Recent observational studies of patients with stage 3–5 chronic kidney disease (CKD) not undergoing dialysis have shown that even slight increases in parathyroid hormone (PTH) levels are associated with an increased cardiovascular risk, regardless of the serum levels of calcium and phosphorus and vitamin D therapy. These studies suggest paying particular attention to monitoring PTH levels from the early stages of CKD, and preventing any mineral metabolism disorders that may trigger the excessive synthesis and secretion of PTH. However, it is not easy to determine when an appropriate response becomes maladaptive and requires the pharmacological suppression of the parathyroid gland because the gland’s adaptive response can vary widely from one person to another. Furthermore, PTH levels are not always a good predictor of bone turnover and current PTH assays have various methodological limitations. Treating the early mineral metabolism abnormalities of CKD may help prevent the cardiovascular complications whose frequency, costs and mortality have a profound effect on society as a whole. For this reason, there is great interest in establishing adequate target ranges for PTH at different stages of CKD, and determining the most appropriate strategies for reaching them.

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