ReviewNutrients2018
Energy-Dense Diets and Mineral Metabolism in the Context of Chronic Kidney Disease⁻Metabolic Bone Disease (CKD-MBD).
Review in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Association of Energy and Macronutrients Intake with S-Klotho Plasma Levels in Middle-Aged Sedentary Adults: A Cross-Sectional Study.The journal of nutrition, health & aging · 2022Article
- Bone Quality in Chronic Kidney Disease Patients: Current Concepts and Future Directions - Part II.Kidney diseases (Basel, Switzerland) · 2021Review
- The Influence of Dietary Interventions on Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD).Nutrients · 2021Review
- Review
- Dietary Habits, Vitamin and Mineral Supplements in Patients with Chronic Kidney Disease (CKD).Nutrients · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The aim of this paper is to review current knowledge about the interactions of energy-dense diets and mineral metabolism in the context of chronic kidney disease⁻metabolic bone disease (CKD-MBD). Energy dense-diets promote obesity and type II diabetes, two well-known causes of CKD. Conversely, these diets may help to prevent weight loss, which is associated with increased mortality in advanced CKD patients. Recent evidence indicates that, in addition to its nephrotoxic potential, energy-dense food promotes changes in mineral metabolism that are clearly detrimental in the context of CKD-MBD, such as phosphorus (P) retention, increased concentrations of fibroblast growth factor 23, decreased levels of renal klotho, and reduction in circulating concentrations of calcitriol. Moreover, in uremic animals, a high fat diet induces oxidative stress that potentiates high P-induced vascular calcification, and these extraskeletal calcifications can be ameliorated by oral supplementation of vitamin E. In conclusion, although energy-dense foods may have a role in preventing undernutrition and weight loss in a small section of the CKD population, in general, they should be discouraged in patients with renal disease, due to their impact on P load and oxidative stress.
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Registered trials
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