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Secondary Hyperparthyroidism: Pathogenesis, Diagnosis, Preventive and Therapeutic Strategies
Mariano Rodríguez Portillo1,2, María E Rodríguez-Ortiz3
1Nephrology Service, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Reina Sofía University Hospital/University of Córdoba, Avda. Menéndez Pidal, S/N, 14004, Córdoba, Spain. juanm.rodriguez.sspa@juntadeandalucia.es.
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Uremic secondary hyperparathyroidism is a multifactorial and complex disease often present in advanced stages of chronic kidney disease. The accumulation of phosphate, the increased FGF23 levels, the reduction in active vitamin D production, and the tendency to hypocalcemia are persistent stimuli for the development and progression of parathyroid hyperplasia with increased secretion of PTH. Parathyroid proliferation may become nodular mainly in cases of advanced hyperparathyroidism. The alterations in the regulation of mineral metabolism, the development of bone disease and extraosseous calcifications are essential components of chronic kidney disease-mineral and bone disorder and have been associated with negative outcomes. The management of hyperparathyroidism includes the correction of vitamin D deficiency and control of serum phosphorus and PTH without inducing hypercalcemia. An update of the leading therapeutic tools available for the prevention and clinical management of secondary hyperparathyroidism, its diagnosis, and the main mechanisms and factors involved in the pathogenesis of the disease will be described in this review.