What is the management of renal osteodystrophy?

Management of Renal Osteodystrophy

The management of renal osteodystrophy should be based on serial assessments of phosphate, calcium, and PTH levels, considered together, with treatment tailored to address specific biochemical abnormalities while preventing complications related to bone turnover disorders. 1, 2

Diagnosis and Assessment

• Begin monitoring serum levels of calcium, phosphate, PTH, and alkaline phosphatase activity starting in CKD G3a (eGFR 45-59 ml/min/1.73m²) 1, 2
• Frequency of monitoring should be based on CKD stage:
  • CKD G3a-G3b: calcium and phosphate every 6-12 months; PTH based on baseline level and CKD progression 1
  • CKD G4: calcium and phosphate every 3-6 months; PTH every 6-12 months 1
  • CKD G5/G5D: calcium and phosphate every 1-3 months; PTH every 3-6 months 1
• Bone mineral density (BMD) testing is recommended for patients with CKD G3a-G5D if results will impact treatment decisions 1, 2
• Bone biopsy remains the gold standard for diagnosis and classification of renal osteodystrophy, particularly when knowledge of the type will impact treatment decisions 1, 2
• Lateral abdominal radiographs can detect vascular calcification, and echocardiograms can detect valvular calcification, both of which indicate highest cardiovascular risk 1

Management of Phosphate and Calcium Abnormalities

• Phosphate management:

  • Target lowering elevated phosphate levels toward the normal range 1
  • Base phosphate-lowering treatment on progressively or persistently elevated serum phosphate, not single values 1
  • Limit dietary phosphate intake, considering phosphate source (animal, vegetable, additives) 1, 3
  • For patients with hyperphosphatemia, restrict the dose of calcium-based phosphate binders to avoid calcium loading 1
  • Avoid long-term use of aluminum-containing phosphate binders due to risk of aluminum intoxication 1
  • For CKD G5D patients with persistent hyperphosphatemia, consider increasing dialytic phosphate removal 1

• Calcium management:

  • Avoid hypercalcemia in adult patients with CKD G3a-G5D 1, 2
  • For CKD G5D patients, use a dialysate calcium concentration between 1.25 and 1.50 mmol/l (2.5 and 3.0 mEq/l) 1
  • Ensure adequate calcium intake through diet and supplements while avoiding excessive calcium loading 1, 2

Management of PTH Abnormalities

• For CKD G3a-G5 (not on dialysis):

  • Evaluate patients with progressively rising or persistently elevated PTH for modifiable factors: hyperphosphatemia, hypocalcemia, high phosphate intake, and vitamin D deficiency 1, 3
  • Avoid routine use of calcitriol and vitamin D analogs due to risk of hypercalcemia 1
  • Reserve calcitriol and vitamin D analogs for patients with CKD G4-G5 with severe and progressive hyperparathyroidism 1

• For CKD G5D (dialysis patients):

  • Maintain intact PTH levels in the range of approximately 2 to 9 times the upper normal limit for the assay 1
  • For PTH-lowering therapy, options include calcimimetics (e.g., cinacalcet), calcitriol, vitamin D analogs, or a combination 1
  • Cinacalcet works by increasing sensitivity of the calcium-sensing receptor to activation by extracellular calcium, directly lowering PTH levels 4
  • Consider parathyroidectomy for patients with severe hyperparathyroidism who fail to respond to medical therapy 1, 3

Bone-Specific Management

• Treatment choices should consider the magnitude and reversibility of biochemical abnormalities and CKD progression 1
• For patients with low BMD and/or fragility fractures, consider bone biopsy to determine the type of renal osteodystrophy before initiating antiresorptive therapy 1
• Be cautious with denosumab in advanced CKD due to risk of severe hypocalcemia; evaluate for CKD-MBD before initiating therapy 5
• Avoid treatments that may exacerbate existing bone turnover abnormalities (e.g., antiresorptives in low turnover disease) 1, 2

Monitoring and Follow-up

• Base treatment decisions on trends in laboratory values rather than single measurements 1, 2
• Monitor for adverse effects of therapies:
  • Hypercalcemia with vitamin D compounds 6, 7
  • Hypocalcemia with calcimimetics 4, 8
  • Adynamic bone disease from oversuppression of PTH 1, 9
• Regularly assess bone health through biochemical markers and, when indicated, imaging or bone biopsy 2, 8

Common Pitfalls and Considerations

• Avoid focusing on a single parameter; the interplay among phosphate, calcium, and PTH is complex 1, 3
• Be aware that treatments targeting one abnormality often affect others (e.g., calcium-based phosphate binders may lead to hypercalcemia and PTH suppression) 1, 2
• The prevalence of adynamic bone disease has increased, possibly due to aggressive use of calcium-based binders and vitamin D analogs 9, 7
• Vascular calcification is associated with positive calcium and phosphate balance, contributing to cardiovascular risk 1, 10
• Recognize that bone disease in CKD is complex with overlapping features of different types of renal osteodystrophy 2, 8