Chronic kidney disease (CKD) describes the progressive loss of kidney function, which affects the body’s ability to maintain balance for various substances. Healthy kidneys manage the concentration of phosphate, a mineral component of bones and genetic material. When kidney function declines, phosphate excretion becomes impaired, leading to a build-up in the bloodstream, known as hyperphosphatemia. This imbalance is part of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), which involves abnormalities in calcium, phosphate, and hormone levels. Phosphate binders are medications used to manage high phosphate levels in advanced CKD.
The Risks of Elevated Phosphate Levels
Controlling phosphate levels is important because sustained hyperphosphatemia causes damage, particularly in the cardiovascular and skeletal systems. High phosphate disrupts mineral balance, leading to the formation of calcium-phosphate deposits outside of the bone. This process, called vascular calcification, is a hardening of the arteries that increases the risk of heart attack, stroke, and cardiovascular mortality.
The excess phosphate also contributes to secondary hyperparathyroidism, where the parathyroid glands overproduce parathyroid hormone (PTH). This hormone imbalance pulls calcium out of the bones, causing renal osteodystrophy. Renal osteodystrophy weakens the bones, making them fragile, and increases the risk of fractures. Elevated phosphate levels are associated with an increased risk of death in people with CKD.
Clinical Triggers for Starting Binder Therapy
The decision to start phosphate binder therapy relies on persistently elevated serum phosphate that cannot be managed through diet alone. Guidelines suggest aiming to keep serum phosphate within the normal range, typically between 2.5 and 4.5 milligrams per deciliter (mg/dL). Binders are initiated when phosphate levels consistently exceed this target range, often above 4.5 or 5.5 mg/dL, particularly in advanced CKD (stages G4 or G5).
Binders are introduced when dietary restriction proves insufficient to maintain the target phosphate concentration. In later stages of CKD, the body’s natural mechanisms to excrete phosphate begin to fail. Phosphate binders are frequently started in CKD Stage G4 and almost universally in those with Stage G5 (kidney failure, including those on dialysis). Regular monitoring of phosphate and calcium levels guides the timing and adjustment of this therapy.
How Phosphate Binders Function
Phosphate binders are oral medications taken with meals and snacks to prevent the absorption of dietary phosphate in the gut. They work by chemically attaching to phosphate molecules found in food within the gastrointestinal tract. This process forms an insoluble complex that cannot be absorbed into the bloodstream.
This complex passes through the digestive system and is excreted in the feces, lowering the body’s overall phosphate burden. Because they only bind phosphate present in food, binders must be taken simultaneously with the meal to be effective. Binders are categorized into calcium-based binders (e.g., calcium acetate) and non-calcium-based binders (e.g., sevelamer or lanthanum carbonate).
The Role of Diet and Dialysis in Phosphate Management
Phosphate binders are one part of a comprehensive strategy for managing hyperphosphatemia in CKD. The initial step is dietary management, which involves restricting foods high in phosphate. This restriction focuses on limiting foods like dairy products, nuts, and processed foods that contain inorganic phosphate additives, which are nearly 100% absorbed.
For people with kidney failure (CKD Stage G5) undergoing dialysis, the procedure removes some phosphate from the blood. However, conventional dialysis is often insufficient to fully control phosphate levels. Most dialysis patients still require binders and dietary restrictions. The dosing of phosphate binders may need frequent adjustment based on dietary intake and treatment efficiency.