UNMODERATED POSTER SESSIONS
a nonobstructive response in the F⫹20 and an equivocal result in the F–15 were seen. One of them underwent surgical operation because of impaired kidney function during the follow-up and 1 was treated conservatively. Overall, obstruction was found in 16 out of 21 patients (76.2 %) by the F – 15 protocol , while it was found in 11 (52.4%) by the F⫹20 protocol (P ⫽ .01 ). The mean kidney spilt function was 55.15 % ⫾ 7.82 % and 54.81 % ⫾ 6.87% in F⫹ 20 and F–15 protocols, respectively (P ⫽ .45). Conclusion: Using the F–15 protocol may reduce the equivocal results of the F⫹20 for diuresis renography. POS-02.81 CT urography using the 64 multidetector CT scanner: correlation with cystoscopic and cytology findings Vriska T, Nehra A, King B, Aadland T, Nienow D Mayo Clinic College of Medicine, Rochester, MN, USA Introduction: At our institution, a 64channel CT urography (CTU) CT scanner was recently introduced. Sixty four-channel CT systems have been recognized to deliver improved spatial resolution over previous multichannel CT systems. Our objectives were to correlate the 64 multidetector CT urographic interpretations with cystoscopy and urine cytologies in 42 consecutive patients with a history of hematuria and/or prior history of TCC. Methods: Twenty six consecutive patients with a history of hematuria and/or history of TCC were scanned with a Sensation 64 multidetector CT scanner (Siemens Medical Solutions), designed to optimize urinary tract distention and 0.4-mm isotropic resolution. Precontrast renal images (3mm/2.8mm) were acquired, ureteral compression applied, and a dualheaded injector used for split-bolus technique and simultaneous acquisition of nephrographic/excretory phase abdominopelvic CT (3mm/2.8mm and 1mm/ 0.8mm reconstructions) immediately after ureteral decompression. CT-scanned-projection-radiographs with compression, without compression, and in the prone position were acquired. Results: Our initial series consisted of 42 consecutive patients. History of transitional cell cancer status post cystectomy and urinary diversion (n⫽12) and a diagnosis of hematuria (n⫽30) were evaluated urologically as well. Cystoscopic and cytology findings were then correlated to the original interpretation of the 64-chan-
256
nel CTU-CT scanner. A small papillary tumor was identified on the CT scanner which was subsequently confirmed cystoscopically. Cystoscopic correlation and cytologic correlation was consistent in all patients in our early and short series of patients. Conclusions: Our initial experience in patients diagnosed with hematuria and prior history of transitional cell cancer is presented. Further experience in this patient population may potentially identify urologic pathology in additional patients during their uroradiologic evaluation. POS-02.82 Laminin-5 immunochemistry identifies bellini ducts and bellini duct carcinoma Krah X1, Henkel B2, Hauschild E1, Eschholz G1, Kosmehl H2 1 Department of Urology, 2Institute of Pathology, HELIOS- Klinikum, Blankenhain, Germany Introduction: The basement membrane protein laminin forms a molecule family. The heterotrimic laminin-5 molecule consisting of an alpha3, beta3 and gamma2chain represents the characteristic laminin isoform of epithelial tissues and can be easily identified using antibodies to the gamma2-chain. The study investigates the laminin-5 expression in normal renal tubules, urothelium of the renal pelvis and their respective tumors. Methods: 5 routine samples of normal human kidney, renal pelvis, renal clear cell, papillary (chromophilic) or chromophobe carcinoma, oncocytoma and pelvic urothelial carcinoma as well as 3 cases of Bellini duct carcinoma were subjected to immunohistochemistry. Primary antibody: D4B5. Further primary antibodies for diagnostis: cytokeratin 19, cytokeratin 20, uroplakin, CD 10. Detection: ChemMate Kit, Autostainer. RT-PCR for gamma2-chain of Laminin-5. Results: In the normal kidney the basement membranes of the tubules were laminin-5 negative with exception of the terminal collecting ducts of Bellini or the basement membrane of the pelvic urothelial mucosa. Renal clear cell and chromophobe carcinomas or oncocytomas were laminin-5 negative. Some of the papillary (chromophilic) renal carcinomas were laminin-5 positiv in the basement membrane. A laminin-5 immunolabelling in the basement membrane and in the cytoplasma was observed in all cases of Bellini duct carcinoma as well as in papillary and invasive urothelial carcinoma of the renal pelvis. Bellini duct carcinoma was sepa-
rated from urothelial carcinoma using cytokeratin 20 and uroplakin. The Bellini duct carcinoma diagnosis was supported by cytokeratin19 immunostaing. Conclusion: The laminin-5-positivity of the Bellini ducts and Bellini duct carcinoma reflects the histogenetic origin from the endoderm. Therefore, laminin-5 immunuhistochemistry is recommended for the discrimination of Bellini duct carcinoma from the other renal cell carcinoma types. Moreover, laminin-5 is an invasion factor in many carcinoma types and may be related to the aggressive course of Bellini duct carcinoma.
Abstract Withdrawn
POS-02.84 Vasculogenic mimicry in renal cell carcinoma Barod R1,2, Tran MGB1, O’Brien TS2, Maxwell PH1 1 Renal Research Section, Imperial College, 2Department of Urology, Guy’s & St Thomas’ NHS Foundation Trust, London, UK Introduction: An abundant blood supply is essential for rapid tumour growth. In addition to conventional forms of angiogenesis, certain tumours have evolved mechanisms to enhance their blood supply. One of these mechanisms is vasculogenic mimicry (VM). In VM, de-differentiated tumour cells begin to behave like vascular endothelial cells and form tube like structures which allow extra blood flow and possibly confer a growth advantage to the tumour. Materials and Methods: We have assembled a series of tissue from 60 patients with renal cell carcinoma (RCC) along with clinical information. We performed immunohistochemistry for markers of endothelium (CD31, CD34), VM structures (VE cadherin), tumour cells & hypoxia (HIF-1␣, HIF-2␣) and proliferation (Ki67). Results: We demonstrate that vasculogenic mimicry occurs in RCC. Furthermore, we show evidence that this process is driven by local hypoxia and occurs in tumour cells with a high proliferation index. We postulate a molecular mechanism for its occurrence and relate this to clinical outcome in the patient. Conclusions: To our knowledge, this is the first description of vasculogenic mimicry in RCC. While it has a supplementary role to the conventional tumour blood supply, it may provide a conduit for the dissemination of tumour cells, leading to metastasis.
UROLOGY 70 (Supplment 3A), September 2007