From the Guidelines
Hyperphosphatemia treatment should focus on reducing elevated phosphate levels in the blood through dietary restrictions, phosphate binders, and addressing underlying causes, with the goal of improving morbidity, mortality, and quality of life. The treatment approach should prioritize individualized decisions based on serial assessments of phosphate, calcium, and parathyroid hormone (PTH) levels, as therapeutic maneuvers aimed at improving one variable often have unintended effects on others 1. Key considerations include:
- Limiting dietary phosphate intake to 800-1000 mg/day by avoiding high-phosphate foods like processed meats, dairy products, nuts, and cola beverages
- Using phosphate binders, such as calcium-based binders (e.g., calcium carbonate 500-1500 mg with meals or calcium acetate 667-1334 mg with meals), non-calcium options (e.g., sevelamer 800-1600 mg with meals, lanthanum carbonate 500-1000 mg with meals), or iron-based binders like ferric citrate (1-2 tablets with meals)
- Optimizing dialysis treatment for patients with kidney disease to remove excess phosphate
- Treating the underlying cause, whether it's kidney dysfunction, vitamin D toxicity, or other conditions It is essential to note that phosphate-lowering therapies may only be indicated in the event of progressive or persistent hyperphosphatemia and not for prevention, as suggested by recent studies 1. Additionally, avoiding hypercalcemia is crucial, and the use of calcium-based phosphate binders should be restricted in patients with hyperphosphatemia across the CKD spectrum 1. The current evidence suggests that excess exposure to calcium may be harmful across all GFR categories of CKD, and phosphate-lowering treatment decisions should be individualized 1. Future research should address the gaps in the knowledge base for treatment of CKD–MBD, including the potential value of hyperphosphatemia prevention in at-risk CKD populations and the benefits and risks of treatment with calcitriol or vitamin D analogues in patients with CKD stage G3a to G5 and mild or severe SHPT 1.
From the FDA Drug Label
The ability of sevelamer hydrochloride to lower serum phosphorus in CKD patients on dialysis was demonstrated in six clinical trials: one double-blind placebo-controlled 2-week study (sevelamer hydrochloride N=24); two open-label uncontrolled 8-week studies (sevelamer hydrochloride N=220) and three active-controlled open-label studies with treatment durations of 8 to 52 weeks (sevelamer hydrochloride N=256). Effectiveness of calcium acetate in decreasing serum phosphorus has been demonstrated in two studies of the calcium acetate solid oral dosage form.
The treatment for hyperphosphatemia (elevated phosphate levels) includes:
- Sevelamer hydrochloride 2: shown to lower serum phosphorus in CKD patients on dialysis
- Calcium acetate 3: demonstrated to decrease serum phosphorus in end-stage renal disease patients
Key points:
- Sevelamer hydrochloride and calcium acetate are both effective in reducing serum phosphorus levels
- The dosage and administration of these medications may vary depending on the individual patient's needs and response to treatment
From the Research
Treatment Options for Hyperphosphatemia
- The treatment of hyperphosphatemia typically involves a combination of dietary restrictions, dialysis, and phosphate binders 4, 5, 6.
- Phosphate binders are used to control blood phosphorus levels, with calcium carbonate being the first choice and sevelamer being an alternative 4.
- Other phosphate binders, such as lanthanum carbonate, are also available, but may have adverse effects such as gastrointestinal disorders and accumulation in bones and brain 4, 7.
- Newer treatments, such as inhibitors of active intestinal phosphate transport, are being developed, but their effectiveness and safety are still being studied 5, 8.
Phosphate Binders
- Calcium-based binders, such as calcium acetate, are effective but can lead to hypercalcemia and/or positive calcium balance and progression of cardiovascular calcification 5, 6.
- Sevelamer, a non-calcium-based binder, appears to have a favorable profile, with reduced progression of vascular calcification, but may cause gastrointestinal adverse events 5.
- Lanthanum carbonate is an effective phosphate binder, but its long-term effects on tissue deposition are still being studied 5, 7.
- Iron-based binders are also available, but their effectiveness and safety are still being evaluated 5.
Dietary Restrictions and Dialysis
- Dietary phosphate restriction is an important part of managing hyperphosphatemia, but can be challenging to implement and maintain 8, 6.
- Dialysis can help remove excess phosphorus from the blood, but may not be sufficient to control hyperphosphatemia on its own 4, 7.
- A multidisciplinary approach, including dietary restrictions, dialysis, and phosphate binders, is often necessary to effectively manage hyperphosphatemia 8, 6.