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Silicosis and renal disease: insights from a case of IgA nephropathy #MMPMID26423329
RICCÒ M; THAI E; CELLA S
Ind Health 2016[Jan]; 54 (1): 74-8 PMID26423329show ga
A 68-yr-old male, smoker, is admitted for proteinuria (2,800?mg/24 h) and reduced renal function (serum creatinine 2?mg/dl, GFR 35 ml/min). Renter, he started working 20-yr-old as a sandstone cave miner. Despite the high levels of silica dusts, he reported no mandatory use of airways protection devices during the first 25?yr of activity. No clinical or radiological signs of silicosis or pneumoconiosis where reported until the year of retirement (1997). Erythrocyte sedimentation rate (91?mm/h) and C reactive protein (35?mg/l) suggested a pro-inflammatory status. High serum IgA was found (465?mg/dl). A renal biopsy identified glomerular sclerosis with IgA deposition, signs of diffuse vasculitis and tubular atrophia suggesting a diagnosis of IgA nephropathy. Chest X-Rays showed emphysema and diffuse nodularity suggesting diagnosis of silicosis. Chest tomography was also positive for mild signs of silicosis with silicotic nodules and without honeycombing. IgA nephropathy is the most common type of glomerulonephritis worldwide. Several clues suggest a genetic or acquired abnormality of immune system as a trigger of the increased production of IgA. In our case report, simultaneous kidney and pulmonary disease could suggest same triggers (e.g. exposure to virus, bacteria or environmental agents) inducing IgA synthesis and pulmonary immune system activation.
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Ind+Health 2016 ; 54 (1): 74-8
