The initial theory that reduced UCaE during the progression of kidney disease was due to decreased renal production of 1,25(OH)2D3 leading to inadequate absorption of calcium from the gastrointestinal tract and increased PTH stimulating enhanced renal tubule calcium reabsorption has been disproven by studies on vitamin D supplementation or decreased PTH, which have failed to alter UCaE in humans [16,17,18]. This evidence concerns the gene PTH and kidney disorder.