In CKD, the renal capacity to synthesize active vitamin D is reduced as a result of the enzyme 1-alpha-hydroxylase’s lower activity, which is ordinarily upregulated by PTH to convert 25-hydroxyvitamin D into its biologically active form, 1,25-dihydroxyvitamin D. The resulting deficiency in active vitamin D diminishes intestinal calcium absorption, triggers compensatory PTH secretion, promotes parathyroid gland hyperplasia, and leads to the development of secondary hyperparathyroidism. This evidence concerns the gene PTH and chronic kidney disease.