|Author(s) (year)||Study design||Subjects||Outcome||Period||Population Total GNa/IgAN||Resultse|
|Porro et al.  (1992)||case–control study||60 biopsy-proven chronic GNa patients in a University hospital in Italy (including 27 IgAN patients)||onset of IgAN||1987–1990||60/27 (reference:120)||
·An increased risk of IgAN was found for occupational solvent exposure group.|
·RRb of IgAN for occupational solvent exposure ; 4.25 (1.18–16.36)
|Stengel et al.  (1995)||case–control study||298 biopsy-proven GNa patients in 5 hospitals in Paris (including 116 IgAN patients)||aggravation of IgAN to CRF||1989–1991||298/116 (reference:298)||
·Among males, clear association was observed between CRF and high exposure to solvents for IgAN; ORc = 3.5 (1.0–11.8), P < 0.05.|
·The OR increased with duration of exposure; OR = 5.6 (1.3–24.1) for ≥10 years exposure, (P = 0.02).
·No relationship was observed for cases without CRF.
|Wakai et al.  (1999)||case–control study||94 biopsy-proven IgAN patients in medical centers in Japan||onset of IgAN||1997–1999||94/94 (reference:185)||· Work-related exposure to organic solvents was found not to be associated with the risk for IgAN; OR = 0.55 (0.27–1.12), (P < 0.10)|
|Jacob et al.  (2007)||retrospective cohort study||338 non-ESRD patients in Paris (including 194 IgAN patients with biopsy confirm)||aggravation of IgAN to ESRD||2002–2004||338/194||
·Solvent exposure was associated with faster progression of IgAN to ESRD, HRd for IgAN is 2.6 (1.3–5.5) for high exposure versus none (p < 0.05).|
·There was a trend increasing HR with exposure duration before and its persistence after diagnosis.
|Jacob et al.  (2007)||retrospective cohort study||269 patients with non-ESRD and biopsy-proven primary GNa diagnosis between 1994 and 2001 in Paris and suburbs (including 167 IgAN patients)||aggravation of IgAN to ESRD||2002–2004||269/167||·This study showed the potential role of toluene and xylene, some petroleum products, ketones and possibly dichloromethane in the progression of GNa to ESRD.|