What is the treatment for hyperphosphatemia (elevated phosphate levels)?

From the Guidelines

Hyperphosphatemia treatment should focus on lowering elevated serum phosphate levels through dietary restriction and phosphate binders, with a preference for non-calcium binders, as excess calcium exposure may be harmful in all GFR categories of CKD, as suggested by recent evidence 1.

Treatment Approach

The treatment approach for hyperphosphatemia involves:

• Dietary phosphate restriction to 800-1000 mg/day by reducing intake of processed foods, dairy products, nuts, and cola beverages
• Phosphate binders, which are the mainstay of treatment and should be taken with meals
• Options for phosphate binders include:
  • Non-calcium binders: sevelamer carbonate (800-1600 mg TID with meals), lanthanum carbonate (500-1000 mg TID with meals), and iron-based binders like ferric citrate (1 gram TID with meals)
  • Calcium-based binders: calcium carbonate (500-1500 mg TID with meals) and calcium acetate (667 mg, 2-3 tablets with meals), which are effective but may increase calcium load

Monitoring and Adjustment

Regular monitoring of serum phosphate, calcium, and PTH levels is crucial to adjust treatment, as hyperphosphatemia treatment is important because elevated phosphate contributes to vascular calcification, secondary hyperparathyroidism, and increased cardiovascular mortality in chronic kidney disease patients 1.

Underlying Cause

Addressing the underlying cause of hyperphosphatemia, such as optimizing renal replacement therapy in patients with chronic kidney disease, is also essential.

Severe Cases

In severe cases, especially with acute kidney injury, hemodialysis may be necessary to rapidly remove phosphate.

Secondary Hyperparathyroidism

Treating secondary hyperparathyroidism with vitamin D analogs (calcitriol 0.25-1 mcg daily) or calcimimetics (cinacalcet 30-180 mg daily) may help regulate phosphate levels, but the use of these agents should be individualized and based on the patient's specific needs and response to treatment 1.

From the FDA Drug Label

Calcium acetate capsules are administered orally for the control of hyperphosphatemia in end-stage renal failure. Calcium acetate, when taken with meals, combines with dietary phosphate to form an insoluble calcium phosphate complex, which is excreted in the feces, resulting in decreased serum phosphorus concentration.

Hyperphosphatemia treatment can be managed with calcium acetate, which acts as a phosphate binder to decrease serum phosphorus levels.

• The medication should be taken with meals to effectively bind to dietary phosphate.
• The dose of calcium acetate may need to be adjusted to control serum phosphorus levels.
• It is essential to monitor serum phosphorus and calcium levels during treatment with calcium acetate. 2

From the Research

Hyperphosphatemia Treatment Options

• Hyperphosphatemia can be induced by three main conditions: a massive acute phosphate load, a primary increase in renal phosphate reabsorption, and an impaired renal phosphate excretion due to acute or chronic renal insufficiency 3
• The most frequent cause of chronic hyperphosphataemia is chronic renal failure, and lowering the phosphate load and maintaining serum phosphorus levels within the normal range are considered important therapeutic goals to improve clinical outcomes in CKD patients 3

Phosphate Binders

• Treatment consists of diminishing intestinal phosphate absorption by a low phosphate diet and phosphate binders, and in CKD patients on dialysis, an efficient dialysis removal of phosphate should be ensured 3
• Aluminium-containing agents are efficient but no longer widely used because of their toxicity, while calcium-based salts are inexpensive, effective, and most widely used, but there is now concern about their association with hypercalcaemia, parathyroid gland suppression, adynamic bone disease, and vascular and extraosseous calcification 3, 4
• Non-calcium-based phosphate binders available include sevelamer, lanthanum carbonate, and magnesium salts, each of which is as effective as calcium salts in lowering serum phosphorus levels depending on an adequate prescribed dose and adherence of the patient to treatment 3, 4, 5

Comparison of Phosphate Binders

• Sevelamer is the only non-calcium-containing phosphate binder that does not have potential for systemic accumulation and presents pleiotropic effects that may impact on cardiovascular disease 3, 5
• Lanthanum carbonate and magnesium salts are absorbed in the gut and their route of excretion is biliary for lanthanum and urinary for magnesium, and there are insufficient data to establish the comparative superiority of non-calcium binding agents over calcium salts for such important patient-level outcomes as all-cause mortality and cardiovascular end points 3, 4
• The choice of phosphate binder should be individualised, considering the clinical context, the costs, and the individual tolerability, the concomitant effects on other parameters of mineral metabolism, such as serum calcium and parathyroid hormone, besides those on serum phosphorus 3