Yeşilbaş Osman, Yıldız Nurdan, Baykan Özgür, Alpay Harika
Department of Pediatrics, Marmara University Faculty of Medicine, İstanbul, Turkey.
Division of Pediatric Nephrology, Departmant of Pediatrics, Marmara University Faculty of Medicine, İstanbul, Turkey.
Turk Pediatri Ars. 2019 Dec 25;54(4):238-245. doi: 10.14744/TurkPediatriArs.2019.93206. eCollection 2019.
Functional iron deficiency seco ndary to inflammation and increased serum hepcidin lead to erythropoietin-resistant anemia in children with chronic kidney disease. Vitamin D deficiency, parathyroid hormone, and phosphate can also participate in chronic inflammation and anemia. The aim of this study was to evaluate the association between hepcidin, bone mineral metabolism, and anemia in non-dialysis pediatric patients with chronic kidney disease.
Thirty-five patients with stage 2-4 chronic kidney disease and 35 healthy subjects were enrolled in the study. Serum creatinine, blood urea nitrogen, uric acid, C-reactive protein, interleukin-6, hepcidin, complete blood count, ferritin, calcium, phosphorus, parathyroid hormone, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and fibroblast growth factor-23 levels were compared between the groups.
Ferritin, C-reactive protein, interleukin-6, blood urea nitrogen, creatinine, uric acid levels, and percentages of reticulocytes were significantly higher than in the controls (p<0.05). The mean serum hepcidin levels in the chronic kidney disease and control groups were 9.6±5.2 (range, 2.15-25.3) and 9.7±4.3 (range, 3.4-22.2) ng/mL and were not significantly different in either group. There were no differences in terms of serum phosphorus, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and fibroblast growth factor-23 levels between the groups (p>0.05). Serum hepcidin levels were not correlated with anemia parameters, serum fibroblast growth factor-23, phosphorus, uric acid, C-reactive protein, parathyroid hormone, and 25-hydroxyvitamin D levels (p>0.05). However, serum hepcidin levels were correlated with 1,25-dihydroxyvitamin D and interleukin-6 levels (p=0.013 and p=0.002, respectively).
Serum hepcidin levels may not increase significantly in non-dialysis pediatric patients with chronic kidney disease despite high levels of inflammatory markers such as C-reactive protein and interleukin-6. The increase of serum hepcidin levels may be inhibited by effective treatment of anemia with iron supplementation and erythropoietin, and the treatment of secondary hyperparathyroidism with phosphate binders and the active form of vitamin D, which decrease serum parathyroid hormone and fibroblast growth factor-23 levels, and control inflammation to some extent.
炎症继发的功能性铁缺乏及血清铁调素升高会导致慢性肾脏病患儿出现促红细胞生成素抵抗性贫血。维生素D缺乏、甲状旁腺激素及磷酸盐也可参与慢性炎症及贫血过程。本研究旨在评估非透析慢性肾脏病患儿中铁调素、骨矿物质代谢与贫血之间的关联。
本研究纳入了35例2-4期慢性肾脏病患儿及35名健康受试者。比较两组间血清肌酐、血尿素氮、尿酸、C反应蛋白、白细胞介素-6、铁调素、全血细胞计数、铁蛋白、钙、磷、甲状旁腺激素、25-羟维生素D、1,25-二羟维生素D及成纤维细胞生长因子-23水平。
铁蛋白、C反应蛋白、白细胞介素-6、血尿素氮、肌酐、尿酸水平及网织红细胞百分比均显著高于对照组（p<0.05）。慢性肾脏病组和对照组的血清铁调素平均水平分别为9.6±5.2（范围2.15-25.3）和9.7±4.3（范围3.4-22.2）ng/mL，两组间无显著差异。两组间血清磷、25-羟维生素D、1,25-二羟维生素D及成纤维细胞生长因子-23水平无差异（p>0.05）。血清铁调素水平与贫血参数、血清成纤维细胞生长因子-23、磷、尿酸、C反应蛋白、甲状旁腺激素及25-羟维生素D水平均无相关性（p>0.05）。然而，血清铁调素水平与1,25-二羟维生素D及白细胞介素-6水平相关（分别为p=0.013和p=0.002）。
尽管非透析慢性肾脏病患儿中C反应蛋白和白细胞介素-6等炎症标志物水平较高，但其血清铁调素水平可能不会显著升高。补充铁剂和促红细胞生成素有效治疗贫血、使用磷结合剂及活性形式的维生素D治疗继发性甲状旁腺功能亢进，可降低血清甲状旁腺激素和成纤维细胞生长因子-23水平，并在一定程度上控制炎症，从而抑制血清铁调素水平的升高。
