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Idiopathic hypercalciuria: hydrochlorothiazide decrease urinary calcium without altered renal response to parathyroid

C J Van Den Berg, R M Tucker, T P Dousa

    The Journal of Clinical Endocrinology and Metabolism
    |July 1, 1982
    PubMed
    Summary
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    Hydrochlorothiazide (HTZ) reduces urinary calcium excretion in idiopathic hypercalciuria (IH). This effect is independent of parathyroid hormone (PTH) levels or kidney sensitivity to PTH.

    Area of Science:

    • Nephrology
    • Endocrinology
    • Pharmacology

    Background:

    • Idiopathic hypercalciuria (IH) is characterized by increased urinary calcium excretion.
    • Hydrochlorothiazide (HTZ) is a diuretic known to reduce urinary calcium.
    • The mechanism by which HTZ reduces urinary calcium, specifically its interaction with parathyroid hormone (PTH), requires clarification.

    Purpose of the Study:

    • To investigate if HTZ therapy sensitizes the kidney to PTH in patients with IH.
    • To determine if changes in PTH secretion contribute to the hypocalciuric effect of HTZ.

    Main Methods:

    • 10 patients with IH were studied before and after 4 weeks of HTZ treatment.
    • Measurements included urinary calcium (UCa V), urinary cAMP (UcAMP V), tubular reabsorption of phosphate (TRP), and plasma PTH.

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  • Renal response to PTH infusion was assessed by changes in UcAMP V and TRP.

    • Main Results:

    • HTZ significantly reduced UCa V.
    • Plasma PTH, UcAMP V, and TRP did not change significantly with HTZ therapy.
    • The renal response to PTH infusion (increased UcAMP V, decreased TRP) was similar before and during HTZ treatment.

    Conclusions:

    • The hypocalciuric effect of HTZ in IH is independent of PTH secretion.
    • HTZ does not alter kidney sensitivity to PTH in these patients.