# Renal osteodystrophy in Egyptian CKD patients: observations from clinically indicated bone biopsies

**Authors:** Nehal Elshabrawy, Mahmoud M. Sobh, Rasha T. Shemies, Mohamed M. Abdalbary, Ahmed Almenshawy, Hanaa I. Okda, Basma O. Sultan, Ehab E. Eltoraby, Amr El-Husseini

PMC · DOI: 10.1186/s12882-026-04776-6 · BMC Nephrology · 2026-02-20

## TL;DR

This study examines bone disease in Egyptian patients with chronic kidney disease and finds high rates of aluminum accumulation in bone biopsies, suggesting environmental exposure as a possible cause.

## Contribution

The paper reports the first bone biopsy-based analysis of renal osteodystrophy in Egypt and Africa, revealing high aluminum staining in patients on dialysis.

## Key findings

- 93% of biopsied patients on hemodialysis showed positive aluminum staining in bone samples.
- 57% of biopsied patients had significant aluminum accumulation, linked to suppressed bone cell activity.
- Aluminum exposure was suspected to come from environmental sources like food, water, or drug manufacturing.

## Abstract

Renal osteodystrophy (ROD) varies among populations. Different genetic and environmental factors and prescription patterns may explain this variation. Egyptian ROD is not sufficiently studied. Although bone biopsy is the gold standard tool, no single study reported the actual ROD spectrum based on bone biopsy in Egypt or Africa. International guidelines must consider the different patterns in developing countries.

The ISN-sistership program enabled us to create an Egyptian bone biopsy consortium that provided a nationwide specialized CKD-MBD service. We included all CKD patients who were referred for unexplained bone pain, osteoporosis, or abnormal CKD-MBD laboratory parameters. Bone biopsy was offered for those who had clinical indications.

Over 2 years, 270 patients were recruited: 118 pre-dialysis, 97 on HD, 21 on PD, and 34 excluded. Non-invasive evaluation suggested that high bone turnover prevailed. Fourteen patients consented to the bone biopsy; all were on HD. Unexpectedly, various degrees of positive aluminum staining were present in 93% of biopsied patients, despite negative results in the dialysate water and nonuse of aluminum-based phosphate binders. Root cause analysis was done, triggering an environmental alarm for potential sources in food, water, and drug manufacturing. Aluminum-induced suppression of bone cells was confirmed by low turnover biomarkers in patients with significant aluminum accumulation. Moreover, FGF23 was significantly higher in the same group (z=-2.082, p-value = 0.037).

To conclude, Aluminum bone disease is still on the differential diagnosis list of ROD. Of the small biopsied patients, 93% had variable degrees of positive aluminum staining, and 57% had significant aluminum accumulation. Extra efforts are needed to eliminate this bone toxin.

The online version contains supplementary material available at 10.1186/s12882-026-04776-6.

## Linked entities

- **Proteins:** FGF23 (fibroblast growth factor 23)
- **Chemicals:** aluminum (PubChem CID 123667)
- **Diseases:** chronic kidney disease (MONDO:0005300), renal osteodystrophy (MONDO:0006946)

## Full-text entities

- **Genes:** FGF23 (fibroblast growth factor 23) [NCBI Gene 8074] {aka ADHR, FGFN, HFTC2, HPDR2, HYPF, PHPTC}, ACP5 (acid phosphatase 5, tartrate resistant) [NCBI Gene 54] {aka HPAP, TRACP5a, TRACP5b, TRAP, TRAcP, TrATPase}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, SOST (sclerostin) [NCBI Gene 50964] {aka CDD, DAND6, SOST1, VBCH}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, KL (klotho) [NCBI Gene 9365] {aka HFTC3, KLA}, PHB2 (prohibitin 2) [NCBI Gene 11331] {aka BAP, BCAP37, Bap37, PNAS-141, REA, hBAP}, PAX5 (paired box 5) [NCBI Gene 5079] {aka ALL3, BSAP, PAX-5}
- **Diseases:** hypertensive retinopathy (MESH:D058437), AL (MESH:D009101), reduced bone volume (MESH:D001523), malignancy (MESH:D009369), diabetic (MESH:D003920), HD (MESH:D006816), DM (MESH:D009223), CKD (MESH:D051436), chronic liver disease (MESH:D008107), metabolic disturbances (MESH:D024821), fibrosis (MESH:D005355), iPTH (MESH:D010279), HPT (MESH:D006961), fracture (MESH:D050723), Bone pain (MESH:D010146), OF (MESH:D005357), PD (MESH:D010300), alcoholism (MESH:D000437), Kidney Disease (MESH:D007674), malignant hypertension (MESH:D006974), low (MESH:D009800), thyrotoxicosis (MESH:C566386), infection (MESH:D007239), cardiovascular diseases (MESH:D002318), PN (MESH:C565820), CKD-MBD (MESH:D012080), aluminum toxicity (MESH:D064420), stones (MESH:D007669), -turnover bone disease (MESH:D001847), OM (MESH:D010018), Osteoporosis (MESH:D010024), vascular calcification (MESH:D061205), death (MESH:D003643), Hypertension (MESH:D006973), HTNB (MESH:C537095)
- **Chemicals:** PD (MESH:D010165), water (MESH:D014867), iron (MESH:D007501), iPTH (MESH:D010281), aluminum sulfate (MESH:C041524), DFO (MESH:D003676), Vit D (MESH:D014807), phosphorus (MESH:D010758), phosphate (MESH:D010710), cinacalcet (MESH:D000069449), sevelamer (MESH:D000069603), bisphosphonates (MESH:D004164), Mg (MESH:D008274), Ca (MESH:D002118), heavy metals (MESH:D019216), Steroid (MESH:D013256), AL (MESH:D000535), 25 (OH) vitamin D (-), prednisolone (MESH:D011239), 25-hydroxyvitamin D (MESH:C104450), tetracycline (MESH:D013752)
- **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/PMC12937528/full.md

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12937528/full.md

## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12937528/full.md

---
Source: https://tomesphere.com/paper/PMC12937528