Long-acting erythropoiesis-stimulating agent (ESA) induces physiological erythropoiesis via improvement of iron availability.

PURPOSE: Previous studies reported that the long-acting erythropoiesis-stimulating agent (ESA) significantly suppresses the expression of hepcidin, which regulates iron availability. In this study, we compared the iron availability for erythropoiesis between short and long-acting ESA over a long period. METHODS: We enrolled 69 hemodialysis patients in this study. All patients were treated with short-acting ESA (epoetin-α or epoetin-ß) for the first 30 months. Then, all patients switched to long-acting ESA (continuous erythropoietin receptor activator-methoxy polyethylene glycol-epoetin beta) for the next 30 months. We measured their blood levels of Hb, ferritin, iron, total iron-binding capacity, intact-parathyroid hormone, calcium, phosphate, albumin, and highly sensitive CRP level. RESULTS: There was no significant change in the dose of short or long-acting ESA during the study period. Compared with the short-acting ESA period, the mean hemoglobin (Hb) and transferrin saturation levels were significantly increased in the long-acting ESA period (from 10.3 ± 0.2 to 10.6 ± 0.3 g/dL). On the other hand, the mean serum ferritin level (from 72 ± 22.2 to 56.3 ± 14 ng/mL) and the dose of IV iron (from 108 ± 63 to 53 ± 27 mg/month) were significantly decreased in the long-acting ESA period. CONCLUSION: In this study, we found that anemia treatment with long-acting ESA attenuated the iron utilization for erythropoiesis and maintained target Hb levels without requiring a higher dose of IV iron or ESA.

The pharmacokinetics of oral metronidazole in patients with metronidazole-induced encephalopathy undergoing maintenance hemodialysis.

BACKGROUND: Metronidazole-induced encephalopathy (MIE) is a rare disease caused by an adverse reaction to metronidazole (MNZ). Furthermore, the pharmacokinetics of MNZ during hemodialysis (HD) treatment have not been revealed. CASE PRESENTATION: In a 70-year-old woman undergoing maintenance HD, MNZ was administered intermittently for the treatment of recurrent hepatic cyst infections. She complained of vomiting, dizziness, and dysarthria after 65 consecutive days of MNZ administration. In brain fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI), we found a high signal intensity in the cerebellar dentate nuclei and splenium of the corpus callosum. We diagnosed the patient with MIE. MNZ administration was withdrawn immediately, and HD treatment was performed for 3 consecutive days. Accompanying the remarkable decrease in serum MNZ levels, MIE symptoms were attenuated after three consecutive days of HD. In a brain MRI at 9 days, the high-intensity areas in the cerebellar dentate nuclei and splenium of the corpus callosum had disappeared. CONCLUSION: In this patient, we diagnosed MIE in the early stage using MRI, and 3 consecutive days of HD rapidly attenuated the symptoms associated with MIE, accompanied by a significant decrease in serum MNZ levels.