Redefining the pathogenesis of CKD-MBD: the critical role of FGF-23

Abstract

Through signals between the kidney, parathyroid gland, and bone, alterations in kidney function lead to changes in serum biochemical values that accompany progressive skeletal disease. Abnormalities in mineral and bone metabolism occur early in the course of chronic kidney disease (CKD) and progress as renal function declines. Traditionally, these abnormalities have been ascribed to an early decline in 1,25(OH)2vitamin D (calcitriol) levels, leading to increases in serum PTH and subsequent alterations in calcium and phosphorus metabolism. However, recent studies have revealed that circulating values of fibroblast growth factor 23 (FGF-23), a key regulator of phosphorus and vitamin D metabolism, rise as renal function declines and may play a key initiating role in the development of abnormal mineral metabolism in patients with CKD.