Diffuse panbronchiolitis and IgA nephropathy

Chronic infections of respiratory tracts are suspected to promote the development of IgA nephropathy. From the study of one case, we discuss the hypothesis that infections by pseudomonas aeruginosa might promote an increased bronchial production of IgA1, which could pass in the serum and settle into immune complexes in the kidney. A 67 years old woman presented simultaneously IgA nephropathy and diffuse panbronchiolitis. The evolution was marked by repeated infections by pseudomonas aeruginosa. The study of lung biopsy by immunohistochemistry showed intense expression of IgA1 in bronchioles, increased when compared to large bronchi. In contrast, expression of the transport receptor (pIgR) was decreased in inflamed bronchioles and preserved in bronchi. The BAL during an infection by pseudomonas aeruginosa showed increased secretory (S-) IgA with predominance of S-IgA1 (28.6 µg/mL versus S-IgA2 8.4µg/mL). In the sera collected during two infectious episodes and compared with an inter-critical sample, we found an increased IgA1 (776 and 549µg/mL versus 455µg/mL), associated with increased polymeric IgA (estimated at 40-50%, versus normally  10%). The increased expression of IgA1 in bronchiolar tissue, BAL and serum in the case of our patient further suggests a putative link between IgA nephropathy and diffuse panbronchiolitis, through exuberant production of IgA1 induced by pseudomonas aeruginosa infections.