Bibliographic Details
| Title: |
Diálogos entre investigadores básicos y clínicos: hiperfosfatemia. |
| Alternate Title: |
Dialogues between basic and clinical researchers: hyperphosphatemia. |
| Authors: |
Rodríguez García, Minerva1, Naves Díaz, Manuel2 mnaves.huca@gmail.com |
| Source: |
Journal of Osteoporosis & Mineral Metabolism / Revista de Osteoporosis y Metabolismo Mineral (Spanish edition). Oct-Dec2024, Vol. 16 Issue 4, p149-153. 10p. |
| Subjects: |
CHRONIC kidney failure, INTESTINAL absorption, METABOLIC regulation, KIDNEY physiology, CALCIFEDIOL |
| Abstract (English): |
Physiological regulation of mineral metabolism is determined by serum levels of phosphorus, FGF23, Klotho, PTH, calcidiol, and calcium. When renal function is normal, the kidney, bone, parathyroid tissue, and intestine collaborate effectively in maintaining this regulation, even in cases of phosphorus excess. The issue arises when renal function is compromised, as the regulators of mineral metabolism become altered, including decreased soluble Klotho, increased PTH and FGF23, and subsequent reductions in calcidiol and calcium. These changes lead to vascular and bone abnormalities, with significant impacts on the morbidity and mortality of renal patients. From a therapeutic standpoint, dietary phosphorus restriction is the initial approach for controlling hyperphosphatemia in patients with chronic kidney disease (CKD). When dietary measures are insufficient, phosphorus binders are used to limit intestinal absorption of this ion. In summary, it is crucial to identify and treat hyperphosphatemia adequately to achieve comprehensive clinical improvements, including a significant reduction in mortality. [ABSTRACT FROM AUTHOR] |
| Abstract (Spanish): |
La regulación fisiológica del metabolismo mineral viene determinada por los niveles séricos de fósforo, FGF23, Klotho, PTH, calcidiol y calcio. Aunque haya un exceso de fósforo, cuando la función renal es normal existe un adecuado funcionamiento del riñón, hueso, tejido paratiroideo e intestino, órganos todos ellos implicados en la regulación del metabolismo mineral. El problema es cuando la función renal se encuentra comprometida ya que los reguladores del metabolismo mineral se ven alterados con un descenso de Klotho soluble, incrementos de PTH y FGF23 y posterior descenso del calcidiol y calcio. Todo ello va a conducir al desarrollo de alteraciones vasculares y óseas, con consecuencias muy importantes en la morbimortalidad de los pacientes renales. Desde el punto de vista terapéutico, en los pacientes con enfermedad renal crónica, la medida inicial para el control de hiperfosfatemia es restringir la ingesta dietética de fósforo. En caso de no lograrlo, disponemos de los captores de fósforo que actúan limitando la absorción intestinal de este ion. Por tanto y a modo de resumen, es crucial subrayar la importancia de identificar y tratar adecuadamente la hiperfosfatemia para lograr una mejora integral en los resultados clínicos, incluyendo una reducción significativa de la mortalidad. [ABSTRACT FROM AUTHOR] |
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Copyright of Journal of Osteoporosis & Mineral Metabolism / Revista de Osteoporosis y Metabolismo Mineral (Spanish edition) is the property of Ibanez y Plaza and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| Database: |
MedicLatina |
