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The in vitro antibacterial activity of cefmetazole sodium on four kinds of clinically isolated bacterial species was determined, and the clinical effect of the drug in 20 cases of postoperative or chroniccomplicated urinary tract infection was studied. l) The maximum sensitivity distribution rate was under 1.56 µg/ml of MIC either on 10[6]cells/ml or 10[8]cells/ml of inoculum size in 25 strains of E. coli, 25 strains of Klebsiella pneumoniae, 25 strains of Genus proteus and 20 strains of Staphylococcus aureus. This indicates that the antibacterial activity of cefmetazole sodium was little influenced by the inoculum size of any of the bacterial species. 2) The patients were 13 males and 7 females with a mean age of 56.7 years. The cause of urinary tract infection was urological tumors in 6 cases, urolithiasis in 4 cases, neurogenic bladder in 3 cases, trauma in 2 cases, inflammation in 2 cases and others in 3 cases. Various operations were performed on 15 patients, and the other 5 patients were not operated on. Catheters were inserted into the urethra or renal pelvis, or ureterocutaneostomy was done in 13 cases; 7 patients did not have catheters inserted. 3) Two to 4 g of cefmetazo1e sodium per day was administered intravenously. The mean duration of chemotherapy was 9.3 days and mean total dose of administration was 25.5 g. 4) The clinical effect of the drug was judged good, unchanged or poor chiefly based on the change of urinalyses. Depending on these criteria, 4 cases which were determined unchanged, were finally judged good as all of them had had catheters inserted. Overall results were good in 12 cases and poor in 8 cases. Effective rate, therefore, was 60%. 5) Comparison of the effectiveness of the drug for the patients who had had catheters inserted to those who had not, showed that the administration of cefmetazo1e sodium was also effective in treating chronic urinary tract infection even when catheters were used. A good effect was seen in 6 of the 7 cases (86%) in which catheters were not used, and in 6 of the 13 cases (46%) in which catheters were used.

Two cases of neurogenic bladder with pituitary adenoma are reported. The pituitary adenomas produced excessive GH (growth hormone). The etiology of the neurogenic bladder was not identified by X-ray examination or any other tests. Urodynamic study, however, indicated a functional cause of neurogenic bladder. Case 1 was a 55-year-old male, who had a relatively small pituitary adenoma with mild symptoms. Urologically, there was complete urinary retention. Cystometrogram showed a flaccid pattern, detrusor-sphincter dyssynergia in sphincter-EMG and ice water test was negative. Case 2 was a 67-year-old female, who had a large pituitary adenoma and severe symptoms. Cystometrogram showed an almost normal pattern, however, there was detrusor-sphincter dyssynergia and ice water test was negative. We suggested that the neuropeptide takes some part in the pathophysiologic cause of neurogenic bladder.

A 56-year-old woman in chronic hemodialysis had been suffering from uncontrollable fever for the past 7 months. Her original disease was diagnosed as familial polycystic kidney and three of her five brothers were found to have the same disease. Her chromosome was 46, XX, 21P+ and laboratory examination revealed severe anemia, malnutrition, liver dysfunction, pyuria and candidiasis of urine. Abdominal echogram and CT scan revealed polycystic kidneys and multiple liver cysts. She was admitted to our hospital and was diagnosed as having pyelonephritis of the right kidney. As her condition was not improved by conservative therapy right nephrectomy was performed. One month later, spiking fever and left tenderness reappeared. Those symptoms could not be controlled by conservative therapy and left nephrectomy was performed again. Pathological examination on nephrectomized kidneys showed interstitial nephritis, hyaline degeneration and proliferative change of glomeruli, microabscess, colloid of tubules and calcification of parts of Henle's loops. Nephrectomy has been performed in 1.6 to 10.0% of polycystic kidneys due to references since 1952. Eight of the 22 polycystic kidneys (36.3%) seen at our hospital during the past 10 years have been removed.