Phosphate-binding agents

Phosphate-Binding Agents When serum phosphorus levels cannot be controlled by restriction of dietary intake, phosphate-binding agents are used to bind dietary phosphate in the GI tract to form an insoluble complex that is excreted in the feces. Phosphorus absorption is decreased, thereby... 

TABLE 23-5. Phosphate-Binding Agents Used in the Treatment of Hyperphosphatemia in CKD... 

Aluminum- and magnesium-containing phosphate-binding agents are not recommended for chronic use in patients with CKD to minimize the risk of aluminum and magnesium accumulation. Aluminum-containing agents may be used for... 

By the time ESRD develops, most patients require a combination of phosphate-binding agents, vitamin D, and calcimimetic therapy to achieve K/DOQI goals. 

Phosphate-binding agents decrease phosphorus absorption from the gut and are first-line agents for controlling both serum phosphorus and calcium concentrations (Table 76-3). 

Patients with chronic renal failure develop hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, and severe metabolic bone disease. The secondary hyperparathyroidism is thought to be due to hyperphosphatemia and decreased 1, 25-(OH)2 formation. Oral or intravenous l,25-(OH)2D3 (calcitriol) therapy along with oral phosphate-binding agents and calcium supplementation is effective in reducing the effects of renal osteodystrophy. 

Calcium acetate and calcium carbonate are used as phosphate-binding agents in hyperphosphataemia. 

Sucralfate, a basic aluminium salt of sucrose octasulfate, probably acts by binding to inflamed surfaces it is possible, however, that its binding properties are more generalized, and it has been used as an intra-alimentary phosphate-binding agent in uremic patients. 

In addition may medication related to the uremic state lead to important trace element accumulation. In the past this has clearly been established for aluminum resulting from the use of aluminum hydroxide as a phosphate binding agent. As aluminum-based phosphate binders may be contaminated with other elements, e.g. strontium the possibility for a simultaneous accumulation of different elements has been suggested [7]. Strontium is mainly eliminated by the kidney and has been associated with bone mineralization defects when present at high concentrations. In view of this the use of strontium ranelate for the treatment and preven-... 

Management of hyperphosphatemia, calcium balance, and secondary hyperparathyroidism includes dietary phosphorus restriction, use of phosphate binding agents, and vitamin D therapy. 

One of the most common obstacles to the success of dietary restriction is patient noncompliance due to the poor palatabUity and inconvenience. Regular counseling by a dietitian is essential to improve patient compliance. As kidney function declines, dietary restriction alone is usually inadequate to control serum phosphorus, and phosphate-binding agents are necessary (see section on pharmacologic therapy). 

I Dosing and Administration. Starting doses of phosphate binding agents are listed in Table 44—6. Doses should be titrated to achieve the recommended serum phosphorus concentrations yet avoid complications such as hypercalcemia. 

Patients with CKD or ESKD often are treated for hyperphosphatemia with phosphorus-restricted diets and phosphate binding agents (see Chaps. 43 and 44). When these patients receive aggressive nutritional support, the combination of refeeding (cellular uptake of phosphorus for synthesis of body cell mass) and vigorous phosphatebinding therapy can result in hypophosphatemia. 

---