What are the effects of Chronic Kidney Disease (CKD) on the thoracolumbar spine and knees?

Effects of Chronic Kidney Disease on the Thoracolumbar Spine and Knees

Chronic Kidney Disease (CKD) significantly impacts the thoracolumbar spine and knees through mineral and bone disorders (CKD-MBD), leading to increased fracture risk, decreased bone mineral density, and structural changes that compromise mechanical integrity.

Pathophysiological Mechanisms

Bone Metabolism Disturbances

• CKD-MBD begins when GFR falls below 60 mL/min/1.73 m² (Stage 3 CKD), with progressive worsening as kidney function declines 1
• Blood levels of PTH rise and vitamin D [1,25(OH)₂D₃] levels fall at this stage, which are central to the development of bone disease 1
• Disturbances in mineral metabolism, uremic toxins, and alterations in immune, endocrine, neurohormonal, and gut systems contribute to bone abnormalities 1

Thoracolumbar Spine Effects

• CKD leads to reduced bone mineral density (BMD) in the lumbar spine, with the lowest BMD levels found in patients with GFR between 6-26 mL/min/1.73 m² (Stage 4 CKD) 1
• Vertebral structural and mechanical properties are compromised in CKD, affecting both trabecular and cortical bone 2
• High PTH levels result in significantly higher bone formation rates (up to 6-fold) but paradoxically reduce the amount of trabecular and cortical bone in the vertebrae 2
• Thoracolumbar spine films are recommended as part of the diagnostic workup for CKD-MBD 1

Knee and Lower Extremity Effects

• CKD affects the knees through similar mechanisms as the spine, with mineral metabolism disturbances leading to bone quality deterioration 3, 4
• Patients with CKD have increased risk of fractures in weight-bearing joints including knees 4
• Electrolyte imbalances and uremia contribute to nerve dysfunction that can affect knee joint function 5

Diagnostic Approach

Imaging Assessment

• Dual-energy X-ray absorptiometry (DXA) of the thoracolumbar spine is recommended for patients with CKD G3a-G5D if results will impact treatment decisions 6
• DXA BMD predicts fractures across all stages of CKD severity 6
• Thoracic/lumbar spine films are specifically recommended to assess skeletal changes in CKD-MBD 1

Laboratory Assessment

• Monitor serum levels of calcium, phosphate, PTH, and alkaline phosphatase activity beginning in CKD G3a 6
• Frequency of monitoring should be based on CKD stage, with more frequent monitoring in advanced stages 6
• Treatment decisions should be based on trends in PTH levels rather than single values 6

Advanced Diagnostics

• Bone biopsy remains the gold standard for diagnosis and classification of renal osteodystrophy affecting the spine and other skeletal sites 1, 6
• Histomorphometric assessment with double tetracycline labeling provides the most accurate diagnosis of metabolic bone disease in CKD patients 1

Clinical Manifestations

Renal Osteodystrophy

• Manifests in the thoracolumbar spine and knees as bone resorption, periosteal reaction, and potential brown tumors 7
• Can present as osteosclerosis (primarily affecting the axial skeleton), osteoporosis, or osteomalacia 7
• Compromises vertebral mechanical properties, increasing fracture risk 2

Other Musculoskeletal Manifestations

• Secondary hyperparathyroidism leads to bone resorption in subperiosteal, subchondral, trabecular, endosteal, and subligamentous locations 7
• Soft-tissue and vascular calcifications can occur around joints including the knees 8, 7
• Long-term hemodialysis can lead to amyloid deposition, destructive spondyloarthropathy, and tendon rupture affecting both spine and knees 8, 7

Management Considerations

Treatment Approach

• Treatment should target underlying mineral metabolism abnormalities to improve bone health in the thoracolumbar spine and knees 6
• Base treatment on serial assessments of phosphate, calcium, and PTH levels, considered together 6
• Lowering elevated phosphate levels toward the normal range is recommended 6
• Treat metabolic acidosis to improve bone health by reducing bone resorption 6

Pharmacological Interventions

• Treatments that reduce bone remodeling are effective in normalizing vertebral structure and mechanical properties only if they also reduce serum PTH 2
• Anti-sclerostin antibody therapy can enhance bone mass and mechanical properties but only when combined with PTH-suppressive treatment 2
• Consider low-dose active vitamin D supplementation to help control PTH, but monitor for hypercalcemia 6

Monitoring

• Regularly assess response to therapy with laboratory monitoring of mineral metabolism parameters 6
• Continue monitoring BMD in patients receiving treatment for CKD-associated osteoporosis 6
• Recognize that bone disease in CKD is complex with overlapping features of renal osteodystrophy and other forms of osteoporosis 6

Clinical Implications and Prognosis

• CKD-MBD significantly increases the risk of vertebral and non-vertebral fractures compared to the general population 2
• The prevalence of bone abnormalities increases with the duration of hemodialysis 7
• Recognition of musculoskeletal manifestations is important in the clinical management of patients with CKD 7
• Once clinical manifestations of CKD-MBD are identified, measures to mitigate disease severity should be initiated to prevent negative outcomes including bone loss and fractures 1