The histological composition of RCCs varied according to the size of the tumor. Sarcomatous components increased with tumor size and were independently associated with a poor prognosis. Further study is warranted to correlate specific genetic alterations with tumor growth-related histological changes in RCCs.

A 76-year-old diabetic woman was referred to our hospital with an episode of high fever and sub-abdominal pain. Computed tomography (CT) of the pelvis revealed gas accumulation within the lumen and wall of the bladder and CT of the abdomen demonstrated bubbles in the inferior vena cava. She recovered by urinary drainage and antibiotic therapy. Urinary culture revealed Escherichia coli. CT after the therapy didn't demonstrate gas accumulation of the bladder and bubbles in the inferior vena cava. Emphysematous urinary tract infections (UTIs) have the high fatality rate, it seems to be a possibility that venous bubbles with emphysematous UTIs contribute to the high fatality rate such as air embolisms. It was suspected that bacterial injury of the bladder wall and high vesical pressure caused by urinary outlet obstruction such as neurogenic bladder lead gas translocation into the venous system. Six previous cases of emphysematous UTIs (three emphysematous cystitis cases and three emphysematous pyelonephritis cases) with venous bubbles have been reported to this day. Our case is seems to be the fourth case report that venous bubbles with emphysematous cystitis was demonstrated.

No abstract

Background: Disease progression after Bacillus Calmette-Guerin (BCG) instillation therapy for bladder cancer is not rare. The purpose of this study was to evaluate the outcome of patients treated with BCG for superficial bladder cancer, focusing on the patients who developed invasive disease during followup. The possible mechanism and risk factors for early progression after BCG therapy are discussed. Methods: A total of 25 patients with superficial bladder cancer (pTa, pTl, and/or pTis) were treated with intravesical BCG instillation (80 mg in 80 mL saline) once a week for eight weeks. Four of the 25 patients received maintenance therapy with BCG (once a month for 3 to 10 months). Patients were followed every three months and underwent cystoscopy, biopsy, and urinary cytology at these intervals. Disease progression was defined as invasion to muscle or prostate, or development of metastatic disease. Clinicopathological features of the patients, especially those with progression, were analyzed. Results: Progression was observed in six of the 25 patients (including four of 19 patients with carcinoma in situ and two of five patients treated prophylactically with BCG). The average time to progression was 8.7 months. Four patients died of cancer despite intensive treatment. Two patients are alive: one without evidence of disease after cystectomy and the other with metastatic disease. Conclusions: Proper patient selection, careful follow-up, and immediate aggressive therapy in case of progression were considered to be important factors to obtain satisfactory results with BCG therapy for bladder cancer.

No abstract