# Exploring the role of quantitative susceptibility mapping in assessing brain iron deposition in hemodialysis patients

**Authors:** GuoLi Ren, QingQing Nie, Daliang Liu, Bo Wang, Xiao Gao, XueHuan Liu, Hao Wang, Jun Liu

PMC · DOI: 10.1186/s13244-025-02197-x · Insights into Imaging · 2026-02-16

## TL;DR

This review explores how quantitative susceptibility mapping can track brain iron buildup in patients on hemodialysis and its link to cognitive decline.

## Contribution

The paper systematically reviews QSM's role in monitoring brain iron dynamics and its clinical implications in hemodialysis patients.

## Key findings

- QSM can noninvasively monitor cerebral iron distribution in hemodialysis patients.
- Brain iron deposition is linked to cognitive impairment and oxidative stress in these patients.
- Future research should focus on standardizing QSM techniques and tracking treatment responses.

## Abstract

Patients with end-stage renal disease (ESRD) develop brain iron deposition due to iron metabolism disorders induced by long-term hemodialysis. This abnormal iron accumulation accelerates cognitive impairment (CI) and neurodegenerative pathologies. Quantitative susceptibility mapping (QSM), a technique capable of precisely quantifying magnetic susceptibility, provides a novel perspective for the noninvasive and dynamic monitoring of cerebral iron distribution. Monitoring brain iron deposition using QSM facilitates the development of individualized clinical treatment strategies. This review systematically examines the application of QSM in studying brain iron deposition in hemodialysis patients, with a focus on analyzing the dynamic patterns of iron deposition pre- and post-dialysis and during follow-up periods. It further explores the relationship between QSM findings and iron metabolism dysregulation, blood-brain barrier (BBB) injury, and oxidative stress. Additionally, the predictive value of QSM for clinical neurological functional prognosis following iron chelation therapy is discussed.

QSM studies on cerebral iron deposition in hemodialysis patients require further monitoring of its spatial-temporal dynamics and changes after iron chelation. Future research should focus on technical standardization, longitudinal tracking, and treatment response to establish a precision neuroimaging-guided framework.

This review exploration is warranted to monitor the spatial distribution and dynamic changes of brain iron deposition in this population.The relationships between QSM findings and iron metabolism dysregulation, blood-brain barrier injury, and oxidative stress are explored.This review focuses on issues in the fields of technology standardization, longitudinal monitoring, and treatment responsiveness.

This review exploration is warranted to monitor the spatial distribution and dynamic changes of brain iron deposition in this population.

The relationships between QSM findings and iron metabolism dysregulation, blood-brain barrier injury, and oxidative stress are explored.

This review focuses on issues in the fields of technology standardization, longitudinal monitoring, and treatment responsiveness.

## Linked entities

- **Diseases:** end-stage renal disease (MONDO:0004375)

## Full-text entities

- **Genes:** APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}, CEBPZ (CCAAT enhancer binding protein zeta) [NCBI Gene 10153] {aka CBF, CBF2, HSP-CBF, NOC1}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, TF (transferrin) [NCBI Gene 7018] {aka HEL-S-71p, PRO1557, PRO2086, TFQTL1}, HAMP (hepcidin antimicrobial peptide) [NCBI Gene 57817] {aka HEPC, HFE2B, LEAP1, PLTR}, TSPO (translocator protein) [NCBI Gene 706] {aka BPBS, BZRP, DBI, IBP, MBR, PBR}
- **Diseases:** PD (MESH:D010300), inflammatory (MESH:D007249), neuropsychiatric complications (MESH:D008107), neurodegeneration (MESH:D019636), dysmetabolism (MESH:D024821), cerebral hypoperfusion (MESH:D002547), iron overload (MESH:D019190), dystonia (MESH:D004421), atrophy (MESH:D001284), neuroinflammation (MESH:D000090862), edema (MESH:D004487), CKD (MESH:D051436), Alzheimer's disease (MESH:D000544), kidney failure (MESH:D051437), calcification (MESH:D002114), confusional (MESH:D003221), stroke (MESH:D020521), mood disorders (MESH:D019964), white matter (MESH:D056784), hemochromatosis (MESH:D006432), hypoxemia (MESH:D000860), iron (MESH:D000090463), small vessel diseases (MESH:D059345), neurological disorders (MESH:D009461), hypotension (MESH:D007022), ischemia (MESH:D007511), pallidal lesions (MESH:D006211), brain abnormalities (MESH:D001927), brain injury (MESH:D001930), iron metabolism (MESH:D019189), Vascular calcifications (MESH:D061205), Anemia (MESH:D000740), vascular (MESH:D057772), Cerebrovascular insults (MESH:D002561), neurocognitive impairment (MESH:D019965), ESRD (MESH:D007676), executive dysfunction (MESH:D006331), dementia (MESH:D003704), neuronal death (MESH:D009410), Kidney Disease (MESH:D007674), Accelerated encephalatrophy (MESH:D015465), movement abnormalities (MESH:D004409), cognitive and motor function decline (MESH:D003072), neuropathology (MESH:D009422), restless legs syndrome (MESH:D012148), calcified (MESH:D018333)
- **Chemicals:** phosphorus (MESH:D010758), deferiprone (MESH:D000077543), Iron (MESH:D007501), TSAT (-), lipid (MESH:D008055), creatinine (MESH:D003404), ROS (MESH:D017382), calcium (MESH:D002118)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12909729/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12909729/full.md

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Source: https://tomesphere.com/paper/PMC12909729