The value of histopathological and immunohistochemical findings in the differential diagnosis of kidney tumors with papillary morphology

Renal cell carcinoma (RCC) is the most aggresive group in urogenital system tumours. RCC compromises 90% of renal tumours and 2-3% of carcinomas. RCC originates from renal tubule epitehelial cells. With technological advances, molecular studies have gained momentum and have led to the identification of new entities in renal tumors as well as in many tumors. In this regard, especially in renal tumors with tubulopapillary architecture, there has been much progress. The new entities proposed by the International Society of Urological Pathology (ISUP) meeting in Vancouver in 2012 were included in the World Health Organization (WHO) classification of kidney tumors published in 2016. In the current classification, clear cell papillary RCC with tubulopapillary morphology, RCC with MIT family translocation, RCC with succinate dehydrogenesis deficiency, RCC with hereditary leiomyomatosis, and tubulocystic carcinoma have been identified. Since renal tumors with tubulopapillary architecture are different in treatment response and prognosis, classification of these tumors is important in order to apply targeted treatment options. The aim of this study is to investigate the relationship between clinical, histopathological, immunohistochemical findings and newly defined entities in renal cell carcinomas with tubulopapillary morphology. 91 patients who were diagnosed as papillary adenoma, papillary renal cell carcinoma (PRCC) and renal cell carcinoma with tubulopapillary architecture that mentioned in the pathology report between 2012 and 2016 were reviewed in terms of histopathological features. evaluated with clinical findings. Seventeen cases were diagnosed with TFE-3 translocation carcinoma, 2 cases with clear cell PRCC, one case with papillary adenoma and one case with type 2 PRCC. The remaining 10 cases were diagnosed as typical papillary RCC in the original report, but were reassessed into the atypical PRCC group that could not be further classified. Eighteen cases (19.8%) were diagnosed as adenoma, 22 cases (24.2%) were type 1 PRCC, 27 cases (29.7%) were type 2 PRCC and 24 cases (26.4%) were atypical. According to morphological and immunohistochemical (IHC) findings, 24 cases in the atypical PRCC group were; 8 cases (25%) had clear cell papillary RCC, 4 cases had tranlocation carcinoma [three of them were TFE-3 (12.5%), one of them was TFE-B (3.1%)] and the remaining 12 cases (50%) were unclassified atypical PRCC. The mean age of the cases was 56.6 years. Atypical RCCs were more common in women. Seven (63.6%) of 11 advanced stage cases and 3 (100%) grade IV patients were in the atypical PBC group. Grade II was more common in type 1 papillary RCC and grade III was more common in type 2 papillary RCC. In the whole group, high-grade tumors were observed more frequently in atypical PRCCs (p = 0.35). Pseudocapsule is seen in 80% of typical PRCCs, while 80% of atypical PRCCs are unencapsulated. Clear cell differentiation is more common in atypical PRCCs (62%). This group consists of clear PRCC and translocation carcinoma cases. Histiocyte infiltration was more common in type 2 PRCCs and psammoma type calcification type 1 papillary RCCs (p> 0.05). Necrosis and cholesterol cleavages were higher in type 2 papillary RCC (p> 0.05). 38 (52%) of the cases had pure papillary pattern. Although solid-papillary pattern was more common in typical PRCC cases and tubular pattern in atypical PRCC cases, it was not statistically significant (p = 0.43). In papillary RCC cases; CK7 was positive in 84.6%, AMACR was positive in 94.3% and Ca9 was negative in 65.4%. Eight of the cases (33.3%) had clear PRCC morphology, positive for CA9 and CK7 in all, 57% for CD10 and 33% for AMACR. Three of the patients were diagnosed with Xp11 translocation carcinoma with TFE3 positivity and one with HMB45 and Melan A positivity with t (6,11) translocation carcinoma. In type 1 and type 2 PRCC's; It was concluded that differential diagnosis can be made by morphological and IHC findings, but it is not possible to make differential diagnosis of atypical PRCC tumors under routine laboratory conditions and it is concluded that IHC's or molecular methods should be applied for these tumors.