To demonstrate specific CKD-induced effects on bone independent of the dysregulation of PTH, active vitamin D, calcium and phosphate, Lund et al. applied a low phosphate diet (0.2%) in CKD mice and supplemented calcitriol to compensate for the lack of renal synthesis of the bioactive form of vitamin D and to prevent HPT and by this was able to also maintain serum phosphate and calcium levels in the normal range [40]. Here, PTH is linked to chronic kidney disease.