Renal amyloidosis in cystic fibrosis: role of colchicine therapy

Cystic fibrosis (CF) is the most common autosomal-recessive condition affecting the white population, with an incidence ranging between 1:2500 and 1:1800 births. It is caused by a mutation in the CFTR gene, encoding the polyprotein CF transmembrane conductance regulator (CFTR), which functions as an ATP-responsive chloride channel in the apical membrane of epithelial cells. Pathologic changes related to CFTR mutations mostly affect secretory cells, resulting in low secretion volume and increased viscosity and promoting mucosal obstruction in the lung, pancreas, biliary tract, sinuses and reproductive tract [1]. Patients with CF currently show a continuing improvement in their life expectancy, an improvement that allows for better multidisciplinary monitoring and earlier therapeutic interventions. Owing to their longer life expectancy, CF patients present complications that were not recorded before [2]. This is illustrated by the following report of two cases of renal AA amyloidosis in women with CF.