Kidney-bone axis: Emerging paradigms in cross-talk between renal function and skeletal health

Figure 1 The figure illustrates both physiological and pathological kidney related conditions which influence bone-mineral metabolism. The figure was created using BioRender (https://biorender.com). A: Under physiological conditions, increased phosphate stimulates the bone to secrete fibroblast growth factor (FGFR)-23, which binds to the FGFR1 receptor with the assistance of the co-receptor klotho. This functional complex is primarily expressed in the distal convoluted tubule and parathyroid glands, where it regulates calcium and phosphate homeostasis; B: In chronic kidney disease, reduced kidney function causes hyperphosphatemia, hypocalcemia, klotho deficiency, and reduced calcitriol production, preventing proper FGF23-receptor binding. These alterations lead to parathyroid hyperplasia and secondary hyperparathyroidism, resulting in vascular calcifications and renal osteodystrophy characterized by increased bone fragility. FGFR: Fibroblast growth factor; PTH: Parathyroid hormone; CKD: Chronic kidney disease.