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March 1986

Massive Cerebral Calcifications Associated With Increased Renal Phosphate Reabsorption

Author Affiliations

From the Division of Nephrology and Catedra de Medicina I, Hospital Universitario de Caracas and National Center for Dialysis and Renal Transplant, Ministerio de Sanidad y Asistencia Social (Drs Weisinger, Bellorin-Font, Riera, Abadí, and Paz-Martínez); and the Division of Neurology, Centro Médico Docente La Trinidad (Drs Mogollón and Lander), Caracas, Venezuela. Dr Riera is now with the University of Carabobo, Valencia, Spain.

Arch Intern Med. 1986;146(3):473-477. doi:10.1001/archinte.1986.00360150071008

• Extensive bilateral cerebral cortical calcifications were demonstrated in a young patient with a history of convulsions since the age of 4 years. Initial metabolic workup showed normal serum calcium levels, hyperphosphatemia, normal renal function, low urinary calcium excretion, and normal serum immunoreactive parathyroid hormone levels. The intravenous infusion of edetate disodium (disodium EDTA) showed a normal phosphaturic and cyclic adenosine monophosphate response, ruling out the diagnosis of pseudohypoparathyroidism. The infusion of acetazolamide produced a blunted phosphaturia with almost no change in the renal phosphorus threshold, suggesting a tubular defect that allows enhanced proximal tubular reabsorption of phosphorus. Although the exact mechanisms responsible for the localized calcifications remain obscure, we suggest that an enhanced proximal tubular reabsorption of phosphorus could be involved in the pathophysiologic basis of this abnormality.

(Arch Intern Med 1986;146:473-477)

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