Spectrum of renal involvement in familial Mediterranean fever

Said, Riyad; Hamzeh, Yousef; Said, Salwa M.; Tarawneh, Musleh S.; Al-Khateeb, Mohamed

doi:10.1038/ki.1992.57

Cited by 62 publications

(40 citation statements)

References 21 publications

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“…They found that among 25 FMF patients, 10 (40%) had NAKD including mainly focal glomerulonephritis and focal segmental glomerular sclerosis. This rate of NAKD is similar to that reported by Said, et al 6 . Contrary to these results, among 2436 patients from the Turkish FMF study group, 12.9% had biopsy-proven amyloidosis (amyloid kidney disease, AKD), while only 0.8% had NAKD 15 .…”

Section: Rheumatologysupporting

confidence: 80%

“…In the report by Said, et al 6 , and in an article by Kukuy, et al in this issue of The Journal 10 , no cases of HSP or PAN were noted, probably because renal biopsy is usually not indicated in patients with HSP and because PAN is rare 6,10 . In these series, types of NAKD were similar to those expected in non-FMF patients, where IgA nephropathy, focal segmental glomerulosclerosis, and mesangial lesions are commonly seen.…”

Section: Rheumatologymentioning

confidence: 99%

“…Both studies were published prior to the introduction of colchicine treatment. More recently, Said, et al reported kidney biopsy pathologies in 15 patients with FMF and proteinuria 6 . Thirteen had urine protein of more than 1 g/24 h. Only 7 had amyloidosis, while 6 had mesangial proliferative glomerulonephritis (with IgA or IgM deposition), and 2 had rapidly progressive glomerulonephritis.…”

Section: The Kidney In Familial Mediterranean Fevermentioning

confidence: 99%

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The Kidney in Familial Mediterranean Fever

Peleg

Ben-Chétrit

2013

J Rheumatol

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Section: Rheumatologysupporting

confidence: 80%

Section: Rheumatologymentioning

confidence: 99%

Section: The Kidney In Familial Mediterranean Fevermentioning

confidence: 99%

See 1 more Smart Citation

The Kidney in Familial Mediterranean Fever

Peleg

Ben-Chétrit

2013

J Rheumatol

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“…Blood analysis revealed a creatinine level of 0.81 mg/dL, urinalysis revealed proteinuria (+), hematuria, and a 24 hour urinary protein collection of 960 mg/day. Serological tests for glomerulonephritis, mesangial IgA nephropathy, IgM nephropathy, diffuse proliferative glomerulonephritis) have also been reported in patients with FMF [7][8][9] . We hereby present nine FMF patients with biopsy proven glomerulonephritis, who have been followed by the Nephrology Department of Cumhuriyet University.…”

Section: Casementioning

confidence: 99%

Biopsy Proven Non-Amyloid Glomerular Diseases in Patients With Familial Mediterranean Fever

Hüzmelí

Koçkara

Candan

et al. 2015

Journal of Nephrology Research

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treatment, patients with more aggressive kidney involvement may require immunosuppressive therapy. Further studies are needed for revealing the relationship between FMF gene mutation and nonamyloid glomerular diseases.© 2015 ACT. All rights reserved. . Mutations of the MEFV gene, on the short arm of chromosome 16, codes for pyrin or marenostrin proteins is responsible for the disease. The MEFV mutation is found in less than 70% of patients diagnosed with FMF. Four mutations have been defined in 85% of patients from the mentioned 4 ethnic groups (M694V, M680I, M694I V726A) [3][4][5] . AA type amyloidosis is the result of serum amyloid A protein deposition in tissues. It is the best understood and the most serious reason for kidney failure in patients with FMF. In a report from Turkey, amyloidosis rates among FMF patients were found to be 7% [6] . There is no publication proving an increase of glomerulonephritis among FMF patients. ABSTRACT AIM: Kidney involvement is the most serious organ involvement of Familial Mediterranean Fever (FMF), while the most common cause is AA type amyloidosis with serum amyloid AA deposition. However, vasculitis and other types of glomerulonephritis (GN) also have been reported. With this study we evaluated biopsy proven non-amyloid glomerular diseases in patients with FMF. METHODS: At our Nephrology clinic, total 950 patients followed by diagnosis of FMF have been evaluated. Nine patients who had positive proteinuria ( >500 mg/day) but had negative amyloidosis in the tissue biopsy were made renal biopsy. RESULTS: Nine patients underwent a renal biopsy, two patients were found to have IgA nephropathy (IGAN), three mesangioproliferative glomerulonephritis (MsPGN), three membranous glomerulonephritis (MGN) and one had immune complex glomerulonephritis. Two patients with IGAN and one patient with MGN with non-nephrotic proteinuria exhibited significant improvement with colchicine and angiotensin receptor blocker (ARB) therapy. Other patients were treated with colchicine, an ARB and immunosuppressive drugs. Upon evaluation for the FMF gene mutation, different mutations have been found for the same glomerulonephritis type. CONCLUSIONS: Other glomerular causes also must be investigated alongside amyloidosis in the case of kidney involvement in FMF patients. While patients with IGAN and other glomerulonephrities with non-nephrotic proteinuria can respond well to colchicine

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“…Said et al reported two patients diagnosed with FMF and IgA nephritis treated with colchicine who were not taking drugs regularly before the GN diagnosis. They had significant improvement at 3-6 months after regular treatment (26). In a recent study, Gok et al described a patient with FMF who presented with gross hematuria and protracted febrile myalgia.…”

Section: Dıscussıonmentioning

confidence: 99%