Recipient-derived cells integrate into renal allografts inducing organ-specific microchimerism. Circulating pluripotent progenitor cells with high plasticity for differentiation were suggested as a potential source of allograft chimerism. Whether or not these cells also contribute to tumor formation in renal transplants is unknown. We analyzed six histologically different tumors in renal allografts for the presence of recipientderived cells. To circumvent dependency on gender mismatch, a polymerase chain reaction assay for highly polymorphic short tandem repeat marker (DNA fingerprinting) in combination with laser microdissection was applied. Pure tumor cell populations were harvested by laser microdissection after immunohistochemical (CD45/CD68) marking of contaminating leukocytes. In cases of gender mismatch (n ؍ 2), results were confirmed by sex chromosome in situ hybridization. Two metanephric adenomas demonstrated microchimerism comprising both donor-and recipient-derived tumor cells. Two clear cell carcinomas, one transitional cell carcinoma, and one renal cortical adenoma were all of donor origin without chimerism. We conclude that except for meta- Microchimerism after organ transplantation has been previously described. 1-9 Pluripotent bone marrow-derived recipient progenitor cells appear to be incorporated into the transplant. These stem cells display plasticity and can adopt various morphological and functional phenotypes in different types of allografts. Examples include renal tubular epithelial cells, endothelial cells, interstitial myofibroblast, hepatocytes, bile duct epithelial cells, cardiomyocytes, pneumocytes, and bronchial epithelial cells. [1][2][3][4][5][6][7][8][9][10][11] Chimerism in organ transplantation is not only generated by recipient-derived stem cells, but also can originate from a spread of graft cells beyond the transplanted organ. Mazal and colleagues 12 showed that donor-derived tubular epithelial cells from renal transplants are the source for nephrogenic adenomas arising in the urinary bladder of allograft recipients. Because neoplasms arise de novo in solid allografts, we investigated six tumors in renal transplants for the presence of recipient-derived cells. We combined laser-microdissection of pure tumor cell populations with genotyping (DNA fingerprinting). [5][6][7][8] This approach enabled analysis of all allografts independent of gender mismatch. In two cases, in which the recipient and donor were of different gender, we detected sex chromosomes by in situ hybridization to confirm short tandem repeat (STR)-polymerase chain reaction (PCR) results.
Materials and Methods
CasesSix tumors arising in renal allografts were investigated. Five neoplasms were retrieved from the archives of the Institute for Pathology of the Medical School, Hannover, Germany. One additional case came from the Pathology