Renal anemia: from erythropoietin deficiency to erythropoietin resistance
- 1Department of Hematology, Baoshan Hospital Affiliated to Shanghai University of Traditional Chinese Medicine
Abstract
Renal anemia is one of the core complications of chronic kidney disease (CKD) and is closely associated with poor patient prognosis. Renal interstitial fibrosis or impaired oxygen sensing leads to insufficient erythropoietin (EPO) production, which constitutes the fundamental mechanism initiating renal anemia. On this basis, multiple pathological factors—including the inflammatory microenvironment in CKD, iron deficiency, and mineral and bone disorders—synergistically induce EPO resistance, further exacerbating anemia and diminishing the response to existing therapies. Currently, the treatment of renal anemia has moved beyond simple EPO replacement and is progressively shifting toward a dual strategy that emphasizes both correction of EPO resistance and enhancement of drug responsiveness. This article summarizes the molecular network through which insufficient EPO synthesis and EPO resistance synergistically aggravate renal anemia, systematically reviews the pharmacological basis, limitations, and safety risks of current drug therapies, and discusses future research directions and potential therapeutic targets in this field.
Related
- Vitamin B6 deficiency as a cause of erythropoietin-stimulating agent-resistant anemia in hemodialysis patients: A report of two cases
- Comparing Erythropoietin, Darbepoetin and No Erythropoiesis-Stimulating Agent Treatment in Preventing Anemia of Prematurity: A Multi-Center Retrospective Study
- The safety and efficacy of oral vitamin C administration on erythropoietin dosing requirements in end stage renal disease patients on regular hemodialysis
- Vitamin C Deficiency Can Present as True Hemolytic Anemia
- Refractory Dysphagia and Severe Iron Deficiency Anemia in a Woman With Plummer-Vinson Syndrome
BibTeX
@article{chu2026renal,
title = {{Renal anemia: from erythropoietin deficiency to erythropoietin resistance}},
author = {Aojiao Chu and Jinyang Bu and Xinfu Zou and Zheng Zhang and Qin Zheng and Ling Shi and Meihong Luo},
journal = {Frontiers in Pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1928390},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1928390/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Renal anemia: from erythropoietin deficiency to erythropoietin resistance
AU - Aojiao Chu
AU - Jinyang Bu
AU - Xinfu Zou
AU - Zheng Zhang
AU - Qin Zheng
AU - Ling Shi
AU - Meihong Luo
PY - 2026
DA - 2026/10/08
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1928390
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1928390/full
AB - Renal anemia is one of the core complications of chronic kidney disease (CKD) and is closely associated with poor patient prognosis. Renal interstitial fibrosis or impaired oxygen sensing leads to insufficient erythropoietin (EPO) production, which constitutes the fundamental mechanism initiating renal anemia. On this basis, multiple pathological factors—including the inflammatory microenvironment in CKD, iron deficiency, and mineral and bone disorders—synergistically induce EPO resistance, further exacerbating anemia and diminishing the response to existing therapies. Currently, the treatment of renal anemia has moved beyond simple EPO replacement and is progressively shifting toward a dual strategy that emphasizes both correction of EPO resistance and enhancement of drug responsiveness. This article summarizes the molecular network through which insufficient EPO synthesis and EPO resistance synergistically aggravate renal anemia, systematically reviews the pharmacological basis, limitations, and safety risks of current drug therapies, and discusses future research directions and potential therapeutic targets in this field.
SN - 1663-9812
ER -