As a result of rapid proteolytic cleavage in circulation, PTH exists as intact PTH (1–84) and various fragments, that is, N-terminal, mid-region and C-terminal PTH, the most abundant being 7–84 PTH.6 Although the plasma half-life of PTH (1–84) is between 2 and 4 min, C-terminal PTH fragments have a longer half-life of several hours because of renal clearance.6,7 The latter may account for more than 20% of circulating PTH in normal kidney function individuals and up to 45% in patients with renal failure.6 This heterogeneity of PTH in circulation has made its measurement challenging. The gene discussed is PTH; the disease is kidney failure.