ArticleBone2022
The combination of aging and chronic kidney disease leads to an exacerbated cortical porosity phenotype.
Article in Bone, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Four weeks of romosozumab treatment increases trabecular bone volume and differentially improves cortical bone in young and aging mice with chronic kidney disease.Calcified tissue international · 2026Article
- Nanostructural changes in bone quality in a mouse model of chronic kidney disease and treatment with calcitonin.Bone reports · 2025Article
- Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.Endocrine reviews · 2024Review
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Authors and funding
6 authors.
Funding
Abstract
purposeChronic kidney disease (CKD) and aging are each independently associated with higher fracture risk. Although CKD is highly prevalent in the aging population, the interaction between these two conditions with respect to bone structure and mechanics is not well understood. The purpose of this study was to examine cortical porosity and mechanical properties in skeletally mature young and aging mice with CKD.
methodsCKD was induced by feeding 16-week and 78-week male mice 0.2% adenine (AD) for six weeks followed by two weeks of maintenance on a control diet for a total study duration of eight weeks of CKD; control (CON) animals of each age were fed a standard diet. Serum biochemistries, μCT imaging, and mechanical properties via four-point bending were assessed at the endpoint.
resultsPhosphorus, parathyroid hormone, and blood urea nitrogen were elevated in both ages of AD mice compared to age-matched CON; aging AD mice had PTH and BUN values higher than all other groups. Femoral cortical porosity was more than four-fold higher in aging AD mice compared to young AD mice and more than two-fold higher compared to age-matched controls. Structural and estimated material mechanical properties were both lower in aging mice, but there were no significant interactions between AD treatment and age.
conclusionThese data show an interaction between CKD and aging that produces a more severe biochemical and cortical bone phenotype. This highlights the importance of studying mechanisms and potential interventions in both young and aged animals to translate to a broader spectrum of CKD patients.
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