Using Cinacalcet to Treat the Hypophosphatemia of Early Kidney Transplant

The purpose of the study is to determine whether cinacalcet, used in patients with secondary hyperparathyroidism to control excessive parathyroid hormone, can normalize low blood phosphorus that is commonly seen in patients who have had a kidney transplant.

Secondary hyperparathyroidism (SHPT), common in ESRD, persists following renal transplantation resulting in profound hypophosphatemia. This can lead to hemolysis, congestive heart failure, rhabdomyolysis. Phosphate repletion is difficult in view of the persistent SHPT: oral phosphate supplementation can lead to hypocalcemia, reduced 1,25-OH Vitamin D production, hypercalcemia and further hyperparathyroidism. In addition, phospho-soda has been associated with phosphate nephropathy and renal failure. Cinacalcet HCl is a calcimimetic agent that has recently become a standard therapy in the treatment of SHPT in ESRD. It suppresses PTH secretion by acting as a modulator of the Calcium-sensing receptor on the PTH cell, causing the PTH cell to decrease production of parathyroid hormone. It is a very effective agent, producing significant reduction of PTH as well as improvement in calcium and phosphate metabolism in the dialysis patient. The drug is well-tolerated with minimal adverse effects. Cinacalcet has also been used to control hypercalcemia in renal transplant patients with persistent hyperparathyroidism. Short-term cinacalcet given for 2 to 4 weeks has normalized serum phosphorus and decreased urinary phosphate wasting in renal transplant recipients with stable graft function. We hypothesize that Cinacalcet HCl will normalize the hypophosphatemia of early renal transplant by reducing the effects of PTH on the proximal renal tubular transport of phosphorus, thereby allowing phosphate reabsorption and decreasing urinary phosphate wasting.