Adynamic Bone Disease in Chronic Kidney Disease: From PTH Suppression-Driven Remodeling Phenotype to Osteoanabolic Therapy. (PubMed, Am J Nephrol) - Sep 1, 2026 - "ABD in advanced CKD represents a PTH suppression-driven skeletal remodeling phenotype characterized by osteoblast, osteoclast, and osteocyte dysfunction together with disruption of osteoblast-osteoclast coupling. Suppression of Wnt/β-catenin signaling, elevated sclerostin expression, impaired mechanotransduction, skeletal resistance to PTH, and accumulation of uremic toxins collectively contribute to globally reduced remodeling activity and defective microdamage repair. In the context of markedly suppressed bone turnover, antiresorptive therapy is biologically unlikely to confer skeletal benefit and may exacerbate impairment of bone remodeling and renewal. By contrast, anabolic strategies aimed at restoring PTH1R-dependent bone formation and remodeling activation are mechanistically appropriate in CKD-associated ABD. Current evidence suggests that intermittent PTH analog therapy, particularly teriparatide, may improve bone formation markers, bone mineral density,..."
Journal • Review • Cardiovascular • Chronic Kidney Disease • Inflammation • Musculoskeletal Diseases • Nephrology • Orthopedics • Renal Disease • FGF23 • SOST
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Chia-Chao Wu; Chien-Lin Lu; Kuo-Cheng Lu; Kuo-Chin Hung; Te-Chao Fang; Yi-Chou Hou
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