At the same time, mechanisms specific to end-stage renal disease, such as the phosphate driven, FGF 23/klotho induced inhibition of 25 D3 1-alpha hydroxylation, or the accumulation of inactive PTH fractions and fragments, have a high force on the increment of PTH, resulting in up to tenfold increased levels of both noxPTH and PTHi [23,24,53]. Here, PTH is linked to chronic kidney disease.