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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Phosphorus excretion in tumoral calcinosis: response to parathyroid hormone and acetazolamide.

The cause of hyperphosphatemia in patients with tumoral calcinosis never been explained. We studied two related patients who had tumoral calcinosis and hyperphosphatemia and two normal controls to determine their renal tubular response to parathyroid hormone ( PTH) and acetazolamide (ACZ). During baseline periods, the patients had abnormally low fractional excretion of phosphorus (FEP) despite their hyperphosphatemia. Values for patients were 0.114 and 0.128; for controls, values were 0.193 and 0.165. PTH caused an increase in FEP and urinary cAMP in both patients and controls. ACZ also increased FEP in both groups, and the effects of PTH and ACZ were additive, suggesting that patients with tumoral calcinosis have normal sensitivities to PTH and normal responses to ACZ. Levels of vitamin D metabolites in the patients were normal. We conclude that patients with tumoral calcinosis have a reduced ability to excrete phosphorus. This defect does not seem to be due to impaired PTH secretion, an abnormal phosphaturic response to this hormone, or a disturbance of vitamin D metabolism.[1]

References

  1. Phosphorus excretion in tumoral calcinosis: response to parathyroid hormone and acetazolamide. Lufkin, E.G., Wilson, D.M., Smith, L.H., Bill, N.J., DeLuca, H.F., Dousa, T.P., Knox, F.G. J. Clin. Endocrinol. Metab. (1980) [Pubmed]
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