PEDIATRICS Vol. 79 No. 3 March 1987, pp. 403-409
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Severe Renal Osteodystrophy Without Elevated Serum Immunoreactive Parathyroid Hormone Concentrations in Hypomagnesemia Due to Renal Magnesium Wasting

Israel Zelikovic MD1, Shermine Dabbagh MD1, Aaron L. Friedman MD1, Mark L. Goelzer MD1, and Russell W. Chesney MD1

1 From the Department of Pediatrics, University of California, Davis, School of Medicine, Center for Health Sciences, The University of Wisconsin, Madison, and Janesville Medical Center, Janesville, Wisconsin

An 8frac12-year-old girl presented with a long history of seizures, growth retardation, muscle weakness, gait disturbance, and hearing loss. Her evaluation revealed chronic moderate renal failure (serum creatinine 2.2 mg/dL), severe hypocalcemia (5 mg/dL), hyperphosphatemia (8.1 mg/dL), hypomagnesemia (1.5 mg/dL), increased urinary magnesium excretion (2 mg/kg/d), high fractional excretion of magnesium (21.7%), hypokalemia (3.2 mEq/L), and hyperkaliuria (26 mEq/L). Low circulating immunoreactive parathyroid hormone levels for the degree of the hypocalcemia (serum N-parathyroid hormone 212 pg/mL) and severe rickets without evidence of osteitis fibrosa cystica were found. The patient probably has primary renal leak hypomagnesemia (magnesuric hypomagnesemia) which caused impaired secretion of immunoreactive parathyroid hormone leading to severe hypocalcemia and calcium deficiency rickets. Treatment with magnesium and calcium supplements, calcitriol, and aluminum hydroxide resulted in marked clinical, biochemical, and radiologic improvement. Calcium deficiency rickets due to primary or secondary renal magnesium wasting in conjunction with moderate renal failure represents a largely unrecognized metabolic bone disease.

Key Words: hypomagnesemia • renal magnesium wasting • hypocalcemia • rickets • immunoreactive parathyroid hormone

Submitted on April 14, 1986
Accepted on June 10, 1986




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