Mineral and Bone Disease in CKD and Kidney Transplantation: Controversies, Gaps, and a Path Forward
Abstract
The pathophysiology of chronic kidney disease (CKD)-related mineral and bone disorder (CKD-MBD) extends far beyond simple mineral imbalances. Evolving from the traditional understanding of secondary hyperparathyroidism, the conceptual framework has recently been updated to recognize 2 distinct but overlapping clinical syndromes: CKD-associated osteoporosis, which encompasses the significantly increased fracture risk and microarchitectural deterioration in this population; and CKD-associated cardiovascular disease, which accounts for vascular and structural cardiac abnormalities, including medial vascular calcification. Unlike traditional osteoporosis, the 2 clinical syndromes emerge from intricate interactions between declining kidney function and dysregulated mineral metabolism. The early rise in fibroblast growth factor-23 (FGF-23) levels; progressive phosphate retention; diminished vitamin D activation; secondary hyperparathyroidism; and uremic toxin accumulation, particularly uric acid and indoxyl sulfate, orchestrate profound disruptions in osteocyte, osteoblast, and osteoclast function. The complex interaction amplifies in the dialysis population, where protein-energy wasting affects most patients; and intensifies following kidney transplantation because of glucocorticoid, immunosuppressive, and anticoagulant treatments. Consequently, fracture rates in patients with CKD exceed those of age-matched controls by >4-fold, with patients on dialysis therapy facing a ≤ 8-fold…
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