# Analysis of Potential Iron Toxicity in Hemodialysis Patients Under Intravenous Iron Treatment

**Authors:** Jessy Korina Peña-Esparragoza, Alina Chávez-Guillén, Paloma Ramos-López, Oscar Rueda-Elías, Susana López-Ongil, Matilde Alique, Rafael Ramírez-Chamond, Julia Carracedo, Diego Rodríguez-Puyol, Patricia Martínez-Miguel

PMC · DOI: 10.3390/medsci14010154 · Medical Sciences · 2026-03-21

## TL;DR

This study examines if high iron doses in hemodialysis patients lead to iron toxicity, finding that while more iron builds up in the liver over time, no signs of toxicity were observed.

## Contribution

The study provides new evidence on hepatic iron deposition in hemodialysis patients and its lack of association with toxicity markers.

## Key findings

- Patients with higher hepatic iron deposition had longer hemodialysis duration and higher ferritin levels.
- No significant differences in plasma protein oxidation or cytokine mRNA levels were observed except for decreased IL-6.
- No evidence of increased toxicity was found in patients with higher hepatic iron deposition.

## Abstract

Background/Objectives: Higher iron doses are used in the anemia treatment of hemodialysis patients, which allows for lower doses of erythropoiesis-stimulating agents; however, there are concerns regarding the risk of iron toxicity. This study aimed to evaluate the potential toxicity of iron deposition in prevalent hemodialysis patients on iron therapy and its relationship with parameters used to assess iron status, plasma protein oxidation, and cellular iron toxicity. Methods: Magnetic resonance imaging was performed in 56 patients to assess hepatic iron deposition, which was related to clinical and analytical parameters. In patients included in the first and fourth quartiles, according to hepatic iron deposition, plasma protein oxidative stress was quantified, as were iron and cytokine levels in peripheral blood mononuclear cells (PBMCs). Results: Patients with higher hepatic iron deposition had a longer time on hemodialysis (42.0 ± 43.0 vs. 4.9 ± 3.4 months, p < 0.001) and higher ferritin levels (1200 ± 516 vs. 429 ± 278 ng/mL, p < 0.001) than those with lower hepatic iron deposition, without differences in transferrin saturation or hepatic enzyme serum concentration. No differences were found in plasma protein oxidation, iron content, or cytokine mRNA content in PBMCs, except for a decrease in IL-6 levels in patients with higher hepatic iron deposition. Conclusions: Patients with longer hemodialysis times had higher iron stores, suggesting that iron treatment over time increases hepatic iron deposition. No parameters supporting increased toxicity in patients with higher hepatic iron deposition were observed.

## Linked entities

- **Diseases:** anemia (MONDO:0002280)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, TF (transferrin) [NCBI Gene 7018] {aka HEL-S-71p, PRO1557, PRO2086, TFQTL1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, ELANE (elastase, neutrophil expressed) [NCBI Gene 1991] {aka ELA2, GE, HLE, HNE, NE, PMN-E}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, HPRT1 (hypoxanthine phosphoribosyltransferase 1) [NCBI Gene 3251] {aka HGPRT, HPRT}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, HAMP (hepcidin antimicrobial peptide) [NCBI Gene 57817] {aka HEPC, HFE2B, LEAP1, PLTR}
- **Diseases:** end-stage renal disease (MESH:D007676), Proinflammatory Cytokine (MESH:D000080424), diabetes (MESH:D003920), Organ damage (MESH:D000092124), Anemia (MESH:D000740), Toxicity (MESH:D064420), nonalcoholic fatty liver disease (MESH:D065626), hepatic iron overload (MESH:D019190), infection (MESH:D007239), injury to (MESH:D014947), homozygous hemochromatosis (MESH:D000090542), Inflammatory (MESH:D007249), kidney failure (MESH:D051437), uremia (MESH:D014511), chronic kidney disease (MESH:D051436), Iron (MESH:D000090463), blood loss (MESH:D016063), hypertension (MESH:D006973), infectious (MESH:D003141), chronic liver disease (MESH:D008107), cancer (MESH:D009369), hemochromatosis (MESH:D006432), cirrhosis (MESH:D005355), hepatic (MESH:D056486), virus infection (MESH:D014777)
- **Chemicals:** lipid (MESH:D008055), iron sucrose (MESH:D000077605), Fe (MESH:D007501), 4-hydroxynonenal- lysine (-), hydrogen (MESH:D006859), heme (MESH:D006418), urea (MESH:D014508), Water (MESH:D014867), vitamin D (MESH:D014807)
- **Species:** Homo sapiens (human, species) [taxon 9606], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395]
- **Mutations:** C282Y

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13028211/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13028211/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC13028211/full.md

---
Source: https://tomesphere.com/paper/PMC13028211