Distal tubular hyperplasia: A novel form of renal tubular proliferation distinct from papillary adenoma

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Conference Proceeding

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Modern Pathology


Background: Papillary adenoma is the only established incipient or preneoplastic lesion in the current classification of renal cell neoplasms. However, we have occasionally encountered a more diffuse proliferation in the setting of chronic renal disease that appears different from papillary adenoma, warranting further study.

Design: Renal specimens showing an unusual proliferation of tubules were retrieved from the authors' archives and studied for clinical and pathologic parameters and immunohistochemical profile. A series of end-stage renal disease specimens from one of the institutions was retrospectively reviewed to establish incidence.

Results: In total, 12 specimens were retrieved showing this tubular proliferation diffusely (n=7) or focally (n=5). Eight were identified from a series of 177 end-stage renal disease specimens from one institution (5%), of which 5 were focal (3%) and 3 diffuse (2%). Eight patients had concurrent renal cell tumors including clear cell (n=4), papillary (n=3), clear cell papillary (n=1), or acquired cystic kidney disease (n=1) renal cell carcinoma (and papillary adenomas, n=5). Four occurred with no neoplasm. All patients had end-stage renal disease, 1 being an explanted allograft; however, there was no definite commonality to the patients' renal disease. In most (n=9), the predominant pattern was indentation of chronic inflammation into renal tubules forming small polypoid structures (Figure A); however, 3 patients had predominantly hyperplastic epithelium with less conspicuous inflammation in the cores (Figure B). In 7 patients both patterns were appreciable at least focally, whereas the remainder (with focal, minimal lesions) had only the inflammatory pattern. Immunohistochemistry was consistently positive for cytokeratin 7, high molecular weight cytokeratin (sometimes weak), and GATA3. Staining for alpha-methylacyl-CoA racemase (AMACR) was negative or weak, dramatically less intense than that of papillary neoplasms or proximal tubules. CD3 and CD20 showed a mixture of B and T lymphocytes in the inflammatory areas.

Conclusions: We describe a novel form of renal tubular proliferation that differs from papillary adenoma in that it shows weak or negative AMACR immunoreaction and in some cases is widely dispersed in sampled renal parenchyma. Based on consistent staining for high molecular weight cytokeratin and GATA3, this appears to be a proliferation of distal tubules, with both inflammatory and hyperplastic patterns.





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