Management of secondary hyperparathyroidism: how and why?

Secondary hyperparathyroidism (SHPT) is a common complication in chronic kidney disease. Currently, various treatment options are available, including vitamin D receptor activators, cinacalcet hydrochloride, and parathyroidectomy. These treatment options have contributed to the successful control of SHPT, and recent clinical studies have provided evidence suggesting that effective treatment of SHPT leads to improved survival. Although bone disease is the most widely recognized consequence of SHPT and remains a major target for treatment of SHPT, there is increasing evidence that parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), both of which are markedly elevated in SHPT, have multiple adverse effects on extraskeletal tissues. These actions may lead to the pathological development of left ventricular hypertrophy, renal anemia, immune dysfunction, inflammation, wasting, muscle atrophy, and urate accumulation. Given that treatment of SHPT leads to decreases in both PTH and FGF23, these data provide an additional rationale for treating SHPT. However, definitive evidence is still lacking, and future research should focus on whether treatment of SHPT prevents the adverse effects of PTH and FGF23.