To the Editor: Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent inflammatory attacks of the serosal and synovial membranes and fever.1 The main complication of the disease is the development of amyloidosis. In most FMFpatients, colchicine treatment prevents inflammatory attacks and development of amyloidosis, whereas the inflammatory crises were not completely suppressed.2 In the literature, cases of amyloidosis of FMF that regressed have rarely been reported. 3–5 We report two cases of nephrotic syndrome due to AA amyloidosis secondary to FMF who recovered colchicine treatment.In May 1999, a 38-year-old man was admitted to the hospital because of attacks of FMF and nephrotic syndrome. Amyloidosis was proved by rectal biopsy. The laboratory findings included urinary protein excretion of 4 g/day, erythrocyte sedimentation rate 90 mm/h, serum creatinine 1.1 mg/dL, albumin 1.6 g/dL, and total protein 5.2 g/dL. Therapy with colchicine (1.5 mg/day) was initiated and was continued during the follow up. The proteinuria disappeared (50 mg/day) in October 2002. He remained proteinuria free during further follow up.In July 2001, a 20-year-old girl was admitted to the hospital with fever, severe abdominal pain, arthralgia, myalgia, and swelling of the hands and feet. She had a history of recurrent abdominal pain and fever for 5 years. Physical examination showed pretibial oedema. Her blood pressure was 100/60 mmHg. Laboratory investigations revealed a hemoglobin level of 12.6 g/dL, a white blood cell count of 13 000/mm3, an erythrocyte sedimentation rate of 79 mm/h, urinary protein excretion 4.3 g/day, serum creatinine 0.91 mg/dL, albumin 3.1 g/dL, and total protein 6.3 g/dL. Mutation analysis of the MEFV (gene for FMF) showed it to be homozygous for the M694 V mutation. A rectal biopsy showed amyloidosis. Colchicine treatment (1.5 mg/day) was started. The proteinuria decreased significantly, and the nephrotic syndrome disappeared at the third to fourth year of colchicine treatment.The most severe manifestation of FMF results from the deposition of amyloid A protein.1,2 The most common clinical manifestation of FMF-related amyloidosis is the development of nephrotic syndrome and eventually uremia. Patients are usually normotensive and non-hematuric.1 Due to widespread use of colchicine, only a minority of FMFpatients now present with amyloidosis. The frequency of amyloidosis differs among various ethnic groups and depends on whether patients are taking colchicine.2 The introduction of long-term colchicine daily prophylactic therapy was shown to be highly effective in preventing or ameliorating the subsequent acute attacks of FMF and amyloidosis. Once it was believed that long-term treatment with colchicine prevents amyloidosis in FMFpatients, but it was not effective for amyloidotic kidney disease when it had reached the nephrotic stage. The presented cases demonstrate that reversal of the nephrotic syndrome by colchicines in amyloidosis of FMF. I conclude that colchicine is of paramount importance in preventing FMF amyloidosis; it may also arrest the progression of amyloidosis in those who already have it, and may even reverse proteinuria.