Acute focal bacterial nephritis (AFBN) is a localized bacterial infection of the kidney presenting as an inflammatory mass without frank abscess formation, which may represent a relatively early stage of renal abscess. The pathogenesis of AFBN is thought to be hematogenous infection or ascending infection from the lower urinary tract. For the majority of children, the pathogenesis may be related to ascending infection, because pre-existing malformative uropathy, especially vesicoureteral reflux (VUR), is common in pediatric patients. Few clinical reports have demonstrated the evolution of this condition into renal abscess in children. We report a girl with AFBN associated with VUR that evolved into a renal abscess despite appropriate intravenous antibiotic therapy. We undertook serial radiological observation of its evolution. It is important to differentiate AFBN from renal abscess because the management of the two entities may be different, and follow-up studies are indispensable to determine appropriate therapy.
Bacterial and crystal adherence to the surfaces of indwelling urethral catheters was investigated by scanning electron microscopy and immunofluorescence method in relation to microbiological examination. Gram-negative bacteria were isolated more frequently than gram-positive bacteria in urine and catheter cultures. Microorganisms and crystals frequently were associated with fibrillar material, some of which was considered to be fibrin. On the surfaces of catheters indwelling for more than 1 week bacteria often were embedded in an amorphous matrix. It was believed that the thick coherent matrix adherent to the catheter served as a protected reservoir of microorganisms that persisted despite antimicrobial chemotherapy. Additionally, urease-producing bacteria attached to the catheter could have an important role in the development of calculous incrustation.
The pharmacokinetics of cefimetazole, a new cephamycin antibiotic, were examined after a 1-h intravenous drip infusion of 1 g to 5 healthy volunteers with normal renal function and 16 Group 1 was composed of five healthy volunteers with creatinine clearances of 95.6 to 155.6 ml/min. Group 2 was composed of four patients with creatinine clearances of 65.5 to 86.8 ml/min. In group 3 were four patients with creatinine clearances of 35.2 to 52.7 ml/ min. Group 4 had four patients with creatinine clearances of 10.2 to 24.8 ml/min. Group 5 was composed of four patients with creatinine clearances of 0 to 9.7 ml/min. Two patients in this group were being treated by hemodialysis twice weekly over 6 to 8 h.All of the subjects were given 1 g of cefmetazole dissolved in 200 ml of 5% dextrose-water. The drug was administered intravenously by drip infusion over a 1-h period. Blood samples were obtained just before infusion and 1, 2, 4, and 6 h after beginning the infusion. Urine specimens were collected from 0 to 2, 2 to 4, and 4 to 6 h. Because only two patients in group 5 were treated by periodic hemodialysis, they were studied between two dialysis sessions.Serum and urine samples were stored at -20°C until assayed. The concentrations of cefinetazole in serum and urine were determined by the thin cupplate method, with Micrococcus luteus ATCC 9341 as the test organism and heart infusion agar as the medium. For the measurement of serum concentrations, a standard solution series was prepared in pooled normal human serum. The assay range was from 200 to 7.8 itg/ml. For the measurement of urinary concentrations, the standard solution series of 20 to 1.25 ,ug/ ml was prepared with 1% phosphate buffer (pH 6.0). Urine was diluted with 1% phosphate buffer (pH 6.0) to give approximately a 5-,ug/ml sample solution. Table 1. The results demonstrated significant negative correlation between the serum concentration and the creatinine clearance (P < 0.05 at 1 h and P < 0.001 at 2, 4, and 6 h). As renal function declined, peak serum concentrations increased, i.e., the mean peak concentration in group 5 (severely impaired renal function) was 1.5 times that of normal subjects.
Objectives:To analyze the clinical effects of flutamide as a second-line anti-androgen for combined androgen blockade in patients with castration-resistant prostate cancer (CRPC) initially treated with bicalutamide as a first-line anti-androgen. Methods: Our study population consisted of 16 patients with CRPC who were treated with flutamide (375 mg daily) as second-line hormonal therapy. Dehydroepiandrosterone (DHEA), androstenedione, androstenediol, testosterone and dihydrotestosterone were measured to investigate the relationship between plasma androgens and outcome following treatment. Furthermore, adrenal androgen levels in a medium of adrenal cancer cell line were also measured. Results: Second-line hormonal therapy using flutamide resulted in a reduction of the prostate-specific antigen (PSA) level in 14 (87.5%) of 16 patients. A PSA decline greater than 50% was observed in 8 (50%) of the 16 patients. The duration of median responsiveness was 6.25 months. PSA elevation of baseline androstenediol level was a predictive factor of PSA responsiveness. The lower DHEA group improved the duration of responsiveness to flutamide. In vitro, 3 mmol/L flutamide suppressed DHEA, androstenedione and androstenediol synthesis compared with bicalutamide in a medium of adrenal cancer cell line. Conclusions: Our data show that flutamide suppresses the adrenal androgens in comparison with bicalutamide. The responsiveness and response duration of flutamide can be predicted in patients with a higher baseline androstenediol level and a lower DHEA level. Metabolites from adrenal androgens contribute to the progression of prostate cancer.
The elimination kinetics of cefotetan (YM09330), a new parenteral semisynthetic cephamycin derivative, were studied in eight healthy volunteers and 41 patients with renal insufficiency after the administration of a single 500-mg dose intravenously. Concentrations of cefotetan in serum and urine were determined by both bioassay and high-pressure liquid chromatography. The pharmacokinetic parameters for cefotetan were calculated on the basis of a two-compartment open model. Serum concentrations of cefotetan immediately after administration were approximately 180 ,ug/ml in all subjects regardless offunction; however, serum concentrations during the P-phase increased directly with the degree of renal impairment. The mean serum half-life during the p-phase was 3.0 h in normal subjects as compared with 13.1 h in hemodialysis patients. There was a linear correlation (P < 0.0001) between the elimination rate constant of cefotetan and creatinine clearance. The mean cumulative urinary recovery of cefotetan in the 24-h urine was 83.3% of the administered dose in normal subjects and decreased with reduced renal function.
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