technetium-tc-99m-pyrophosphate and Hypocalcemia

Patients with rhabdomyolysis (RBD) and acute renal failure (ARF) are hypocalcemic during the oliguric phase of ARF and over 30% develop hypercalcemia during the diuretic phase. The present study examined the factors underlying these derangements in calcium metabolism in 15 patients: 7 with RBD and ARF, 4 with RBD only, and 4 with ARF only. All patients had hypocalcemia on admission and the hypocalcemia was more pronounced in those with RBD and ARF. All patients with RBD independent of the presence or absence of ARF had calcium deposition in soft tissues as documented by technetium-99 scan. In 4 patients with RBD and ARF, hypercalcemia developed during the diuretic phase at a time when Serum PTH levels were undetectable. Only patients with RBD and ARF had a significant increase in serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D [1,25(OH)2D] during the diuretic phase and both the increments in and the levels of 1,25(OH)2D were significantly greater in those who were hypercalcemic. The data indicate that 1) hypocalcemia occurs in RBD independent of ARF and is most likely related to calcium deposition in injured tissues, and 2) elevation in serum levels of 1,25(OH)2D plays an important role in the genesis of hypercalcemia during the diuretic phase of patients with RBD and ARF. Our observations suggest that extrarenal production of 1,25(OH)2D may occur in these patients, and/or that the renal production of 1,25(OH)2D may not be so tightly controlled as it is in normal subjects.

Topics: Acute Kidney Injury; Adult; Calcinosis; Calcitriol; Diphosphates; Diuresis; Female; Humans; Hypercalcemia; Hypocalcemia; Male; Middle Aged; Parathyroid Hormone; Radionuclide Imaging; Rhabdomyolysis; Technetium; Technetium Tc 99m Pyrophosphate; Time Factors

A patient with hypokalemic metabolic alkalosis, hypophosphatemia, and hypomagnesemia/hypocalcemia is described. Electrocardiography demonstrated the pattern of acute anterior myocardial infarction. Further evaluation revealed that the patient had not actually had the acute myocardial infarction and that the electrocardiographic change was a mere simulation. The possible role of hypomagnesemia in the pathogenesis of the electrocardiographic change and the interrelation between the metabolic disturbances noted are discussed.

Topics: Alkalosis; Diagnosis, Differential; Diphosphates; Electrocardiography; Humans; Hypocalcemia; Hypokalemia; Hypophosphatemia, Familial; Magnesium; Male; Metabolism, Inborn Errors; Middle Aged; Myocardial Infarction; Radionuclide Imaging; Technetium; Technetium Tc 99m Pyrophosphate