Control of phosphorus and prevention of fractures in the kidney patient
Por:
González-Parra E, Bover J, Herrero J, Sánchez E, Molina P, Martin-Malo A, Bajo Rubio MA, Lloret S, Navarro J and Arenas MD
Publicada:
1 ene 2021
Ahead of Print:
25 sep 2020
Resumen:
Patients with chronic kidney disease have a higher risk of fractures than the general population due to the added factor of uraemia. Although the mechanisms behind uraemia associated fractures are not fully understood, it is widely accepted that the decrease in bone mineral content and alteration in bone architecture both increase bone fragility. As chronic kidney disease progresses, the risk of fracture increases, especially once the patient requires dialysis. Among the many causes of the increased risk are advanced age, amenorrhoea, steroid exposure, decreased vitamin D, increased parathyroid hormone (PTH), malnutrition and chronic inflammation. Serum phosphorus, whether high or very low, seems to correlate with the risk of fracture. Moreover, increased serum phosphate is known to directly and indirectly affect bone metabolism through the development of adaptive hormonal mechanisms aimed at preventing hyperphosphataemia, such as the increase in PTH and fibroblast growth factor 23 (FGF23) and the reduction in calcitriol. These adaptive mechanisms are less intense if the intestinal absorption of phosphorus is reduced with the use of phosphorus captors, which seem to have a positive impact in reducing the risk of fractures. We describe here the possible mechanisms associating serum phosphorus levels, the adaptive mechanisms typical in kidney disease and the use of drugs to control hyperphosphataemia with the risk of fractures. We found no studies in the literature providing evidence on the influence of different treatments on the risk of fractures in patients with chronic kidney disease. We suggest that control of phosphorus should be an objective to consider. (C) 2020 Sociedad Espanola de Nefrologia. Published by Elsevier Espana, S.L.U.
Filiaciones:
González-Parra E:
Hospital Universitario Fundación Jiménez Díaz, Madrid, España
Bover J:
Fundación Puigvert, Barcelona, España
Herrero J:
Hospital Clínico, Madrid, España
Sánchez E:
Hospital Universitario de Cabueñes, Gijón, España
:
Hospital de Peset, Valencia, España
Martin-Malo A:
Hospital Reina Sofía, Córdoba, España
Bajo Rubio MA:
Hospital de La Paz, Madrid, España
Lloret S:
Fundación Puigvert, Barcelona, España
Navarro J:
Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, España
Arenas MD:
Hospital del Mar, Barcelona, España
Green Published, gold
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