ETHAN A. NATELSON, M.D.; EDWARD C. LYNCH, M.D., F.A.C.P.; ROBERT A. HETTIG, M.D., F.A.C.P.; CLARENCE P. ALFREY JR., M.D., F.A.C.P.
In a patient with the nephrotic syndrome prolonged whole blood clotting and defective intrinsic thromboplastin generation resulted from an acquired deficiency of factor IX. His urine and that from eight additional patients with massive proteinuria, in contrast to normal urine, contained a procoagulant with factor IX activity. The extraction of this substance as a barium sulfate adsorbate from urine is described, and its ability to correct the abnormality in thromboplastin generation of patients with congenital factor IX deficiency and elicit rabbit antisera that inactivate human serum factor IX is demonstrated. These findings support excessive urinary loss of factor IX as a potential cause for acquired factor IX deficiency in certain patients with massive proteinuria.
NATELSON EA, LYNCH EC, HETTIG RA, et al. Acquired Factor IX Deficiency in the Nephrotic Syndrome. Ann Intern Med. 1970;73:373–378. doi: https://doi.org/10.7326/0003-4819-73-3-373
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Published: Ann Intern Med. 1970;73(3):373-378.
Coagulopathies, Hematology/Oncology, Nephrology, Nephrotic Syndrome.
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