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Acute oxalate nephropathy after massive ascorbic acid administration.

J M Lawton, L T Conway, J T Crosson

    Archives of Internal Medicine
    |May 1, 1985
    PubMed
    Summary
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    High-dose intravenous ascorbic acid therapy can cause oxalate nephropathy, leading to acute kidney injury. This study highlights the risk of calcium oxalate deposition in the kidneys following high ascorbic acid administration.

    Area of Science:

    • Nephrology
    • Biochemistry
    • Pathology

    Background:

    • Primary amyloidosis and nephrotic syndrome can lead to kidney complications.
    • Ascorbic acid (vitamin C) is a metabolic precursor to oxalate.

    Observation:

    • A patient received a 45-g intravenous dose of ascorbic acid as adjuvant therapy.
    • The patient subsequently developed acute oliguric renal failure.
    • Postmortem examination revealed intratubular calcium oxalate crystal deposition in the kidneys.

    Findings:

    • Elevated plasma concentrations of both oxalate and ascorbic acid were observed.
    • Histopathology confirmed extensive intratubular calcium oxalate deposition, indicating oxalate nephropathy.
    • No extrarenal calcium oxalate deposits were found.

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    Implications:

    • High-dose ascorbic acid administration is a potential cause of oxalate nephropathy.
    • Clinicians should consider the risk of oxalate nephropathy when administering high-dose intravenous vitamin C.
    • This finding is crucial for managing patients with kidney disease and those receiving high-dose vitamin C therapy.