Atypical epithelial proliferations in acquired renal cystic disease harbor cytogenetic aberrations

Department of Pathology, Queen Elizabeth Hospital, Kowloon, Hong Kong, SAR China.
Human Pathlogy (Impact Factor: 2.77). 08/2002; 33(7):761-5. DOI: 10.1053/hupa.2002.125370
Source: PubMed


Acquired renal cystic disease (ARCD) complicating end-stage renal failure confers an increased risk for renal cell carcinoma, and atypical epithelial proliferation in the cysts may represent the precursor lesion. In this report we used an interphase cytogenetic technique to analyze the karyotypic features of various forms of atypical epithelial proliferations in a patient with ARCD. Both kidneys harbored numerous simple and atypical cysts. In addition, papillary tufts and a hitherto undescribed cribriform epithelial proliferation were found in the right kidney. The left kidney contained a 10-mm renal cell carcinoma with features indeterminate between clear cell and papillary types. There was gain of chromosome 7 in the papillary tufts; gain of chromosomes 7 and 17 in the cribriform lesion; gain of chromosomes 7, 12, 17, 20, and Y in the atypical cysts; and gain of chromosomes 7, 12, 17, and 20 in the renal cell carcinoma. These chromosomal aberrations suggest that atypical epithelial proliferations in ARCD represent early neoplastic lesions.

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    • "Renal cysts and ACKD are major risk factors for RCC in renal transplant recipients [6,14]. Nephron loss associated with renal insufficiency may promote hyperplasia of tubular epithelial cells, resulting in cyst formation, and atypical epithelial proliferation in the cyst may represent a precursor lesion to RCC [15]. In this study, all patients had renal cysts at the time they were diagnosed with RCC. "
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    ABSTRACT: BACKGROUNDAIMS: We investigated the incidence and clinical characteristics of renal cell carcinoma (RCC) in the native kidney of renal transplant recipients. Between 1991 and 2010, 1,425 patients underwent kidney transplantation at our institution. We retrospectively evaluated the clinical features and outcomes in renal transplant patients with RCC in the native kidney after renal transplantation. The patients included three males and two females with a mean age of 63 years (range, 52 to 74). The incidence of RCC was 0.35%. The median interval between renal transplantation and RCC occurrence was 16.2 years (range, 9 to 20). All of our patients with RCC had developed renal cysts either before (n = 3) or after (n = 2) renal transplantation. The mean duration of dialysis was 12 months (range, 2 to 39). Of the five patients, four underwent dialysis treatment for less than 8 months. All the RCCs were low grade at the time of diagnosis. Four patients underwent radical nephrectomy, and one patient refused the operation. The four patients who underwent radical nephrectomy showed no evidence of local recurrence or distant metastasis during the median follow-up of 2.9 years. However, the patient who did not undergo surgery developed spinal metastasis from the RCC 6 years later. This study suggests that the follow-up period is an important factor for the development of RCC in renal transplant recipients, and more vigorous screening with a longer follow-up period is required in renal transplant recipients.
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    ABSTRACT: The acquired cystic disease of the kidney-associated renal cell carcinoma (ACDK-RCC) in the current study occurred in a kidney with multiple cysts and was composed of cells with eosinophilic cytoplasm and prominent nucleoli. There were extensive calcium oxalate deposits in both non-neoplastic cysts and tumor. The tumor cells were positive for RCC Ma, CD10, and EMA, focally positive for CK7, negative for vimentin. Interphase in situ hybridizations (FISH) were performed for chromosome 1, 2, 7, 10, 13 and 17. No chromosomal abnormality was observed in the non-neoplastic cysts. Polysomies of chromosomes 1, 2, 7, 10, 13, 17 were observed in the tumor. Trisomy 13 was first reported in this type of tumor, which warranted further study.
    Open Journal of Pathology 01/2012; 02(01). DOI:10.4236/ojpathology.2012.21001
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