The major findings were that (i) renal impairment did not markedly alter normal daily variations in circulating minerals or hormonal regulators in low‐normal dietary phosphate conditions, (ii) that the generation of severe hyperphosphatemia in CKD was associated with an attenuated diurnal variation in phosphate and PTH, (iii) the development of VC in CKD was predicted by an early increase in the circulating level of FGF‐23, but not PTH or hyperphosphatemia, and (iv) the presence of VC associated with an altered diurnal variation in circulating phosphate. The gene discussed is FGF23; the disease is hyperphosphatemia.