It is this period of rapid CKD‐MBD progression, where the increased PTH and FGF23 moves from appropriate compensation for decreased renal excretion of phosphate to a state where the persistent increase of PTH and FGF23 can no longer compensate, and end‐organ effects of CKD‐MBD such as bone loss due to cortical porosity, vascular calcification, and LVH ensue in humans,[38] as we saw in our rats. Here, PTH is linked to chronic kidney disease.