Management of Hyperphosphatemia in Chronic Kidney Disease
In patients with CKD G3a-G5D, initiate treatment only for progressively or persistently elevated serum phosphate—not for prevention—starting with dietary phosphate restriction, followed by phosphate binders with restricted calcium-based binder dosing, and increasing dialytic removal in dialysis patients with persistent hyperphosphatemia. 1, 2
When to Initiate Treatment
- Base treatment decisions on serial assessments of phosphate, calcium, and PTH levels considered together, not isolated single values 1, 2
- Start phosphate-lowering therapy only for progressive or persistent hyperphosphatemia, not for prevention or normophosphatemia 1, 3
- The 2017 KDIGO guidelines abandoned the previous recommendation to maintain phosphate in the normal range for CKD G3a-G4 patients due to lack of evidence that phosphate binders improve outcomes in this population and unproven safety 1
Stepwise Treatment Algorithm
Step 1: Dietary Phosphate Restriction (First-Line)
- Limit dietary phosphate intake as initial therapy, either alone or combined with other treatments 1, 2, 3
- Consider phosphate source when counseling patients 1, 2:
- Guide patients toward fresh and homemade foods rather than processed foods to avoid phosphate additives 1
Pitfall to avoid: Aggressive dietary phosphate restriction can compromise adequate protein intake, particularly problematic in dialysis patients at risk for malnutrition 1
Step 2: Phosphate Binders
Initiate phosphate binders when dietary restriction alone fails to control progressive or persistent hyperphosphatemia 1, 2
Restrict the dose of calcium-based phosphate binders in adult patients with CKD G3a-G5D receiving phosphate-lowering treatment 1, 2
Further restrict calcium-based binders in the presence of: 1
- Persistent or recurrent hypercalcemia
- Arterial calcification
- Adynamic bone disease
- Persistently low serum PTH levels
Avoid long-term use of aluminum-containing phosphate binders due to risk of aluminum intoxication 1, 2
Sevelamer hydrochloride effectively lowers serum phosphorus by approximately 2 mg/dL, with average doses of 4.9-6.5 g daily 4
Pitfall to avoid: Excess calcium exposure from calcium-based binders may contribute to cardiovascular calcification across all CKD stages, though calcium acetate remains more cost-effective than alternatives 5, 6
Step 3: Increase Dialytic Phosphate Removal
- For patients with CKD G5D with persistent hyperphosphatemia, increase dialytic phosphate removal 1, 2
- Use dialysate calcium concentration between 1.25-1.50 mmol/L (2.5-3.0 mEq/L) 1, 2
Management of Associated Abnormalities
Addressing Secondary Hyperparathyroidism
- Evaluate patients with progressively rising or persistently elevated PTH for modifiable factors including hyperphosphatemia, hypocalcemia, high phosphate intake, and vitamin D deficiency 1, 2
- For CKD G5D patients, maintain intact PTH levels at approximately 2-9 times the upper normal limit for the assay 1, 2
Calcium Management
- Avoid hypercalcemia in adult patients with CKD G3a-G5D 1, 2
- In children, maintain serum calcium in age-appropriate normal range and base phosphate binder choice on serum calcium levels 1, 2
Pitfall to avoid: Overly aggressive PTH suppression can lead to adynamic bone disease, which is associated with increased fracture risk and may worsen with excessive calcium-based binder use 2
Special Populations and Considerations
- Patients with vascular or valvular calcification should be considered at highest cardiovascular risk, which should guide more aggressive restriction of calcium-based binders 1, 2
- Novel agents targeting gastrointestinal phosphate transport proteins (tenapanor, nicotinamide) may offer future alternatives by reducing phosphate absorption 7