Nonetheless, these directions are biologically credible: CKD causes mineral metabolism abnormalities, secondary hyperparathyroidism, and cortical bone loss as components of CKD–MBD [33], while systemic inflammation, reduced mobility, elevated RANKL activity, and frequent use of glucocorticoids contribute to greater fracture risk in RA [34]. This evidence concerns the gene TNFSF11 and secondary hyperparathyroidism.