HYDROCARBON EXPOSURE AND TUBULAR DAMAGE - ADDITIONAL FACTORS IN THE PROGRESSION OF RENAL-FAILURE IN PRIMARY GLOMERULONEPHRITIS

To investigate the role of hydrocarbon exposure in the progression of glomerulonephritis, 68 patients (12 female) with biopsy-proven primary glomerulonephritis (60 proliferative cases, 8 membranous) were blindl y assessed for chronic hydrocarbon exposure by a validated questionnai re. Serum creatinine, proteinuria, and urinary excretion of markers of renal tubular damage were measured. Patients were assessed for eviden ce of progressive renal failure (PRF) (defined as persistent rise of s erum creatinine >50 mu mol/l above the baseline) during a mean follow up period of 5 years. Patients were divided according to the presence or absence of PRF, (group 1, n=29, with PRF) and (group 2, n=39, witho ut PRF). The two groups were comparable in age, sex, duration of diagn osis (since the time of biopsy) and blood pressure control. The derive d chronic hydrocarbon exposure scores were significantly higher in gro up 1 than 2 (p<0.001). Moreover, hydrocarbon exposure score since the diagnosis of glomerulonephritis was significantly higher in group 1: t han 2 (p<0.001). In group 1, 73% of patients continued to be exposed t o hydrocarbons at their work site after the diagnosis of glomeruloneph ritis, compared to only 13% in group 2 (p<0.001). At renal biopsy, gro up 1 had a significantly higher mean serum creatinine than group 2 but the degree of proteinuria and proportion of patients with hypertensio n were similar. During follow-up serum creatinine pose significantly i n group 1 but not in group 2. In group 2, proteinuria fell significant ly during follow-up but remained unchanged in group 1. A higher propor tion of patients from group 1 developed hypertension requiring antihyp ertensive drugs (84% vs. 28%; p<0.001). Urinary marker secretion data indicated a possible association between tubular damage and renal impa irment. These results suggest that chronic hydrocarbon exposure and re nal tubular damage are important additional risk factors in the progre ssion of primary glomerulonephritis.