Concern for hyperphosphatemia?

From the Guidelines

Concern for hyperphosphatemia should focus on patients with overt hyperphosphatemia, as current evidence does not show benefit to maintaining normal serum phosphate levels in patients not receiving dialysis, and there are safety concerns associated with aggressive phosphate-lowering therapy. According to the Kidney Disease: Improving Global Outcomes 2017 clinical practice guideline update 1, treatment approaches for CKD–MBD should be based on serial assessments of biochemical variables (serum phosphate, calcium, and PTH) taken together.

Some key points to consider:

• Dietary modifications should be implemented first, including reducing intake of phosphorus-rich foods such as processed foods, dairy products, nuts, and cola beverages.
• Increase water intake to 2-3 liters daily to help flush excess phosphorus.
• If you have kidney disease, consult with your nephrologist as phosphate binders like calcium acetate (PhosLo), sevelamer (Renvela), or lanthanum carbonate (Fosrenol) may be prescribed to take with meals.
• The elevated phosphorus level is concerning because it can lead to calcium-phosphate deposits in blood vessels and tissues, contributing to cardiovascular disease and bone disorders.
• High phosphorus levels often indicate decreased kidney function, as healthy kidneys typically excrete excess phosphorus.
• Follow-up testing in 2-4 weeks is recommended to monitor if dietary changes are effective, with more frequent monitoring if you have chronic kidney disease.

It's also important to note that new evidence suggests that hypercalcemia may be harmful in all GFR categories of CKD, prompting the recommendation to avoid inappropriate calcium loading in adults whenever possible 1. Additionally, the use of calcium-based phosphate binders should be restricted in patients with hyperphosphatemia across the CKD spectrum 1.

Overall, the management of hyperphosphatemia should be individualized and based on the patient's specific needs and circumstances, taking into account the potential risks and benefits of different treatment approaches 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). Eighty-four CKD patients on hemodialysis who were hyperphosphatemic (serum phosphorus >6 mg/dL) following a two-week phosphate binder washout period received sevelamer hydrochloride and active-control for eight weeks each in random order. Both treatments significantly decreased mean serum phosphorus by about 2 mg/dL (Table 5). Two hundred CKD patients on hemodialysis who were hyperphosphatemic (serum phosphorus >5. 5 mg/dL) following a two-week phosphate-binder washout period were randomized to receive sevelamer hydrochloride 800 mg tablets (N=99) or an active-control (N=101). The two treatments produced similar decreases in serum phosphorus. At week 52, using last observation carried forward, sevelamer hydrochloride and active-control both significantly decreased mean serum phosphorus (Table 6)

Sevelamer hydrochloride is effective in lowering serum phosphorus levels in patients with chronic kidney disease (CKD) on dialysis, as demonstrated by significant decreases in mean serum phosphorus levels in several clinical trials 2 2.

• The medication has been shown to decrease mean serum phosphorus levels by approximately 2 mg/dL in patients with hyperphosphatemia.
• Sevelamer hydrochloride can be used to treat hyperphosphatemia in CKD patients on dialysis.
• The recommended dosage should be individualized based on the patient's serum phosphorus level and clinical response.

From the Research

Concern for Hyperphosphatemia

Hyperphosphatemia is a common condition in the late stages of chronic kidney disease (CKD) and is associated with elevated parathormone levels, abnormal bone mineralization, extraosseous calcification, and increased risk of cardiovascular events and death 3, 4, 5, 6.

Causes and Treatment Options

The most frequent cause of chronic hyperphosphatemia is chronic renal failure 5. Treatment consists of diminishing intestinal phosphate absorption by a low phosphate diet and phosphate binders 5. Several classes of oral phosphate binders are available to help control plasma phosphorus levels, including aluminum, calcium-based binders, lanthanum, and sevelamer 3, 4, 5, 7, 6.

Phosphate Binders

• Aluminum has potentially serious toxic risks 3, 4, 6
• Calcium-based binders are effective but can lead to hypercalcemia and/or positive calcium balance and cardiovascular calcification 3, 4, 5, 6
• Lanthanum is an effective phosphate binder, and long-term effects of tissue deposition seem clinically irrelevant 4
• Sevelamer appears to have profiles that would lead to less vascular calcification, and the main adverse events seen with these agents are gastrointestinal effects 3, 4, 5, 7
• Lanthanum carbonate is more efficacious in lowering serum phosphate concentrations and effectively managing hyperphosphatemia as compared to sevelamer carbonate 7

Management of Hyperphosphatemia

Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake 6. 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 5.