Secondary hyperparathyroidism (SHP) associated with chronic kidney disease (CKD) represents a significant health concern, contributing to morbidity and mortality. Despite its clinical importance, the underlying causes of CKD-SHP and the related parathyroid signaling pathways remain elusive. Our previous research demonstrated the activation of the parathyroid mTORC1 pathway in CKDSHP. Utilizing novel genetically modified mouse models and clinical data from 106 healthcare organizations, we reveal intricate connections between mTORC1 activity, parathyroid gland structure, and the response to CKD.
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Naveh‐Many et al. (2024) studied this question.
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