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Amyloid Deposition in a Renal Transplant in Familial Mediterranean Fever

MERRILL D. BENSON, M.D., F.A.C.P.; MARTHA SKINNER, M.D.; and ALAN S. COHEN, M.D.; F.A.C.P.
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Grant support: by grants from the U.S. Public Health Service, National Institute of Arthritis and Metabolic Diseases (AM-04599 and T1-AM-5285); the General Research Centers Branch of the Division of Research Resources, National Institutes of Health (RR533 and 5-SO1 RR-05487-13); the Massachusetts Chapter of the Arthritis Foundation; the Arthritis Foundation; and the John A. Hartford Foundation.

▸Requests for reprints should be addressed to Merrill D. Benson, M.D.; Rheumatology Section, Veterans Administration Hospital, 1481 W. 10th St.; Indianapolis, IN 46202.


Boston, Massachusetts


Ann Intern Med. 1977;87(1):31-34. doi:10.7326/0003-4819-87-1-31
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A patient with familial Mediterranean fever and amyloidosis who received a cadaver renal transplant 6½ years ago was studied to determine the relation of the serum precursor of secondary amyloid (SAA) to the clinical course and to the deposition of amyloid in the transplant. Amyloid fibrils extracted from the patient's kidneys contained protein AA as a major constituent, which identified the amyloid as secondary. Protein AA antiserum was used in an indirect immunofluorescent technique to stain amyloid deposits in sections of the original kidney. A renal biopsy at 2 years showed no amyloid, but a renal biopsy at 4 years showed amyloid. Serum levels of SAA from 3 years before transplant to 6 years after transplant were elevated throughout most of the course.

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