Patients, whose end stage renal disease is likely to upregulate the level of PTHi and noxPTH via several mechanisms: (a) Impaired clearance of non-functional or only partially functional, oxidised PTH [20], (b) decreased clearance of receptor modulating PTH fragments [21,23,24,53], (c) The regulatory cascade of renal function decline, starting with deteriorating phosphate clearance, ensuing increase in FGF23 levels, decrease of 1,25 D3 and hypocalcaemia, resulting in secondary renal hyperparathyroidism [47]. This evidence concerns the gene FGF23 and chronic kidney disease.