Progression of Renal Amyloidosis of FMF and Relation to Serum SAA Level
Information source: Sheba Medical Center
ClinicalTrials.gov processed this data on August 20, 2015 Link to the current ClinicalTrials.gov record.
Condition(s) targeted: Observational
Phase: N/A
Status: Not yet recruiting
Sponsored by: Sheba Medical Center Official(s) and/or principal investigator(s): Avi Livneh, MD, Principal Investigator, Affiliation: Sheba Medical Center
Summary
Purpose of this study is to determine whether keeping SAA on normal or near normal level
will delay progression of renal failure in patients with amyloidosis secondary to FMF.
Clinical Details
Official title: Progression of Renal Amyloidosis of FMF and Relation to Serum SAA Level
Study design: Observational Model: Case Control, Time Perspective: Prospective
Detailed description:
FMF is an inherited inflammatory disorder typically presented in most causes as recurrent
episodes of fever and serositis. Phenotype II, another kind of this disorder, has atypical
courses, when the inflammation proceeds without any clinical sign.
Each FMF attack is accompanied by sharp elevation of inflammatory markers in the serum, and
serum amyloid A (SAA) one of them. The level of these inflammatory markers returns to
normal with termination of the attack. The SAA is the main component of amyloids fibrils
and constantly high level of SAA after the attack (as occurs in undiagnosed or
undertreated disease) is the significant risk factor responsible for development of
amyloidosis. On the other hand, in patients with phenotype II the amyloidosis occurs despite
absolute absence of the attacks.
The kidney is one of the first organ suffers from amyloid deposits. The spectrum of kidney
damage spread wildly from mild proteinuria to obvious nephrotic syndrome with disturbance
in renal function and progression to end stage renal failure.
It is well known that deterioration of renal disease in AA amyloidosis links to level of
SAA in serum. The permanently high SAA level is a major factor responsible to progression of
renal disease. Occasionally, however, decline in the renal function occurred despite normal
or near normal levels of SAA. Renal impairment in these cases may be explained by
mechanisms existing in other kidney diseases when uncontrolled proteinuria aggravates renal
dysfunction. The purpose of the study is to find whether a cohort of patients followed in
our clinic and receiving colchicine for FMF- amyloidosis according to the SAA levels,
monitored periodically, have better prognosis than an historical cohort receiving colchicine
according to the attack status
Eligibility
Minimum age: 18 Years.
Maximum age: N/A.
Gender(s): Both.
Criteria:
Inclusion Criteria:
- FMF patients with amyloidosis AA
- 18 year and older
Exclusion Criteria:
- patients with AA amyloidosis not related to FMF
- evidence of other primary renal disease or renovascular pathology
- evidence of renal disease secondary to any systemic illness
- presence of inflammatory, autoimmune conditions or chronic infection that could lead
to high SAA level
- pregnancy
- inability to provide legal consent
Locations and Contacts
Sheba Medical Center, Tel Hashomer 52621, Israel; Not yet recruiting Avi Livneh, MD, Principal Investigator
Additional Information
Related publications: Lachmann HJ, Goodman HJ, Gilbertson JA, Gallimore JR, Sabin CA, Gillmore JD, Hawkins PN. Natural history and outcome in systemic AA amyloidosis. N Engl J Med. 2007 Jun 7;356(23):2361-71. Gillmore JD, Lovat LB, Persey MR, Pepys MB, Hawkins PN. Amyloid load and clinical outcome in AA amyloidosis in relation to circulating concentration of serum amyloid A protein. Lancet. 2001 Jul 7;358(9275):24-9. Yalçinkaya F, Cakar N, Acar B, Tutar E, Güriz H, Elhan AH, Oztürk S, Kansu A, Ince E, Atalay S, Girgin N, Doğru U, Aysev D, Ekim M. The value of the levels of acute phase reactants for the prediction of familial Mediterranean fever associated amyloidosis: a case control study. Rheumatol Int. 2007 Apr;27(6):517-22. Epub 2006 Nov 14.
Starting date: September 2010
Last updated: August 16, 2010
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