Management of Hyperphosphatemia in Chronic Kidney Disease
The management of hyperphosphatemia in CKD patients should focus on lowering elevated phosphate levels toward the normal range through dietary phosphate restriction, appropriate phosphate binders, and increased dialytic removal in patients on dialysis. 1
Evaluation and Monitoring
- Treatment decisions should be based on serial assessments of phosphate, calcium, and PTH levels, considered together rather than in isolation 1
- Phosphate-lowering treatment should be initiated for progressively or persistently elevated serum phosphate, not for prevention or isolated single elevated values 1
- Regular monitoring of calcium, phosphorus, and PTH levels is essential, with PTH measurements recommended at least every 3 months in ESRD patients 2
Dietary Management
- Limiting dietary phosphate intake is recommended as a first-line approach for treating hyperphosphatemia, either alone or in combination with other treatments 1
- Consider phosphate source when making dietary recommendations - animal-based phosphate is absorbed at 40-60%, plant-based phosphate (with phytates) at 20-50%, while inorganic phosphate in food additives has much higher absorption 1, 3
- Focus patient education on identifying and avoiding "hidden" sources of phosphate, particularly in processed foods with phosphate-containing additives 1, 4
Pharmacological Management
Phosphate Binders
For patients with CKD G3a-G5D with persistently elevated phosphate levels, phosphate binders are indicated 1
Choice of phosphate binder should consider:
- CKD stage
- Presence of other CKD-MBD components
- Concomitant therapies
- Side effect profile 1
In adult patients with CKD G3a-G5D receiving phosphate-lowering treatment, restrict the dose of calcium-based phosphate binders 1
Avoid long-term use of aluminum-containing phosphate binders due to risk of aluminum toxicity 1
Non-calcium-based binders like sevelamer have shown efficacy in lowering serum phosphorus by approximately 2 mg/dL in clinical trials 5
Resin-based binders (sevelamer, colestilan) may lead to less vascular calcification but can cause gastrointestinal side effects 6
Management of Secondary Hyperparathyroidism
- Patients with progressively rising or persistently elevated PTH should be evaluated for modifiable factors including hyperphosphatemia, hypocalcemia, high phosphate intake, and vitamin D deficiency 1
- For patients with CKD G5D, maintain intact PTH levels in the range of approximately 2-9 times the upper normal limit 1, 2
- In patients with severe hyperparathyroidism who fail to respond to medical therapy, parathyroidectomy should be considered 1
Dialysis Management
- For patients on dialysis (CKD G5D) with persistent hyperphosphatemia, increasing dialytic phosphate removal is recommended 1
- Use a dialysate calcium concentration between 1.25 and 1.50 mmol/l (2.5 and 3.0 mEq/l) 1
Special Considerations
- Patients with vascular or valvular calcification should be considered at highest cardiovascular risk 1
- In children with CKD G3a-G5D, base the choice of phosphate-lowering treatment on serum calcium levels and maintain serum calcium in age-appropriate normal range 1
- Avoid hypercalcemia in adult patients with CKD G3a-G5D 1
Emerging Therapies
- Novel therapeutic targets include gastrointestinal transport proteins:
- These agents may overcome limitations of existing phosphate-lowering strategies by reducing phosphate uptake from the gut 7
Potential Pitfalls and Caveats
- Overly aggressive PTH suppression can lead to adynamic bone disease 2
- Excess calcium exposure from calcium-based binders may contribute to cardiovascular calcification 1, 9
- Normal or low PTH levels in ESRD may indicate adynamic bone disease, which is also problematic 2
- Treatment decisions should consider trends in PTH levels rather than single values 2
- Sevelamer may interact with certain medications, including ciprofloxacin, mycophenolate mofetil, levothyroxine, cyclosporine, and tacrolimus 5