Microalbuminuria in the course of familial Mediterranean fever.

Abstract

Sir, In their interesting paper, Lobato et al. [1] studied the importance of microalbuminuria as a predictor of symptomatic disease and clinical nephropathy in familial transthretin related amyloidosis. They demonstrated that microalbuminuria represents a first stage of clinical amyloid nephropathy and that it could be premonitory of neuropathy. They recommend the systematic and regular search for urinary albumin excretion in symptomatic gene carriers and patients, instead of renal biopsy, as a non-invasive method for estimating the progression of amyloidosis. Previously, it has been shown that in cases of essential hypertension and diabetic nephropathy, early renal glomerular damage can be detected by microalbuminuria [2]. Saatci et al. [3] previously showed increased urinary b2-microglobulin excretion and microalbuminuria during familial Mediterranean fever (FMF) attacks. FMF is characterized by recurrent fever and serositis. The most important complication of the disease is AA amyloidosis. Proteinuria and renal failure may complicate the clinical course. We have measured the microalbuminuria and urinary glycosaminoglycan (GAG) levels as predictors of amyloidosis in patients with FMF in an attack-free period. We found that mean urinary GAG levels of the patients with FMF secondary amyloidosis were lower than those of FMF patients without amyloidosis [4]. When we examined the duration of disease in the FMF group without amyloidosis, we saw that median GAG levels were significantly lower in patients having the disease for >10 years compared with those having the disease for <3 years. Also, microalbuminuria levels tended to increase with the duration of the disease. In FMF patients with low GAG levels, colchicine dose was increased and urinary GAG and microalbuminuria levels were re-examined after 2 weeks. In these patients, urinary GAG levels increased significantly with increments in the colchicine dose. Microalbuminuria decreased along with the increase in urinary GAG when colchicine dose was increased. These results suggest that urinary GAG and microalbuminuria may be predictors of amyloidosis in FMF patients. We also suggest that effective colchicine dosing may be monitored by following urinary GAG excretion and microalbuminuria. Our results are in agreement with the recommendation by Lobato et al.