Quantitative adjuvant zinc therapy using polaprezinc was performed to examine the correlation between zinc concentration and anemia in maintenance hemodialysis patients to propose appropriate treatment. Anemia and serum zinc concentration were measured in 117 patients with chronic renal failure receiving outpatient maintenance hemodialysis at Tsuyama Chuo Kinen Hospital. Two bags of polaprezinc (containing zinc 34 mg/day) were administered to 58 patients with lower than normal zinc levels (Zn < 80 mg/dl) as adjuvant zinc therapy to assess anemia improvement. Zinc concentration and all anemia parameters showed significant positive correlation, indicating that anemia improves in patients with high serum zinc levels. Regarding the effects of adjuvant zinc therapy for improving anemia, hemoglobin levels were found to increase significantly to the highest value at 3 weeks. During treatment, the dosage of erythropoietin was reduced significantly from baseline at all assessment points. No zinc poisoning from therapy was seen, but two patients had diarrhea (1.9%). Zinc-treated patients required iron therapy due to the development of iron deficiency. Most maintenance hemodialysis patients suffer from zinc deficiency anemia, and zinc-based polaprezinc has been confirmed to be an effective and safe adjuvant zinc treatment. Most patients diagnosed as refractory anemia with no response to erythropoietin also suffer from zinc deficiency anemia, many of whom are expected to benefit from zinc therapy to improve their anemia. Possible zinc deficiency anemia should be considered in the treatment of refractory anemia with no response to erythropoietin.
To determine the spectrum of mutations of the COL4A5 gene encoding type IV collagen among Japanese Alport syndrome (AS) patients, 60 unrelated patients (47 males and 13 females) from all over the country were recruited. Screening for mutations in all the exons (1 to 51) of the COL4A5 gene was carried out by PCR-SSCP analysis. A mobility shift was observed in 22 of 60 patients, and their genomic DNA were analyzed by the direct sequence method and using cloned ssDNA. Nine of these had missense mutations in the collagenous domain (in exons 39, 37, 31, 29, 28, 27, 21, 20, 19). Eight of these mutations were observed in a codon of glycine residue. Two were altered to arginine, two to valine, two to glutamic acid and two to aspartic acid. The other missense mutation was a change from isoleucine to serine in a interruption region. Five patients had small size base deletions and one had a 4 bp insertion resulting in frameshift (in exons 49, 41, 19, 14, 13). Three had a splice site mutation (in exons 49, 47, 27). One had a nonsense mutation (in exon 17). These mutations seemed to be pathogenic, but the phenotype, which includes extrarenal manifestations, can vary with respect to both expression and severity. The remaining mutations were three silent ones (in exons 19, 39, 46). In addition, major gene rearrangement seemed to be rare in Japanese AS patients.
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