Nephrologists and dietitians spend a significant amount of their time managing hyperphosphatemia. Phosphorus retention, which occurs in moderate to advanced CKD, is thought to contribute to secondary hyperparathyroidism and excessive vascular calcification.
Diet counseling to reduce phosphorus intake is usually the first step in management. In most cases, however, the physician feels compelled to prescribe a so-called “phosphorus binder” to reduce GI absorption of phosphorus in the food.
In recent years, several new binders have reached the market or await FDA approval, providing welcome flexibility to patients, physicians, and dietitians. The variety of agents, however, has also led to some confusion. Many physicians are not sure which binder is the best choice.
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Nephrologists may feel overwhelmed by information about different mechanisms of various binders, both in reducing phosphorus absorption and offering “bonus” effects such as reducing lipid levels, improving acidosis, lowering pill burden, mitigating inflammation, and so forth. Contradictory data add to the confusion, as pharmaceutical companies emphasize the strengths of their binder and the pitfalls of those sold by competitors.
Nephrologists should reconsider their priorities and focus on the bigger picture of phosphorus management.
First, emerging data indicate that, at least in dialysis patients, dietary management of hyperphosphatemia by restricting protein intake may worsen nutritional status, leading to hypoalbuminemia, protein-energy malnutrition, and poor outcomes. Instead of asking dialysis patients to “eat less” because their phosphorus is high, we should be encouraging them to keep their protein intake at adequate levels. In this context, diligent use of binders is even more warranted.
Second, binders are underutilized in patients with earlier CKD stages who are not yet on dialysis. Hyperparathyroidism and vascular calcification usually develop prior to the dialysis initiation. Currently none of the binders are FDA-approved for non-dialysis patients. There are very few studies about the role of hyperphosphatemia in CKD progression and pre-dialysis mortality.
When it comes to phosphorus management in CKD, there are more important problems to consider than which binder to use, such as protein malnutrition by dietary restriction and pre-dialysis phosphorus control. Solving these problems will require the combined efforts of patients, nephrologists and dietitians. Let’s work toward that end.
