“…Marked hy pocalcemia, which occurred during the oliguric phase, is a well-recognized biochemical feature of this disorder, and those patients who are initially hypocalcemic, may become hypercalcemic during the diuretic phase of acute renal failure [1][2][3]. Early studies suggest that the severity of hypocalcemia varies directly with hyperphospha temia, is related with the intensity of muscle injury and may be due to the rapid deposition of calcium salts in traumatized skeletal muscle and cytoplasmic sequestra tion [I, 2], Possible explanations for hypercalcemia in clude mobilizations of calcium already sequestered in muscle [4,5], volume depletion and autonomous secre tion of parathyroid hormone (PTH) [6,7].…”