Treatment of Hyperphosphatemia
For patients with elevated phosphate levels, begin with dietary phosphate restriction to 800-1,000 mg/day, then add phosphate binders if levels remain persistently elevated, starting with calcium-based binders (limiting elemental calcium to ≤1,500 mg/day) in early CKD stages, but strongly preferring non-calcium binders (sevelamer or lanthanum) in dialysis patients with vascular calcification, hypercalcemia, or suppressed PTH. 1, 2
When to Initiate Treatment
- Only treat progressively or persistently elevated phosphate levels—not isolated single values or for prevention. 3, 1, 4
- Base treatment decisions on serial assessments of phosphate, calcium, and PTH considered together, not phosphate alone. 3, 1, 2
- The target is to lower elevated phosphate toward the normal range (3.5-5.5 mg/dL for dialysis patients). 3, 2
Step 1: Dietary Phosphate Restriction (First-Line)
- Limit dietary phosphate intake to 800-1,000 mg/day while maintaining adequate protein intake of 1-1.2 g/kg/day. 1, 2, 4
- Consider phosphate source when counseling patients: 3, 1, 4
- Animal-based phosphate: 40-60% absorbed
- Plant-based phosphate (with phytates): 20-50% absorbed
- Inorganic phosphate in food additives: >90% absorbed
- Avoid processed foods with phosphate additives, which have the highest bioavailability. 1, 4
- Dietary restriction alone is usually insufficient in most CKD patients, requiring addition of binders. 4
Step 2: Phosphate Binders
For CKD Stages 3a-4 (Non-Dialysis)
- Start with calcium-based binders (calcium acetate or calcium carbonate) when serum phosphorus exceeds 4.6 mg/dL despite dietary restriction. 2, 4
- Calcium acetate combines with dietary phosphate in the gut to form insoluble calcium phosphate complex, which is excreted in feces. 5
- Limit elemental calcium from binders to ≤1,500 mg/day, with total calcium intake (including dietary) not exceeding 2,000 mg/day. 3, 2, 4
- Calcium acetate dosing: Start with 2 capsules (667 mg each = 169 mg elemental calcium per capsule) per meal, titrate as needed. 5
For CKD Stage 5D (Dialysis Patients)
- Either calcium-based or non-calcium binders can be used as primary therapy, but strongly prefer non-calcium binders in these high-risk situations: 1, 2
- Severe vascular or soft-tissue calcifications present
- Hypercalcemia (corrected calcium >10.2 mg/dL)
- Suppressed PTH (<150 pg/mL)
- Adynamic bone disease
- Non-calcium binder options: 1, 2, 6, 7
Critical Dosing Limits
- Never use calcium-based binders in hypercalcemic patients or those with PTH <150 pg/mL—this worsens outcomes. 2, 4
- Restrict calcium-based binder doses to avoid excess calcium exposure, which contributes to cardiovascular calcification across all CKD stages. 3, 2, 4
Aluminum-Based Binders
- Avoid long-term use of aluminum-containing binders due to aluminum toxicity risk. 3, 1, 6, 7
- May use short-term only (maximum 4 weeks, single course) for severe hyperphosphatemia (>7.0 mg/dL), then switch to other agents. 4
Step 3: Combination Therapy
- If hyperphosphatemia persists (>5.5 mg/dL) despite monotherapy, combine calcium-based and non-calcium-based binders for additive benefit. 1, 2, 4
Step 4: Increase Dialytic Phosphate Removal
- For dialysis patients with persistent hyperphosphatemia despite binders, increase dialytic phosphate removal by considering more frequent or longer dialysis sessions. 3, 1, 2, 4
- Use dialysate calcium concentration between 1.25-1.50 mmol/L (2.5-3.0 mEq/L). 3, 1, 2
- Conventional hemodialysis three times weekly removes approximately 900 mg phosphorus per session. 9
Monitoring Targets
- Maintain corrected total serum calcium in the normal range, preferably 8.4-9.5 mg/dL (lower end of normal) for dialysis patients. 2, 4, 9
- Avoid hypercalcemia in all adult CKD patients. 3, 1
- Maintain calcium × phosphorus product <55 mg²/dL². 2, 9
- Monitor phosphate and calcium every 1-3 months in CKD G5D, every 3-6 months in CKD G4. 3
Management of Secondary Hyperparathyroidism
- Evaluate patients with progressively rising or persistently elevated PTH for modifiable factors: hyperphosphatemia, hypocalcemia, high phosphate intake, and vitamin D deficiency. 3, 1, 2
- Correcting hyperphosphatemia is the critical first step before addressing PTH directly. 2
- For CKD G5D patients requiring PTH-lowering therapy, maintain intact PTH in the range of approximately 2-9 times the upper normal limit (roughly 130-585 pg/mL). 1, 2
Special Populations
- In children with CKD G3a-G5D, base phosphate binder choice on serum calcium levels and maintain calcium in age-appropriate normal range. 3, 1, 2
Critical Pitfalls to Avoid
- Patients with vascular or valvular calcification are at highest cardiovascular risk—this should guide management toward non-calcium binders. 3, 1, 2
- Overly aggressive PTH suppression can lead to adynamic bone disease; normal or low PTH in ESRD may indicate this problematic condition. 1, 2
- Excess calcium exposure from calcium-based binders may contribute to cardiovascular calcification across all CKD stages. 2, 4
- Sevelamer can decrease bioavailability of ciprofloxacin by 50% and reduce mycophenolate levels; separate dosing by several hours. 8
- Cases of increased TSH have been reported with sevelamer and levothyroxine coadministration. 8
- Take calcium acetate with meals for optimal phosphate binding; counsel patients to avoid calcium supplements and nonprescription antacids. 5