SUMMARY We report for the first time to our knowledge the histopathological findings in the eye of a patient with type II mesangiocapillary glomerulonephritis (dense deposit disease) in which a deposit of material morphologically very similar to that which is pathognomonic for the disease in the kidney was demonstrated in Bruch's membrane. The nature of the deposit in the renal lesion is unknown but is considered to represent a structural alteration secondary to a reaction with anticomplement antibody. Clinically the fundus appearance resembled that seen in drusen.

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Forty cases of mesangiocapillary glomerulonephritis are reviewed for whom both light and electron microscopy and full clinical data were available. Immunofluorescence microscopy (IF) was performed on 23 cases and complement screening (CH50, C4 and C3) on 25 cases, with follow-up period of 5-22 y. The results of EM revealed 17 cases (42 per cent.) of Type I and 23 cases (58 per cent.) of Type II MCGN but only 52 per cent. of Type II cases were correctly identified by light microscopy. Epimembranous deposits were seen as frequently in Type II as in Type I (26 per cent. and 30 per cent.) and fragmentation of glomerular capillary basement membranes (GBM) was seen in 27 per cent. of Type I cases. Overall patient survival was 49 per cent. at 10 y and that of patients who presented with nephrotic syndrome was poor (39 per cent. at 10 y). Persistent hypocomplementaemia with C3 Nephritic Factor was present in 40 per cent.; the survival of these patients was less than those with normal complement levels (70 per cent. vs 100 per cent. at 5 y) and they were also more likely to develop renal failure. Renal failure was more likely to develop in those with a creatinine clearance of less than 100 ml/min at presentation and where the biopsy showed substantial crescents in greater than 20 per cent. of glomeruli. Mean CH50, C3 and C4 was lower in the hypocomplementaemic as compared to normocomplementaemic patients, and there were no differences between Type I and Type II. IF showed immunoglobulins and fibrin as well as C3 in both Type I and Type II cases. Our results support the concept of an immune-complex mediated phase in both types of MCGN, and we further suggest that (a) epimembranous deposits are common in both Type I and Type II and (b) cases with fragmentation of the GBM should be designated Type Ia.

Exposure to organic solvents was compared by interview and questionnaire in 50 patients with biopsy-proven proliferative glomerulonephritis in whom there was no evidence of systemic disease or preceding infection with that of 100 control subjects matched for age, sex and social class. The interview was conducted by a lay person who did not know whether the interviewee was a patient with glomerulonephritis or a control subject. The exposure scores derived from the results of the questionnaires were significantly greater in the patients with glomerulonephritis than the control subjects (13,186 ± 3,716 vs. 3,030 ± 1,152, p < 0.01). The degree of exposure was higher in those patients with the more severe diffuse endocapillary proliferative glomerulonephritis than in those with mesangial proliferative glomerulonephritis. In the glomerulonephritis patients solvent exposure was mainly occupational in origin and involved fuels, paints and degreasing agents in most cases. This occupational exposure was significantly greater than in the control subjects (13,061 ± 3,858 vs. 2,878 ± 1,146, p < 0.01). It is suggested that exposure to organic solvents may participate in the pathogenesis of non-systemic proliferative glomerulonephritis.

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