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Acquired Factor IX Deficiency in the Nephrotic Syndrome

ETHAN A. NATELSON, M.D.; EDWARD C. LYNCH, M.D., F.A.C.P.; ROBERT A. HETTIG, M.D., F.A.C.P.; and CLARENCE P. ALFREY JR., M.D., F.A.C.P.
[+] Article and Author Information

Dr. Natelson was supported in this study by Fellow in Hematology grant HE-0572-04, U.S. Public Health Service, Washington, D.C.

Presented in part December 5, 1969, at the Regional Meeting of the American College of Physicians, Houston, Tex.

▸Requests for reprints should be addressed to Ethan A. Natelson, M.D., Special Hematology Division, The Methodist Hospital, Texas Medical Center, Houston, Tex. 77025


Houston, Texas


Ann Intern Med. 1970;73(3):373-378. doi:10.7326/0003-4819-73-3-373
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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.

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