Phosphate imbalance: a culprit or victim in renal failure?

Abstract

The kidneys have an important role in the maintenance of phosphate balance. About 80% to 85% of the phosphate filtered at the glomeruli is reabsorbed. Glomerular filtration rate (GFR) declines with renal failure. With the initial fall in GFR, filtered phosphate load as well as excretion are diminished. The net effect will be phosphate retention and a small increase in the plasma phosphate concentration. This small increase in phosphate will combine with ionized calcium. The lowered ionized calcium level stimulates secretion of parathyroid hormone (PTH) and results in secondary hyperparathyroidism, as proposed in the trade-off hypothesis (3,4). However, the initial minor increase in phosphate may not be sufficient to cause a significant hypocalcemia to enhance hypersecretion of PTH (5). Recent studies have demonstrated that phosphate may directly enhance PTH secretion (6). In early chronic renal failure, phosphate retention suppresses 1ahydroxylase activity, thus the renal synthesis of 1,25-dihydroxyvitamin D3 that has inhibitory effect on the parathyroid gland. Dietary phosphate restriction may restore vitamin D3 levels and diminish PTH secretion (7,8).