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Urology | 2000

Outcome of surgery in cystic renal cell carcinoma.

Shigehiko Koga; Masaharu Nishikido; Tomayoshi Hayashi; Fukuzo Matsuya; Yutaka Saito; Hiroshi Kanetake

OBJECTIVES To review cases of cystic renal cell carcinoma treated surgically at our institution and define their clinical and histopathologic features. METHODS Between 1986 and 1998, 21 patients with cystic renal cell carcinoma were treated surgically. Cystic renal cell carcinoma was categorized using Hartmans classification. RESULTS Histopathologic examination demonstrated cystic necrosis in 11 patients, multilocular cystic renal cell carcinoma in 9, and unilocular cystic renal cell carcinoma in 1 patient. Tumors were incidentally found during an evaluation of unrelated disease or a general health checkup in 14 patients (67%). The mean tumor size was 5.6 cm (range 0.5 to 12) for cystic necrosis and 5.4 cm (range 2 to 9) for multilocular cystic renal cell carcinoma. All 9 cases of multilocular cystic renal cell carcinoma were of the clear cell type and tumor grade 1. The mean follow-up period was 65 months (range 9 to 141). The 5-year disease-specific survival rates for multilocular cystic renal cell carcinoma and cystic necrosis were 100% and 80%, respectively. CONCLUSIONS The prognosis for patients with cystic renal cell carcinoma is better than that for patients with solid tumors. In particular, the prognosis of multilocular cystic renal cell carcinoma is excellent. Multilocular cystic renal cell carcinoma represents a distinct subtype of renal cell carcinoma that can be completely cured by surgery.


Biochemical and Biophysical Research Communications | 1992

Gene expression and immunohistochemical localization of basic fibroblast growth factor in renal cell carcinoma

Jiro Eguchi; Koichiro Nomata; Shigeru Kanda; Tsukasa Igawa; Masakatsu Taide; Shigehiko Koga; Fukuzo Matsuya; Hiroshi Kanetake; Yutaka Saito

Renal cell carcinoma is known as a neoplastic condition of renal tubular cells and usually shows a hypervascular tumor in angiographic examination. We examined the presence of basic fibroblast growth factor (bFGF) in human renal cell carcinoma. To determine if alterations in bFGF gene expression are present in human renal cell carcinoma, paired samples of normal and neoplastic renal tissue from 6 patients were analyzed for bFGF mRNA content by Northern blot hybridization. In 4 out of 6 patients, tumor tissue expressed bFGF mRNA 2 to 4 times greater than corresponding normal tissue. Two patients showed minimal elevation of tumor bFGF mRNA. The localization of bFGF in the renal cell carcinoma tissue was also examined using immunohistochemical staining, and it was found that bFGF was positively stained at the nuclei of tumor cells and the cell surface. These results suggest that increased expression of bFGF may be associated with neoplastic growth in renal tubular epithelial cells and neovascularization.


Diabetes Care | 1991

Effects of Cyclosporin A and Low Dosages of Steroid on Posttransplantation Diabetes in Kidney Transplant Recipients

Hidefumi Yamamoto; Shoichi Akazawa; Yoshihiko Yamaguchi; Atsushi Yokota; Hironori Yamasaki; Toshiaki Nakanishi; Daigo Tahara; Fukuzo Matsuya; Yutaka Saito; Shigenobu Nagataki

Objective To investigate the adverse effects of cyclosporin A (CsA) on pancreatic beta-cell function in kidney transplant recipients. Research Design and Methods The study consisted of 73 patients without a history of diabetes mellitus who had undergone kidney transplantation in our clinic. Results We experienced a higher incidence of posttransplantation diabetes mellitus (PTDM) in patients receiving CsA and low dosages of methylprednisolone (6/20, 30%, P < 0.05) than in patients receiving conventional therapy of azathioprine methylprednisolone (4/53, 7.5%) since the introduction of CsA. In all 6 patients in the CsA-treated group, PTDM occurred within 3 mo after transplantation. The CsA level during the initial 3 mo posttransplant was significantly higher in diabetic than nondiabetic subjects, and the highest CsA level was observed shortly (1 mo) before the development of PTDM. After an average of 71 days of insulin therapy, there was complete remission of PTDM in 5 of 6 diabetic patients, with a corresponding decrease in CsA level. For the patients who were in remission for > 1 yr, a significant improvement of glucose intolerance was observed in association with a significantly higher insulin response to oral glucose load; however, their glycemic profile still showed a significantly higher plasma glucose concentration and a prolonged continuous elevation without initial peak of the insulin-response curve in contrast to the normal pattern found in nondiabetic subjects in the CsA-treated group. Conclusions This study suggests that CsA in combination with low dosages of steroid may have adverse effects on glucose metabolism, which may lead to effects similar to those in non-insulin-dependent diabetes mellitus.


Pathology International | 1997

Primary renal angiosarcoma: A case report and review of the literature

Nobuo Tsuda; Paritosh Roy Chowdhury; Tomayoshi Hayashi; Masanobu Anami; Masachika Iseki; Shigehiko Koga; Fukuzo Matsuya; Hiroshi Kanetake; Yutaka Saito; Yoshio Horita

Primary renal angiosarcoma is very rare. To our knowledge, only 15 cases have been reported to date. A 77‐year‐old Japanese man with a unilateral kidney presented with massive hematuria followed by renal failure. A renal tumor was suspected and a left nephrectomy was performed. The histopathological diagnosis was angiosarcoma of the kidney. A hemorrhagic tumor measuring 10 × 5 cm and clotted blood was found in the modularly area. The atypical tumor cells had a sinusoidal and solid appearance, and showed Immunohistochemically positive reactions for some of the endothelial markers. The patient died about 21 months after the nephrectomy and the autopsy revealed massive metastases to the liver and retroperitoneum. One of the differential diagnoses of the case was anglomyolipoma, because the tumor cells were relatively bland in their histological appearance with entrapped fat cells in the pelvic area. Fifteen case reports with titles that included the term ‘hemangiosarcoma/anglosarcoma’, ‘hemangioendothelloma/endothelloma’ or ‘vascular sarcoma’ of the kidney were reviewed and compared to the present case.


The Journal of Urology | 1993

Acute Hemorrhagic Cystitis Caused by Adenovirus Following Renal Transplantation: Review of the Literature

Shigehiko Koga; Kazuhiko Shindo; Fukuzo Matsuya; Tateo Hori; Shigeru Kanda; Hiroshi Kanetake

We report on 4 male patients with acute hemorrhagic cystitis caused by adenovirus following renal transplantation. These patients showed symptoms of gross hematuria, urinary frequency, burning urination and fever. Adenovirus was isolated in all patients and 3 were positive for serotype 11. Complement-fixing antibody was positive for adenovirus in all cases. Acute hemorrhagic cystitis caused by adenovirus was self-limiting and reduction of immunosuppression was not required for its resolution. Clinical presentation of these patients is described and the literature is reviewed.


International Journal of Urology | 2004

Erectile dysfunction in hemodialysis patients with diabetes mellitus: Association with age and hemoglobin A1c levels

Yasuyoshi Miyata; Kazuhiko Shindo; Fukuzo Matsuya; Mitsuru Noguchi; Masaharu Nishikido; Shigehiko Koga; Hiroshi Kanetake

Abstract  Aim:  Erectile dysfunction (ED) is common in patients with diabetes mellitus (DM) as well as those undergoing hemodialysis (HD). The purpose of this study is to investigate the frequency and severity of ED in HD patients with DM and those without DM. In addition, we examined the relationship between erectile function and several risk factors, including presence of DM and hemoglobin A1c levels in HD patients.


Urologia Internationalis | 1986

Acute hemorrhagic cystitis caused by adenovirus type 11 after renal transplantation.

Kazuhiko Shindo; Toshio Kitayama; Toshio Ura; Fukuzo Matsuya; Yasuyuki Kusaba; Hiroshi Kanetake; Yutaka Saito

A case of acute hemorrhagic cystitis caused by adenovirus type 11, which occurred in an allograft recipient 6 months after a living-related renal transplantation, is described. The patient lacked a neutralizing antibody to adenovirus type 11 before transplantation. Adenovirus type 11 was isolated from his urine and he developed a neutralizing and complement-fixing antibody to this virus. Although adenovirus type 11 isolates had been obtained from 2 of 18 renal allograft recipients, only 1 patient suffered acute hemorrhagic cystitis. Adenovirus type 11 may play a role in acute hemorrhagic cystitis in renal allograft recipients during immunosuppressive therapy.


BJUI | 2007

Cavernous nerve graft reconstruction using an autologous nerve guide to restore potency

Masaki Fujioka; Isao Tasaki; Riko Kitamura; Aya Yakabe; Mikio Hayashi; Fukuzo Matsuya; Taishi Miyaguchi; Junji Tsuruta

To present our experience of cavernous nerve graft reconstruction, using an autologous nerve vein‐guide technique, to restore potency.


International Urology and Nephrology | 1991

Multiloculated renal cell carcinoma.

Shigehiko Koga; A. Yamasaki; Masaharu Nishikido; R. Matsuo; Fukuzo Matsuya; Y. Yushita; Hiroshi Kanetake; Yutaka Saito

Multiloculated renal cell carcinoma and multilocular renal cyst with renal cell carcinoma are uncommon diseases. We report on 2 cases of multiloculated renal cell carcinoma. To our knowledge 16 cases of multiloculated renal cell carcinoma and multilocular renal cyst with renal cell carcinoma have been previously described in detail. The authors review the literature and discuss the aetiology and diagnosis of the disease.


Pathology International | 2011

De novo papillary renal cell carcinoma in an allograft kidney: Evidence of donor origin

Yuki Naruke; Masahiro Ito; Yumi Mihara; Yasushi Umezaki; Fukuzo Matsuya; Mikio Hayashi; Masahiro Nakashima; Shinji Khono

To the Editor: An increased incidence of primary malignancies has been recognized in transplant recipients. Renal cell carcinomas (RCC) represent 4.6% of all malignancies in renal transplant recipients, whereas RCC constitutes 2% of all cancers in the general population. According to the Cincinnati Transplant Tumor Registry, there are fewer instances of RCC that develop in the allograft kidneys (up to 10%), while nearly 90% of RCC in renal transplant recipients have been found in native kidneys. De novo RCC has been described as the opposite of pre-existing tumors before transplantation. Pathological characteristics of de novo RCC occurring in the allograft kidney have not been well described. Furthermore, genetic studies to determine the tumor origin, whether from the donor or the recipient, have been performed in only a few reported RCC cases, although it is clinically important considering the association of tumor transmission. We report a case of de novo papillary RCC developing in an allograft kidney diagnosed 13 years after renal transplantation, and which was genetically confirmed to be of donor origin. A 49-year-old Japanese male presented with end-stage renal disease secondary to chronic glomerulonephritis of unknown etiology when he was at the age of 25. The patient had no family history of renal disease. After 5 years of hemodialysis, he underwent renal transplantation at the age of 29 from a deceased donor. The donor was a 37-year-old Japanese male who died of cerebral hemorrhage. The donor had no significant medical illness in his family history or past history according to medical records. Immunosuppressive therapy was maintained with methylprednisolone, cyclosporine and mizoribine. The patient presented with an episode of chronic rejection that successfully treated by steroids 7 years after transplantation. At that point, ultrasonography showed no evidence of a solid or cystic lesion in the allograft kidney. Graft function had been stable with serum creatine level of 1.1 to 1.3 mg/dL, although the patient exhibited 30 mg/dL of proteinuria on rare occasions. However, 13 years after transplantation, ultrasonography revealed a 2.3 cm solitary cystic lesion in the lower pole of the allograft kidney. During the following 7 years, the cyst had increased in size to 4.0 cm with slight blood flow inside, which led to suspicion of malignancy. There was no other cystic lesion in the allograft kidney or native kidneys. An extensive workup ruled out any primary or metastatic lesion. The patient underwent a partial nephrectomy of the allograft kidney in 2010, 20 years after transplantation. No recurrence has been found on most recent evaluation. Graft function has resumed and the patient has maintained dialysis-free status. The contralateral kidney of this particular donor, which had been transplanted to a Japanese female and resected 12 years after transplantation due to chronic rejection, presented no solid or cystic lesion. In the resected specimen, a well-circumscribed tumor was located in the renal cortex. The tumor measured 4.0 ¥ 3.5 ¥ 3.5 cm in size. The cut surface was solid and yellowish-white with tiny hemorrhages. No necrosis was noted. Histologically, a unilocular cyst was densely filled with small cuboidal cells with scanty basophilic cytoplasm. The cuboidal cells also lined the cyst wall (Fig. 1a). The tumor cells formed papillae and tubules, arranged in a single layer on the basement membrane. The nuclei were small, uniform and had hyperchromatic chromatin with a finely granular pattern. The papillary cores frequently contained aggregates of foamy macrophages and hemosiderin laden macrophages. Kidney parenchyma around the tumor showed mild interstitial fibrosis and slight tubular atrophy. Formalin-fixed paraffinembedded tissue sections were immunohistochemically stained. The antibodies used were vimentin (DAKO, Glostrup, Denmark, monoclonal, clone V9, dilution 1:100), high molecular weight cytokeratin (DAKO, monoclonal, clone 34bE12, dilution 1:100), cytokeratin 7 (DAKO, monoclonal, clone OV-TL12/30, dilution 1:100), CD10 (DAKO, monoclonal, clone SS2/36, dilution 1:100), and alpha-methylacylcoenzyme A racemase (AMACR) (DAKO, monoclonal, clone 13H4, dilution 1:100). Prostate tissue and the allograft kidney parenchyma around the tumor were used as positive control. The tumor cells were positive for vimentin, cytokeratin 7 (Fig. 1b), CD10 and AMACR, but negative for high molecular weight cytokeratin (Fig. 1c). Pathological diagnosis was papillary RCC type 1, Fuhrman’s nuclear grade 2, and stage pT1aN0M0. Comparative microsatellite analysis was performed to detect tumor origin according to a previously described method. Recipient peripheral blood and paraffinembedded tissue from the tumor and the allograft kidney parenchyma (donor tissue) were used. In total, 15 short tandem repeat (STR) markers were compared for microsatellite analysis. All of the analyzed STR markers were detected and the predominant DNA patterns of the tumor matched those of the donor, confirming that the tumor was of donor origin (Fig. 1d). The present case provides some insights into the nature of de novo RCC developing in an allograft kidney. First, the present case of RCC was confirmed to be of donor origin by microsatellite analysis on genomic DNA. It is of clinical Pathology International 2011; 61: 694–696 doi:10.1111/j.1440-1827.2011.02714.x

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