The adsorption of the anticoagulant nafamostat mesilate (FUT-175) by five different hemodialysis mem-brane\ was studied in vivo and in vitro. In vivo, FUT-

Background/Aim: In this study, we compared the dialysis efficiency, oxidative stress, and nutritional conditions between predilution on-line hemodiafiltration (pre-OL-HDF) and conventional hemodialysis (HD) using a super-flux dialyzer (CHD). Method: This was a crossover study of 38 maintenance HD patients. All patients were treated with CHD for the first 4 months (1st CHD period), then were switched to pre-OL-HDF for 4 months (pre-OL-HDF period), and were returned to CHD for the next 4 months (2nd CHD period). Results: We found no significant difference in the removal ratio of small uremic substances or the indices of inflammation or nutritional states between the pre-OL-HDF and CHD periods. However, we found higher removal of β2 micro-globulin in the pre-OL-HDF period, and the human mercapto-albumin (Alb)/human serum Alb ratio was significantly higher in the pre-OL-HDF period. Conclusion: Treatment with pre-OL-HDF enabled enhanced removal of middle molecule uremic toxins and better Alb redox than did CHD.

The influence of magnesium (Mg) deficiency on the concentration of calcium (Ca) in the aorta, heart, and kidney was evaluated in uremic rats. A total of 32 rats were randomly assigned to two groups: one group made uremic by the 5/6 nephrectomy method, and the other serving as sham-operated controls. Both groups were randomly assigned to two subgroups: one group given a Mg-deficient diet and the other fed a Mg-supplemented diet. After 12 weeks on the regimen, all animals were sacrificed. In Mg-supplemented uremic rats, the concentration of Ca in the aorta was higher than in Mg-supplemented control rats. The concentration of Ca in the aorta was further increased in Mg-deficient uremic rats. The concentrations of Ca in the heart and the kidney were also increased in Mg-deficient uremic rats, as compared with Mg-supplemented uremic rats. The concentration of Mg was decreased in the aorta and increased in the kidney of Mg-deficient rats. There was no significant influence of Mg deficiency on the concentration of phosphate in tissue. Results suggest that Mg deficiency in uremia may increase aortic calcification.

Sevelamer hydrochloride, a non-aluminum-and non-calciumcontaining hydrogel, is an effective phosphate binder in dialysis patients. The suppressive effect of the switching from calcium carbonate to sevelamer hydrochloride on the progression of vascular calcification was examined by measuring areas of calcification on routine chest X-rays using image-analyzing software. The data of 69 maintenance hemodialysis patients were analyzed retrospectively. Over a period of 18 months, 19 patients took only sevelamer hydrochloride as a phosphate binder, while the other 50 patients took only calcium carbonate. The area of calcification increased in the calcium carbonate group, but did not change significantly in the sevelamer group. While the usefulness of computed tomography in detecting vascular calcification in hemodialysis patients has been reported previously, the suppressive effects of switching from calcium carbonate to sevelamer hydrochloride on the progression of aortic calcification can be observed without computed tomography by using the plain chest X-ray films that are routinely performed in hemodialysis clinics.

The concentration of calcium was measured in the aorta, heart, and kidney of uremic rats treated with 100 ng/kg/day 1,25-dihydroxyvitamin D3 (1,25 D3) or 60 mg/kg/day diltiazem for 12 weeks. The concentration of calcium was increased in the aorta, heart, and kidney of uremic rats, and was further increased by administration of 1,25 D3. The 1,25 D3-induced increase in calcium in the aorta was inhibited by diltiazem, but this effect was not accompanied by a decrease in serum calcium x phosphate products. Diltiazem had no effect on the 1,25 D3-induced increase of calcium in the heart and kidney. Thus, in uremia 1,25 D3 may promote the calcification of the aorta; calcium antagonists may protect against calcification without a reduction in serum calcium x phosphate products.