# Osteoporosis and CKD-Metabolic Bone Disease Under the Same Umbrella: Insights From a Joint Scientific Symposium

**Authors:** David W. Dempster, Pieter Evenepoel, Thomas L. Nickolas, Ziad A. Massy, Sandro Mazzaferro, Nicholas C. Harvey, Paul D. Miller, Michael Pazianas

PMC · DOI: 10.1016/j.ekir.2026.106362 · Kidney International Reports · 2026-02-17

## TL;DR

Osteoporosis and CKD-metabolic bone disease often overlap, especially in older people, but are frequently managed separately, leading to gaps in diagnosis and treatment.

## Contribution

The paper highlights the need for integrated management of osteoporosis and CKD-MBD to improve diagnosis and treatment in aging populations.

## Key findings

- Adynamic bone in CKD-MBD resembles low-turnover osteoporosis, making differentiation difficult without clinical context.
- Current diagnostic approaches for osteoporosis and CKD-MBD remain limited, leading to clinical misclassification.
- Interdisciplinary strategies, such as intermittent PTH administration, may improve skeletal and cardiovascular outcomes in CKD.

## Abstract

Osteoporosis and chronic kidney disease (CKD)–metabolic bone disease (MBD) (CKD-MBD) are increasingly recognized as overlapping conditions, particularly in the aging population. Declining renal function and skeletal fragility often coexist, because CKD-MBD may develop in a skeleton already compromised by preexisting osteoporosis. Adynamic bone, often resulting from excessive suppression of parathyroid hormone (PTH) and now a common form of renal osteodystrophy (ROD), may histologically resemble low-turnover osteoporosis; distinguishing between the 2 under light microscopy remains difficult, and reliable differentiation often depends on clinical context. Nevertheless, nephrologists and nonnephrologist bone specialists frequently work in parallel rather than in collaboration.This separation has contributed to persistent diagnostic gaps and fragmented management, especially in patients with advanced CKD. Advances in imaging, biochemical markers, and bone histomorphometry have improved insight into disease mechanisms; however, limitations in current diagnostic approaches remain. Osteoporosis therapies are frequently underused in CKD, despite growing evidence supporting efficacy and safety across a broader range of kidney function than previously assumed. Despite efforts to refine the definition of osteoporosis beyond bone mineral density (BMD) alone, clinical misclassification continues.Beyond skeletal health, vascular calcification (VC)—driven by disordered calcium–phosphate homeostasis—remains insufficiently prioritized in clinical decision-making, despite its strong association with cardiovascular morbidity and mortality in CKD. Emerging concepts, such as intermittent PTH administration, an established treatment in osteoporosis, illustrate the potential for interventions that may restore mineral balance and improve skeletal integrity in selected CKD populations. Whether such strategies can also favorably influence cardiovascular risk remains uncertain and warrant investigation. This integrated framework may improve interdisciplinary care.

## Linked entities

- **Diseases:** osteoporosis (MONDO:0005298)

## Full-text entities

- **Genes:** PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}
- **Diseases:** MBD (MESH:D001851), VC (MESH:D061205), skeletal fragility (MESH:D005600), Declining renal function (MESH:D060825), Adynamic bone (MESH:D001847), Osteoporosis (MESH:D010024), CKD (MESH:D051436), ROD (MESH:D012080)
- **Chemicals:** calcium (MESH:D002118)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC12995437/full.md

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Source: https://tomesphere.com/paper/PMC12995437