CKD Patients: The Dilemma of Serum PTH Levels

Abstract

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.

Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

“…Parathyroid hormone (PTH) levels are associated with increased cardiovascular risk in CKD patients [21]. miR-223 presented a strong negative correlation with PTH, while miR-155 was positively correlated with PTH.…”

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

“…Upregulation of phosphorus, FGF-23, and parathyroid hormone is associated with worsening kidney disease and a higher likelihood of death [17,18]. This study demonstrated a marked decrease in adenineinduced increases in serum phosphorus, FGF-23, and parathyroid hormone levels in rats, suggesting the preventative effects of resveratrol against adenine-mediated kidney disorders.…”

Rosiglitazone alleviates injury in rats with adenine-induced chronic kidney disease

“…Mineral and bone metabolism may be viewed as a complex system in which three hormones (PTH, calcitriol and FGF-23) act on three key organs (the kidneys, intestines and bones) to adjust plasma, calcium and phosphorus concentrations (19). Mineral disorders, including an increase in FGF-23 and PTH, and hyperphosphatemia, are independent risk factors in CKD progression and mortality (3,20,21). The present data revealed that ROG reduced the serum levels of FGF-23, PTH and phosphorus in the CKD rats, indicating that ROG may have a beneficial effect on the kidney through the attenuation of mineral disorders in adenine-induced CKD models.…”