A mathematical model of parathyroid gland biology

We built a model of the parathyroid gland biology in hemodialysis patients based on the regulation of the calcium ‐sensing receptor. The model spans several timescales, from the fast release of parathyroid hormone in the case of induced hypocalcemia to the development of cell hyperplasia in the case of reduced phosphate clearance and impaired vitamin D metabolism. The model provides a ready‐to‐use tool to analyze the complex system underlying secondary hyperparathyroidism. AbstractAltered parathyroid gland biology in patients with chronic kidney disease (CKD) is a major contributor to chronic kidney disease ‐mineral bone disorder (CKD‐MBD). This disorder is associated with an increased risk of bone disorders, vascular calcification, and cardiovascular events. Parathyroid hormone (PTH) secretion is primarily regulated by the ionized calcium concentration as well as the phosphate concentration in the extracellular fluid and vitamin D. The metabolic disturbances in patients with CKD lead to alterations in the parathyroid gland biology. A hallmark of CKD is secondary hyperparathyroidism, characterized by an increased production and release of PTH, reduced expression of calcium‐sensing and vitam in D receptors on the surface of parathyroid cells, and hyperplasia and hypertrophy of these cells. These alterations happen on different timescales and influence each other, thereby triggering a cascade of negative and positive feedback loops in a highly complex manner. Due to...
Source: Physiological Reports - Category: Physiology Authors: Tags: Original Research Source Type: research