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Julius J. Sachs, M.D.; Robert R. Henderson, M.D.
JAMA. 1952;148(10):839-841. doi:10.1001/jama.1952.02930100057012.
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The concept that impaired renal function is a contraindication to bishydroxycoumarin (dicumarol®) therapy had its origin in early animal experiments. Bollman and Preston1 produced renal damage in dogs by subcutaneous injection of uranium acetate or by bilateral ligation of the ureters and found a marked sensitivity to bishydroxycoumarin. They noted a similar effect after bilateral nephrectomy. Richards and Steggerda2 found that bilateral nephrectomy in rats greatly increased the effect of bishydroxycoumarin. An early clinical report by Allen, Barker, and Waugh3 stated that the effect of bishydroxycoumarin on prothrombin time is excessive in cases of renal insufficiency and advised that the drug be used very cautiously or not at all in these patients. Allen, Barker, and Hines4 cited cases of two patients treated with this drug, in whom suppression of urine developed owing to the accumulation of crystals of sulfonamide compounds in the renal pelvis. The prothrombin time, which was increased in association with the anuria, returned to normal when urine again was excreted by the kidneys.


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