In hemodialysis patients, oxidative stress results from an imbalance between the production of reactive oxygen species and antioxidant defense mechanisms. Recently, a new dialysis multi-layer membrane has been developed, by modifying the inner surface of regenerated cellulose to support a vitamin E coating. The aim of our study was to investigate the effects of hemodialysis treatment with vitamin E-modified membrane on anemia and erythropoietin requirement in a group of chronic uremic patients. Ten uremic, non diabetic, patients on standard bicarbonate dialysis were treated with vitamin E-bonded dialysis membrane for 12 months. Hematological parameters, erythropoietin requirement, serum vitamin E and serum malonyldialdehyde (MDA) were evaluated before starting the study and monthly. No significant changes in hemoglobin level, RBC count, hematocrit and EPO requirement were observed. Basal vitamin E levels were in the normal range (13.0 +/- 2.88 mg/L vs. 14.79 +/- 3.12 mg/L; NS). On the contrary, basal MDA levels were higher than those observed in the control group (1.87 +/- 0.36 vs. 1.13 +/- 0.18 mmol/mL; p < 0.01) and a significant decrease of MDA levels was found after 1 month of Excebrane treatment (1.39 +/- 0.25 nmol/mL; p < 0.02). In conclusion, the role of the "oxidative hemolysis" in the pathogenesis of anemia in CHD patients is still not clearly defined, but it could be of minor clinical relevance. Although the effectiveness of vitamin E-coated membranes as a scavenger of ROS allows a better control of intradialytic oxidative stress, it doesn't seem to contribute to clinical management of anemia in these patients.

The purpose of this case report is to illustrate the diagnostic difficulties of pericardial tamponade and to suggest that focused cardiac ultrasound be included in the resuscitative care of pediatric shock. Three cases of cardiac tamponade are presented. Each patient had a syncopal episode and presented with altered mental status and hypotension. Muffled heart tones, distended neck veins, and electrocardiogram and chest radiograph abnormalities were not present. Hypotension was not responsive to intravenous volume expansion treatment. Diagnostic delays would have been prevented if focused cardiac ultrasound had been included in the resuscitative care of shock.

The effect of tolazamide on in vitro rates of gluconeogenesis, ketogenesis, and glycogenesis was determined in liver tissue from fasted normal and diabetic rats. Hormones were not added to the incubation mixture. Two concentrations of the drug were tested, one of which was therapeutic (40 micrograms/ml) and other immoderately elevated (400 micrograms/ml). Neither drug concentration affected hepatic glycogen synthesis. However, the low dose of tolazamide inhibited ketogenesis in the diabetic liver by 39% and in the control liver by 32%; oxidative CO2 production from palmitate was reduced in parallel with ketogenesis. The drug did not alter ketogenesis in isolated intact mitochondria. Similarly, this same therapeutic dose curtailed hepatic gluconeogenesis only in control liver (74% inhibition); this reaction was unaltered by this drug concentration in the explants derived from the diabetic rats. The logarithmically higher dose inhibited hepatic gluconeogenesis in both control and diabetic liver tissue by 56% and 51%, respectively. Hence, possibly acting at a postreceptor site, therapeutic concentrations of tolazamide can decrease rat hepatic in vitro gluconeogenesis and ketogenesis.

Clinical usefulness of calcium acetate (CAA) as phosphorus binder was assessed in 19 stable hemodialysis patients with persistent hyperphosphatemia. All were dialysed thrice weekly with a constant dialytic schedule and a dialysate calcium of 3.5 mEq/l. One month prior the study beginning all patients stopped assumption of Ca and vitamin D supplements. In the first period of the study CAA (mean daily doses 2.2 g) was administered for one month followed by 15 days of withdrawal. The mean serum phosphorus decreased from 7.6 +/- 1.4 to 5.8 +/- 0.8 mg% (p < 0.005). After 15 days of withdrawal mean serum phosphorus reached the pretreatment value. Then the patients entered a long term study with personalized doses of CAA (between 1 and 4 g/day) and administration in 8 of them of alpha-calcidol. After a mean follow-up period of 5.4 +/- 1.5 months serum phosphorus was reduced from 7.5 +/- 1.1 to 5.6 +/- 1.1 mg% (p < 0.0005) while calcemia increased from 9.0 +/- 0.7 to 9.6 +/- 0.6 mg% (p < 0.005). Only one patient developed mild hypercalcemia. We concluded that CAA is a safe alternative to calcium carbonate for the control of hyperphosphatemia of uraemic patients for the most efficient phosphorus binding and the lesser absorption of calcium.