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We report here our 10-year experience of a biopsy performed at day 14 after transplantation in 304 patients with stable graft function. The factors that may have influenced subclinical rejection were analyzed according to histology. The incidence of subclinical rejection was 13.2%. Addition of mycophenolate mofetile (MMF) as a primary immunosuppressant significantly decreased the incidence of subclinical rejection compared with patients without such treatment (odds ratio, 0.23; p < 0.05). On the other hand, HLA-DR antigen mismatch (odds ratio, 2.39) and unrelated donor (odds ratio, 2.10) were also significantly associated with decreased subclinical rejection (p < 0.05). The incidence of acute rejection in patients with normal findings was lower than in those with borderline changes or subclinical rejection (0.23 ± 0.05 vs. 0.48 ± 0.07 and 0.60 ± 0.11, respectively; p < 0.05). The graft survival rates in patients with subclinical rejection were lower than in patients with normal or borderline changes at 1 (88.4% vs. 97.9% and 99.1%; p < 0.05), 5 (77.8% vs. 96.2% and 95.9%; p < 0.05) and 10 (62.3% vs. 96.2% and 93.7%; p < 0.05) years. Thus, a protocol biopsy performed on day 14 after transplantation is useful for predicting graft survival. Triple therapy including MMF, related donor and HLA-DR antigen match are important factors for reducing subclinical rejection in living-donor renal transplantation.

In this report, we summarized the clinicopathologic features of 9 cases of plasmacytoid transitional cell carcinoma (TCC) of the urinary bladder, a rare variant of TCC. All 9 patients were men with a mean of age 64.3 years (range, 46 to 81 y). All but 1 patient presented with gross hematuria; the remaining patient had urgency and microscopic hematuria. Cystoscopic findings revealed a dominant solid mass with surrounding multiple papillary lesions in 6 cases and multiple masslike lesions in 3 other cases. The initial diagnosis of plasmacytoid TCC was made on transurethral resection in 8 cases and cystoscopic biopsy in 1. One patient had TNM stage I disease, 2 had stage II disease, 3 had stage III disease, and 3 had stage IV disease. Four patients were treated by radical cystectomy with chemotherapy, 2 by radical cystectomy alone, 1 each by chemotherapy or intravesical bacillus Calmette-Guerin infusion alone, and 1 did not receive any further therapy. Microscopically, all tumors contained plasmacytoid cells, which composed 30% to 100% of the entire tumor. Eight of 9 cases were associated with high-grade TCC, and transitional cell carcinoma in situ was present in 4 cases. The plasmacytoid tumor cells were characterized by eccentrically located nuclei and abundant eosinophilic cytoplasm. Interestingly, plasmacytoid transitional cell carcinoma in situ was noted in 1 case. Immunohistochemical staining demonstrated that both plasmacytoid and conventional TCC components were positive for cytokeratins 7 and 20. The mean Ki-67 labeling index was 30% (range, 10% to 50%), and p53 expression in the majority of cases was low (5% to 10%), except for in 2 cases (70% and 80%). The mean follow-up in 8 patients was 24.5 months (range, 5 to 47 mo); the other patient was lost to follow-up. Five patients died of disease from 5 to 36 months, 2 patients were alive with disease at 30 and 47 months, and 1 patient was alive and well at 36 months with no evidence of disease. In summary, plasmacytoid TCC tends to present at an advanced stage and to have a poor prognosis. Morphologic recognition and distinction from other plasmacytoid malignant neoplasms is critical for its clinical management and immunohistochemical studies may be required for differential diagnosis.

Cystic renal neoplasms represent an isolated cystic mass not accompanied by cystic change of the renal parenchyma. Although cystic change may be seen in any type of renal neoplasm, a few (i.e., cystic renal cell carcinoma, cystic nephroma, cystic partially differentiated nephroblastoma, mixed epithelial and stromal tumor) are characterized by constant cystic change that may involve the entire tumor. Cystic kidney disease is characterized by cystic change, which usually involves the kidneys in a bilateral and diffuse pattern, does not create a discreet mass, and is due to hereditary or developmental conditions. Some of the cystic kidney diseases are not known to give rise to renal neoplasm; others such as autosomal polycystic kidney disease or multicystic dysplastic kidney may fortuitously coexist with renal neoplasms. Three conditions (acquired cystic kidney disease, tuberous sclerosis, and von Hippel-Lindau disease) are associated with renal neoplasms with such a high frequency that they are considered preneoplastic. This article reviews the differential diagnoses among cystic neoplasms. It also focuses on the underlying genetic and molecular mechanisms for the relationship between cystic renal diseases and renal neoplasms.