Phosphate Homeostasis in Cimetidine Treated Uremic Dogs

More than a decade ago, a secondary hyperparathyroidism (HPTH) was postulated to be directed at the maintenance of phosphate homeostasis in chronic uremia (1). Each decrement in glomerular filtration rate would be associated with transient hyperphosphatemia, hypocalcemia and an increase in PTH secretion. Secondary HPTH would cause phosphaturia and restore phosphate balance, thereby normalizing serum phosphate and calcium levels. As renal function deteriorates, phosphate balance would be maintained at the expense of increasingly severe HPTH.