Nephrogenic adenoma in renal transplant recipients: a truly benign lesion?

• Published in: Urology (Ridgewood, N.J.) Vol. 52; no. 5; pp. 756 - 761
• Main Authors: Pycha, Armin, Mian, Christine, Reiter, Werner J, Brössner, Clemens, Haitel, Andrea, Wiener, Helene, Maier, Ulrich, Marberger, Michael
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.11.1998; Elsevier Science
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Biological and medical sciences; Child; Chromosomes - genetics; Diagnosis, Differential; DNA - analysis; Female; Genes, p53 - genetics; Humans; Ki-67 Antigen - genetics; Kidney Transplantation - adverse effects; Male; Medical sciences; Metaplasia - etiology; Middle Aged; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Surgery of the urinary system; Urinary Bladder - chemistry; Urinary Bladder - pathology; Urinary Bladder Neoplasms - chemistry; Urinary Bladder Neoplasms - etiology; Urinary Bladder Neoplasms - pathology; Kidney disease; Human; Postoperative; Urinary system disease; Exploration; Transplantation; Adenoma; Urinary tract; Homotransplantation; Kidney; Metaplasia; Treatment; Surgery; Renal failure; Complication; Benign neoplasm
• ISSN: 0090-4295; 1527-9995
• DOI: 10.1016/S0090-4295(98)00371-9

Objectives. Nephrogenic adenoma is a benign metaplastic lesion of the urinary bladder, reported to occur as a response to inflammation, trauma, intravesical therapies, and after renal transplantation. The aim of this study was to evaluate on the basis of chromosomal analysis whether nephrogenic adenoma really is benign. Methods. Twelve renal transplant recipients with histologically verified nephrogenic adenoma were analyzed for numerical aberrations of chromosomes 7, 9, and 17. Results were related to total DNA content, p53 and Ki-67 positivity, and clinical outcome. Ten patients with superficial bladder cancer and 10 healthy renal transplant recipients formed the control groups. Results. All 12 patients with nephrogenic adenoma had monosomy 9 in a mean of 24.3% (range 20% to 30%) of the evaluated cells; 3 patients had an additional trisomy 7 in a mean of 8% (range 6% to 10%) of the counted cells. Chromosome 17 was disomic in all patients. DNA histograms were diploid in 11 of the 12 patients and aneuploid in 1 patient. No p53 and Ki-67 positivity was present in this group. All patients with superficial bladder cancer had monosomy 9 in a mean of 79.8% (range 75% to 85%) of the counted cells. Two patients were found to have an additional trisomy 7 in 50% and 65% of the cells, respectively. The latter had an aneuploid histogram; the others had haploid/diploid histograms. p53 was negative in all specimens. Ki-67 positivity was present in 70% of these patients. All healthy transplant recipients had disomic chromosomal patterns according to diploid DNA histograms and negative immunocytochemical results. Conclusions. Even if in a lower percentage of cells, aberrations of chromosome 7 and 9 were detected in nephrogenic adenoma. It therefore cannot be excluded that nephrogenic adenomas in immunosuppressed renal transplant recipients may develop into malignant lesions.