Journal of the American Society of Nephrology
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Published ahead of print on November 29, 2006
J Am Soc Nephrol 18: 274-281, 2007
© 2007 American Society of Nephrology
doi: 10.1681/ASN.2006060652

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Epidemiology and Outcomes

Effect of Organic Solvent Exposure on Chronic Kidney Disease Progression: The GN-PROGRESS Cohort Study

Sophie Jacob*,{dagger}, Michel Héry{ddagger}, Jean-Claude Protois{ddagger}, Jérôme Rossert§ and Bénédicte Stengel*,{dagger}

* INSERM, Unit 780, and {dagger} University Paris-Sud, Faculty of Medicine, IFR69, Villejuif, {ddagger} INRS, Vandoeuvre-les-Nancy, and § INSERM, Unit 652, Paris-Descartes University, Faculty of Medicine, and AP-HP, Hôpital Européen Georges Pompidou, Service Néphrologie, Paris, France

Address correspondence to: Dr. Sophie Jacob, INSERM Unit 780, 16, avenue Paul Vaillant-Couturier, 94807 Villejuif cedex, France. Phone: +33-1-45-59-51-08; Fax: +33-1-45-59-51-52; E-mail: jacob-s{at}vjf.inserm.fr

Received for publication June 23, 2006. Accepted for publication October 10, 2006.

It has been suggested that solvent exposure may have a role in the progression of glomerulonephritis (GN) to ESRD, but this has never been tested with an appropriate cohort study design. A total of 338 non-ESRD patients with a first biopsy for primary GN between 1994 and 2001 were included: 194 IgA nephropathies (IgAN), 75 membranous nephropathies (MN), and 69 FSGS. ESRD, defined as an estimated GFR <15 ml/min per 1.73 m2 or dialysis, was registered during a mean follow-up period of 5 yr. Patients’ lifelong solvent exposures before and after diagnosis were recorded by interview and assessed by industrial hygienist experts. Cox models were used to estimate adjusted hazard ratios (HR) of ESRD related to exposures. Overall, 15 and 14% of the patients had been exposed at a low and a high level before diagnosis, respectively. Forty-two with IgAN, 12 with MN, and 22 with FSGS reached ESRD. A graded relationship was observed for MN (age- and gender-adjusted HR [95% confidence interval] for low exposure versus none was 3.1 [0.5 to 18.2] and for high exposure versus none was 8.2 [1.9 to 34.7]) and for IgAN (1.6 [0.7 to 3.9] and 2.2 [1.0 to 4.8]) but not for FSGS. Solvent risk was mediated only partly by baseline proteinuria: Adjusted HR for high exposure versus none was 5.5 (1.3 to 23.9) for MN and 1.8 (0.8 to 3.9) for IgAN. In patients with IgAN, there was a trend in increasing HR with exposure duration before and its persistence after diagnosis. These findings support the hypothesized association of solvent exposure with the progression of GN to ESRD. They should prompt clinicians to give greater attention to patients’ occupational exposures and possibly to consider professional reclassification.


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