Renal Disease

End Stage Renal Disease (ESRD) obligates the replacement of lost kidney function through dialysis or transplantation. Prevention and treatment of ESRD related electrolyte and metabolic imbalances, such as hyperphosphatemia are the primary treatment goals in dialysis patients.

Even with current therapy, hyperphosphatemia persists in 70% of the dialysis population. More importantly, although the exact mechanism has not yet been elucidated, this condition has been shown to significantly increase ESRD patient mortality and morbidity.

Soft-tissue cardiac calcification may explain the hyperphosphatemia-mortality relationship, as many authors have demonstrated a link between elevated serum phosphorus, calcium- phosphate product and cardiac calcification, a known cardiovascular risk. In Canada, cardiovascular disease is responsible for approximately 40% of deaths among patients with ESRD treated by either hemodialysis (HD) or peritoneal dialysis (PD). This is roughly 10-20 times higher than the general population even after stratification by age, gender, race and presence of diabetes.

Hyperphosphatemia has additional morbidity implication due to its enhancement and promotion of secondary hyperparathyroidism, which leads to renal osteodystrophy. This latter condition results in one of several metabolic bone pathologies. This disturbance of bone metabolism manifests as pathologic fracture and impaired mobility.

Approaches to Treatment

Hyperphosphatemia in ESRD is managed through serum phosphorus removal via dialysis, diet modification and utilization of phosphorus binders to inhibit dietary absorption of ingested phosphorus.

Due to the inadequacy of dialysis and the challenges of dietary phosphorus restriction, almost all dialysis patients rely on a phosphate binder to reduce phosphorus absorption and prevent hyperphosphatemia. Currently, the most utilized phosphate binding agents include calcium carbonate and aluminum hydroxide.

Aluminum hydroxide is mainly used as rescue therapy due to known aluminum toxicities such as aluminum bone disease, dementia, myopathy and anemia.

Calcium salts (calcium carbonate and calcium acetate) have been shown to effectively control serum phosphorus; however the consequences of calcium absorption and excess calcium load lead to hypercalcemia and soft tissue calcification. Additionally, the use of Vitamin D analogs in the treatment of hyperparathyroidism may exacerbate the unwanted consequences of calcium-based phosphate binders due to an increase in absorbed calcium.

The development of Renagel^® (sevelamer hydrochloride), a non-calcium, non-metal phosphate binder is as effective as calcium based binders and has the distinct advantage of not contributing to overall body calcium load.

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