The association of hepcidin, reticulocyte hemoglobin equivalent and anemia-related indicators on anemia in chronic kidney disease

Author:

Gao Zhaoli1,Hu Yingying2,Gao Yanxia1,Ma Xiaotian3,Hu Zhao4ORCID

Affiliation:

1. Department of Nephrology, Qilu Hospital of Shandong University (Qingdao), Qingdao, Shandong, China

2. Qilu Hospital of Shandong University, Jinan, Shandong, China

3. Department of Medicine Experimental Center, Qilu Hospital of Shandong University (Qingdao), Qingdao, Shandong, China

4. Department of Nephrology, Qilu Hospital of Shandong University, Jinan, Shandong, China.

Abstract

Hepcidin is an essential regulator of iron homeostasis in chronic kidney disease (CKD) anemia, reticulocyte hemoglobin equivalent (RET-He) can be used to evaluate the availability of iron for erythropoiesis. Previous research has found that hepcidin indirectly regulates RET-He. This study aimed to investigate the association of hepcidin, RET-He and anemia-related indicators on anemia in chronic kidney disease. A total of 230 individuals were recruited, including 40 CKD3-4 patients, 70 CKD5 patients without renal replacement therapy, 50 peritoneal dialysis patients, and 70 hemodialysis patients. The serum levels of hemoglobin (Hb), reticulocyte, RET-He, serum iron, serum creatinine, serum ferritin, total iron binding capacity, hepcidin-25, high sensitivity C-reactive protein, transferrin, erythropoietin, intrinsic factor antibody, soluble transferrin receptor and interleukins-6 (IL-6) were measured. Hepcidin-25 was positively associated with IL-6, and negatively with total iron binding capacity, intrinsic factor antibody, and transferrin. Reticulocyte Hb equivalent was associated positively with Hb, serum ferritin, serum iron, transferrin saturation, and negatively with serum creatinine, reticulocyte, IL-6, STfR. Hepcidin-25 was not associated with RET-He, while IL-6 was independently associated with hepcidin-25 and RET-He, suggesting that hepcidin has no effffect on the iron dynamics of reticulocytes in CKD, may be related to IL-6, indicate a likelihood of a threshold for stimulation of hepcidin-25 expression by IL-6 in order to indirectly regulates RET-He.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

General Medicine

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