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Submitted: 18 Jun 2026
Revision: 01 Aug 2026
Accepted: 09 Aug 2026
ePublished: 22 Sep 2026
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J Renal Inj Prev. 2026;15(4): e38781.
doi: 10.34172/jrip.38781
  Abstract View: 197075
  PDF Download: 134203

Original

The association of exposure to depleted uranium and markers of mineral and bone metabolism in chronic kidney disease patients; a prospective analytical, cross-sectional study

Ihsan Maher Abdulameer 1 ORCID logo, Seyed Alireza Mesbah-Namin 1* ORCID logo, Arif Sami Malik 2 ORCID logo, Sameera Ahmed Ebrahiem 3 ORCID logo

1 Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
2 Department of Medicine, College of Medicine, Al-Nahrain University, Baghdad, Iraq
3 Department of Physics, College of Education for Pure Science, Ibn Al-Haitham, University of Baghdad, Baghdad, Iraq
*Corresponding Author: Seyed Alireza Mesbah-Namin, Email: mesbahna@modares.ac.ir

Abstract

Introduction: Environmental exposure to depleted uranium (DU) has raised growing concerns about its potential systemic toxicity, yet its impact on mineral and bone metabolism in patients with chronic kidney disease (CKD) remains poorly defined. Given that disturbances in vitamin D, calcium, parathyroid hormone (PTH), and phosphorus are central to the development of CKD‑mineral and bone disorder, clarifying whether uranium burden contributes to these abnormalities may have important implications for risk stratification and clinical management in this vulnerable population.

Objectives: This prospective analytical study aimed to evaluate the correlation between internal exposure to DU and key markers of mineral and bone metabolism, including serum 25(OH)D, calcium, PTH, and phosphorus, in patients with CKD.

Patients and Methods: This cross‑sectional study included 100 male patients with CKD who were referred to several hospitals and medical centers in Iraq from February to August 2024. After obtaining informed written consent, demographic and clinical data were recorded; a blood sample was collected for measurement of DU and assessment of markers of mineral and bone metabolism, including serum 25‑hydroxyvitamin D (25(OH)D), calcium, PTH, and phosphorus, and these variables were subsequently analyzed using appropriate statistical methods.

Results: The results indicated that DU levels were significantly correlated with lower 25(OH) D concentrations (B = −0.015, 95% confidence interval [CI]: −0.028 to −0.001 and B = −0.016, CI: −0.030 to −0.001), reduced serum calcium (B = −0.003, 95% CI: −0.006 to −0.001 and B = −0.004, 95% CI: −0.007 to −0.001), and increased PTH (B = 0.022, 95% CI: 0.010 - 0.033 and B = 0.014, 95% CI: 0.002 - 0.026) in the unadjusted and adjusted (age and hemodialysis status) models, respectively. While no significant relationship emerged with serum phosphorus.

Conclusion: Greater internal exposure to DU was associated with a pattern of altered mineral and bone markers, with consistently lower 25(OH)D and calcium levels and higher PTH concentrations. A lack of link with phosphorus, suggesting that phosphate homeostasis may be maintained or shaped by additional determinants beyond uranium exposure in this setting.



Implication for health policy/practice/research/medical education:

In this study, we found that higher internal exposure to depleted uranium (DU) was linked to lower circulating 25‑hydroxyvitamin D (25(OH)D) and calcium levels, together with higher parathyroid hormone (PTH) concentrations, pointing toward a shift in mineral and bone metabolism compatible with secondary hyperparathyroidism. At the same time, phosphorus levels did not show a meaningful association with uranium burden, suggesting that phosphate balance may be maintained or more strongly governed by other clinical or treatment‑related factors in this setting.

Please cite this paper as: Abdulameer IM, Mesbah-Namin SA, Sami Malik A, Ebrahiem SA. The association of exposure to depleted uranium and markers of mineral and bone metabolism in chronic kidney disease patients; a prospective analytical, cross-sectional study. J Renal Inj Prev. 2026; 15(4): e38781. doi: 10.34172/jrip.38781.

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