Skip to main content
. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Semin Nephrol. 2018 Nov;38(6):542–558. doi: 10.1016/j.semnephrol.2018.08.001

Figure 1. Simplified Schematic of Mineral and Bone Disorder (MBD) Physiology in Chronic Kidney Disease.

Figure 1.

Solid lines and arrows depict dominant physiologic effects on circulating MBD factors including: (1) effects of fibroblast growth factor 23 (FGF23) to lower serum phosphorus by inhibiting 1α-hydroxylase that converts 25-hydroxyvitamin D (25-D) to 1,25-dihydroxyvitamin D (1,25-D) and stimulating urinary phosphorus excretion; (2) effects of parathyroid hormone (PTH) to raise serum calcium by stimulating 1α-hydroxylase and increasing urinary calcium reabsorption and bone remodeling; (3) effects of vitamin D to promote gastrointestinal absorption of calcium and phosphorus and feedback on FGF23 (stimulation) and PTH (inhibition). Dashed lines and arrows depict additional non-dominant effects of FGF23 to increase urinary calcium reabsorption and PTH to increase urinary phosphorus excretion and FGF23 transcription. In each case, arrows (→) represent actions that raise the associated MBD factor whereas capped lines (┤) represent actions that lower the associated MBD factor. Altogether, the physiology encompasses major effects of FGF23 to reduce phosphorus and vitamin D and major effects of PTH to increase calcium and vitamin D, along with substantial redundancy, feedback, and crosstalk.