Adynamic bone disorder in chronic kidney disease: meta-analysis and narrative review of potential biomarkers as diagnosis and therapeutic targets.

Adynamic bone disorder, common in chronic kidney disease (CKD), results from reduced bone turnover, often due to medications such as calcimimetics or high-dose vitamin D analogs that induce low parathyroid hormone (PTH) levels. Numerous factors contributing to PTH hyporesponsiveness, which also induces low bone turnover, include deficient PTH, uremic toxins like indoxyl sulfate, malnutrition, inflammation, and diabetes. Diagnosis typically involves bone biopsy, although it is inconvenient. Biomarkers like bone-specific alkaline phosphatase (BALP) and intact PTH (iPTH) show promise in distinguishing between low and high bone turnover. Meta-analysis suggests that levels of iPTH below 150 pg/mL or BALP levels below 20 μg/l indicate low bone turnover. Treatments aim to improve bone density without hindering repair, with osteo-anabolic medications being favored for low PTH levels and anti-resorptive agents being cautioned. Romosozumab, while effective, has safety concerns that limit its use. Uremic toxins are reduced by AST-120 treatment, which alleviates PTH hypo-responsiveness and bone toxicity. Adjunctive measures include addressing vitamin D deficiency, and diabetes, and utilizing antioxidant and anti-inflammatory therapies. Overall, BALP and iPTH appear as potential promising biomarkers for diagnosing and monitoring adynamic bone disorder in CKD, effectively guiding therapeutic interventions.