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We determined the impact of the extent of regional lymphadenectomy on survival in patients with urothelial carcinoma of the upper urinary tract.Between January 1989 and January 2006, 169 patients with nonmetastatic urothelial carcinoma of the upper urinary tract underwent curative surgery. We previously reported the primary sites of nodal metastases in urothelial carcinoma of the upper urinary tract. Nodal sites where the incidence of metastases was 30% or more were considered regional lymph nodes. When all primary sites were resected, this was considered complete lymphadenectomy. Regional lymphadenectomy without the removal of all primary sites was considered incomplete lymphadenectomy. We retrospectively analyzed the influence of the extent of lymphadenectomy on patient survival.A total of 45 patients (26.6%) underwent complete lymphadenectomy. Lymphadenectomy was performed in an additional 36 patients (21.3%) but it was incomplete. Lymphadenectomy was not performed in 88 patients. Cancer specific survival did not significantly differ between the groups when all patients were analyzed. However, patient survival significantly depended on the extent of lymphadenectomy when we focused on patients with T stage pT3 or higher. Patient survival was likely to improve when the number of lymph nodes removed increased. Multivariate analysis showed that complete lymphadenectomy was a significant prognostic factor for cancer specific survival (p = 0.009) as well as T stage (pT3 or less p = 0.0004) and tumor grade (G3 p = 0.0001).Although further investigation is required to make a definite conclusion, the extent of lymphadenectomy may significantly influence its therapeutic effect, especially for patients with advanced disease.

To our knowledge the influence of sex hormones on urinary stone formation remains undetermined. We investigated the effect of castration on urinary lithogenic factors and renal osteopontin expression in rats previously treated with ethylene glycol.Sprague-Dawley rats were divided normal males, castrated males, males with 2 weeks of 0.75% ethylene glycol treatment, castrated males with 2 weeks of 0.75% ethylene glycol treatment, normal females, castrated females, females with 2 weeks of 0.75% ethylene glycol treatment and castrated females with 2 weeks of 0.75% ethylene glycol treatment. We analyzed 24-hour urine samples for urinary constituents, such as calcium, oxalate, citrate, uric acid, phosphate, magnesium, sodium, potassium and creatinine. The kidneys were examined for osteopontin expression by Northern blot analysis and for crystal deposition by histological examination.In intact male rats calcium and citrate excretion decreased and oxalate excretion increased significantly after ethylene glycol treatment. Castrated male rats with ethylene glycol had greater calcium and less oxalate excretion than male intact rats with ethylene glycol. In intact female rats uric acid excretion decreased and only calcium excretion increased significantly after ethylene glycol treatment. Castrated female rats with ethylene glycol excreted significantly more oxalate and less calcium than intact female rats with ethylene glycol. Renal osteopontin expression was the same in male intact and castrated rats, and in female intact and castrated rats. In males with ethylene glycol expression was stronger in castrated than in intact rats. In females with ethylene glycol expression was weaker in castrated than in intact rats. No crystal deposits were found in the kidneys in any group.Testosterone appears to promote stone formation by suppressing osteopontin expression in the kidneys and increasing urinary oxalate excretion. Estrogen appears to inhibit stone formation by increasing osteopontin expression in the kidneys and decreasing urinary oxalate excretion.

We evaluate the efficacy of a new technique of minimally invasive treatment for benign prostatic hyperplasia involving direct injection of dehydrated ethanol.Dehydrated ethanol was injected transurethrally with lumbar or sacral and urethral anesthesia in 10 patients with prostatic hyperplasia. Endoscopic injection was performed at 4 to 8 sites in the prostate and 3.5 to 12.0 ml. ethanol were used.There were no intraoperative complications but postoperative urinary retention occurred transiently in all patients which required catheterization for a mean of 8.8 days. Mean symptom score plus or minus standard deviation was 12.2+/-5.8 at 3 months postoperatively, which was significantly improved from 23.1+/-7.0 preoperatively (p0.01). Mean quality of life score also improved significantly from 5.1+/-0.6 preoperatively to 3.2+/-1.5 at 3 months postoperatively (p0.01), mean peak urinary flow rate increased from 8.0+/-2.2 (9 patients) to 13.1+/-3.6 ml. per second (p0.05) and mean residual urine volume decreased from 129.1+/-55.3 (9 patients) to 49.3+/-34.7 ml. (p0.05). There was no significant change in prostate volume. Acute epididymitis and chronic prostatitis occurred in 1 patient each.This technique can be performed as an outpatient procedure and appears to be safe and cost-effective. Retrograde ejaculation can be avoided.

To investigate the role of basic fibroblast growth factor (FGF) in renal cell carcinoma growth, we have analyzed the expression of mRNA of basic FGF. In 7 of 15 cases, basic FGF mRNA level in renal cell carcinoma tissues was higher than that in corresponding normal tissues. However, the tumor-to-normal ratios of expression levels are chiefly less than 2.0 and, in 5 cases, are even less than 1.0. Furthermore, there was no correlation between the ratio and the clinical stage. In protein analysis, we could not find any difference between basic FGF extracted from renal cell carcinomas and that from normal kidney tissues in bioactivity, immunoreactivity, molecular weight and affinity to heparin. On the other hand, anti-basic FGF monoclonal antibody inhibited the growth of a renal cell carcinoma cell line, VMRC-RCW, and this inhibition was reversed by an extraphysiological amount of exogenous basic FGF (100 ng./ml.). These results suggest that basic FGF itself may have no pivotal role in renal cell carcinoma etiology but is involved in the growth of renal cell carcinomas in an autocrine manner.