Control del fósforo y prevención de fracturas en el paciente renal / Control of phosphorus and prevention of fractures in the kidney patient

El paciente con enfermedad renal tiene incrementado el riesgo de fracturas, y a los factores habituales de la población general se suman otros propios de la uremia. Los mecanismos que favorecen las fracturas en la uremia no son suficientemente conocidos, aunque es ampliamente aceptado que la disminución del contenido mineral óseo y la alteración en la arquitectura ósea son responsables de un aumento en la fragilidad ósea. Con la progresión de la enfermedad renal crónica (ERC), el riesgo de fractura aumenta, siendo especialmente evidente cuando el paciente requiere diálisis. Dentro de las numerosas causas implicadas en el aumento de fracturas óseas se encuentran la edad avanzada, la amenorrea, la exposición a esteroides, el descenso de la vitamina D, el aumento de la hormona paratiroidea (PTH) y también la desnutrición y la inflamación crónica. La concentración de fósforo sérico ya sea alto o muy bajo también se ha correlacionado con el riesgo de fractura. El aumento del fosfato sérico puede afectar el metabolismo óseo directamente e indirectamente a través del desarrollo de mecanismos hormonales adaptativos que tratan de prevenir la hiperfosfatemia, como el aumento de PTH y el factor de crecimiento de fibroblastos 23 (FGF23), y la disminución del calcitriol. Estos mecanismos de adaptación son de menor intensidad si la absorción intestinal de fosforo se disminuye con el uso de captores de fósforo; los cuales parecen tener un impacto positivo en la reducción del riesgo de fracturas. En este documento se describirán los posibles mecanismos que relacionan el riesgo de fracturas con: los niveles de fósforo sérico, los mecanismos adaptativos propios de la enfermedad renal y el uso de fármacos para controlar la hiperfosfatemia. No existen estudios que proporcionen evidencia sobre la influencia de diversos tratamientos en el riesgo de fracturas en pacientes con enfermedad renal crónica. Sugerimos que el control del fósforo debería ser un objetivo a tener en cuenta

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

Control of phosphorus and prevention of fractures in the kidney patient. / Control del fósforo y prevención de fracturas en el paciente renal.

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.