell organelles. Unlike the classic ChRCC, the cytoplasm of this tumor was filled with crowded microvesicles diffusely interspersed between mitochondria, leading to less prominence or absence of perinuclear clearing (halo) by light microscopy. Previous studies have suggested that the microvesicles are derived from mitochondria because of the close relationship between microvesicles and mitochondria at the ultrastructural level;(8) although the possibility of endoplasmic reticulum being the origin has also been suggested.(1), (7) In addition, clear cell RCC can occasionally show a somewhat granular cytoplasm leading to potential confusion with ChRCC.(4), (7) However, clear cell RCC usually demonstrates alveolar or acinar growth patterns with delicate thin-walled blood vessels by light microscopy and abundant cytoplasmic lipid vacuoles and glycogen granules by electron microscopy. Immunohistochemically and histochemically, clear cell RCC is usually positive for antibodies against vimentin, RCC marker and CD10, and negative for CD117 and colloidal iron.

ChRCC was first described in 1985 as a tumor composed of cells with unique histomorphologic and ultrastructural features.(1) The tumor is presumably derived from intercalated cells of the collecting ducts.(5) Histologically, ChRCC is characterized by polygonal cells with distinct nuclear borders and evenly distributed, finely granular, translucent and pale cytoplasm. The classic architectural appearance is that of sheets or wide trabeculae of cells often separated by incomplete fibrovascular septations. Occasional, papillary, tubulocystic and nested patterns may be present.(1), (4) The nuclei often are hyperchromatic with nuclear membrane irregularity (raisinoid) and coarse chromatin. Binucleation or multinucleation are also common. Classically, perinuclear cytoplasmic clearing (halo) is present. Interestingly, it appears that nuclear grade as determined by the Fuhrman system may not reflect the clinical or biological behavior of chromophobe RCC as closely as it does for the other subtypes.(9)

The eosinophilic variant of ChRCC was first reported in 1997.(10) It usually shows small to medium-sized, eosinophilic granular/oncocytic cells arranged in sheets.(11) Compared with the classic ChRCC, our case showed smaller cell size, less prominent cell borders and thinner or absent perinuclear halos. However, similar to classic ChRCC, the eosinophilic variant is a tumor of low malignant potential with reported 5-year and 10-year survival rates of 78-100% and 80-90%, respectively.(1), (11) It is also believed that the cytogenetic abnormalities of this variant are similar to those of the classic ChRCC, including losses of chromosomes 1, 2, 6, 10, 13, 17 and 21.(12), (13)

ChRCC with microcystic and adenomatous patterns was first described in 1998.(14) Because of the tubulocystic architectures identified in the current case, a differential diagnosis that includes tubulocystic carcinoma of the kidney is needed. The tubulocystic carcinoma of the kidney is a recently recognized subtype of renal tumor that is not listed in the 2004 WHO classification.(3) Besides the packed tubules and cysts separated by bland fibrous stroma, the lining tumor cells of this newly described entity are cuboidal to columnar with abundant eosinophilic cytoplasm and usually large nuclei with prominent nucleoli.(15) These features are readily separable from the current case by routine histology. In addition, the genetic signatures of the tubulocystic carcinoma of the kidney are gains of chromosome 7 and 17.

In conclusion, we report for the first time a unique case of an eosinophilic variant of ChRCC that contained tubulocystic features. Because ChRCC is associated with a different prognosis from those conditions which mimic it, accurate identification of this tumor has important clinical implications. Even if the cytological features of this eosinophilic variant of ChRCC are extremely similar to that of renal oncocytoma, we believe that the combination of careful evaluation of the architectural patterns, cytologic characteristics and special stain profile of adequately sampled tumor will be very helpful for its accurate identification. If needed, ultrastructural study will yield a definitive diagnosis. Likewise, the unique morphologic and architectural patterns will help to distinguish the eosinophilic variant of ChRCC from clear cell RCC with granular cells and tubulocystic carcinoma of the kidney. Further elucidation of the characteristic cytogenetic abnormalities will provide a foundation for molecular classification of the neoplasm.

Acknowledgement
The authors thank Dr. Peter Kragel for his advices and critical comments on the manuscript and Debra Laich for her expert help in electron microscopy.

Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

References
(1) Thoenes W, Storkel S, Rumpelt HJ. Human chromophobe cell renal carcinoma. Virchows Arch B Cell Pathol Incl Mol Pathol 1985;48(3):207-217.
(2) Przybycin CG, Cronin AM, Darvishian F, Gopalan A, Al-Ahmadie HA, Fine SW, et al. Chromophobe renal cell carcinoma: a clinicopathologic study of 203 tumors in 200 patients with primary resection at a single institution. Am J Surg Pathol 2011 Jul;35(7):962-970.
(3) Eble JN, Sauter G, Epstein JI, Sesterhenn IA. World Health Organization Classification of Tumours. Pathology and genetics of tumors of the urinary system and male genital organs. Lyon: IARC Press; 2004.
(4) Amin MB, Paner GP, Alvarado-Cabrero I, Young AN, Stricker HJ, Lyles RH, et al. Chromophobe renal cell carcinoma: histomorphologic characteristics and evaluation of conventional pathologic prognostic parameters in 145 cases. Am J Surg Pathol 2008 Dec;32(12):1822-1834.
(5) Truong LD, Shen SS. Immunohistochemical diagnosis of renal neoplasms. Arch Pathol Lab Med 2011 Jan;135(1):92-109.
(6) Ortmann M, Vierbuchen M, Fischer R. Sialylated glycoconjugates in chromophobe cell renal carcinoma compared with other renal cell tumors. Indication of its development from the collecting duct epithelium. Virchows Arch B Cell Pathol Incl Mol Pathol 1991;61(2):123-132.
(7) Tickoo SK, Lee MW, Eble JN, Amin M, Christopherson T, Zarbo RJ, et al. Ultrastructural observations on mitochondria and microvesicles in renal oncocytoma, chromophobe renal cell carcinoma, and eosinophilic variant of conventional (clear cell) renal cell carcinoma. Am J Surg Pathol 2000 Sep;24(9):1247-1256.
(8) Moreno SM, Benitez IA, Martinez Gonzalez MA. Ultrastructural studies in a series of 18 cases of chromophobe renal cell carcinoma. Ultrastruct Pathol 2005 Sep-Oct;29(5):377-387.
(9) Paner GP, Amin MB, Alvarado-Cabrero I, Young AN, Stricker HJ, Moch H, et al. A novel tumor grading scheme for chromophobe renal cell carcinoma: prognostic utility and comparison with Fuhrman nuclear grade. Am J Surg Pathol 2010 Sep;34(9):1233-1240.
(10) Erlandson RA, Shek TW, Reuter VE. Diagnostic significance of mitochondria in four types of renal epithelial neoplasms: an ultrastructural study of 60 tumors. Ultrastruct Pathol 1997 Sep-Oct;21(5):409-417.
(11) Manipadam MT, Korula A, Chandrasingh J, Devasia A. Chromophobe renal cell carcinoma: A report of two cases with unusual histological features. Indian J Urol 2008 Jan;24(1):123-125.
(12) Brunelli M, Eble JN, Zhang S, Martignoni G, Delahunt B, Cheng L. Eosinophilic and classic chromophobe renal cell carcinomas have similar frequent losses of multiple chromosomes from among chromosomes 1, 2, 6, 10, and 17, and this pattern of genetic abnormality is not present in renal oncocytoma. Mod Pathol 2005 Feb;18(2):161-169.
(13) Yusenko MV. Molecular pathology of chromophobe renal cell carcinoma: a review. Int J Urol 2010 Jul;17(7):592-600.
(14) Michal M, Hes O, Svec A, Ludvikova M. Pigmented microcystic chromophobe cell carcinoma: a unique variant of renal cell carcinoma. Ann Diagn Pathol 1998 Jun;2(3):149-153.
(15) Azoulay S, Vieillefond A, Paraf F, Pasquier D, Cussenot O, Callard P, et al. Tubulocystic carcinoma of the kidney: a new entity among renal tumors. Virchows Arch 2007 Nov;451(5):905-909.

Gross rz

Figure 1. The upper pole mass was homogeneously tan-pink in color with dark brown areas suggestive of old hemorrhage.

Fig2 rz

Figure 2. The majority of tumor cells were arranged in sheets or wide trabeculae. (hematoxylin and eosin, 100x)

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Figure 3. Adjacent to wide trabeculae, tumor cells show tubulocystic growth pattern. (hematoxylin and eosin, 100x)

Fig4 rz

Figure 4. The polygonal tumor cells have abundant granular eosinophilic cytoplasm with relatively welldefined cellular borders. There was mild to moderate nuclear pleomorphism, with occasional thin-rim perinuclear halo. (hematoxylin and eosin, 400x )

Fig5 rz

Figure 5. Selected photomicrographs of the renal mass with immunohistochemical and Hale’s colloidal iron stains are shown. (x100)

Fig6 rz

Figure 6. Ultrastructurally, the tumor cells show abundant microvesicles, admixed with mitochondria, distributed diffusely throughout the cytoplasm. Nuclei were rounded with irregular nuclear membranes and coarse chromatin.

Fig7 rz

Figure 7. The crowded microvesicles show smooth single membranes, measure 200 – 500 nm in diameter, and pack the spaces between mitochondria. A small number of lysosomes, lipid vacuoles and glycogen granules are also present.

Date added to bjui.org: 06/11/2012

DOI: 10.1002/BJUIw-2012-048-web

 

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