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 blindly assessed for chronic hydrocarbon exposure by a validated questionnaire. Serum creatinine, proteinuria, and urinary excretion of markers of renal tubular damage were measured. Patients were assessed for evidence of progressive renal failure (PRF) (defined as persistent rise of serum creatinine > 50 mumol/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, without PRF). The two groups were comparable in age, sex, duration of diagnosis (since the time of biopsy) and blood pressure control. The derived chronic hydrocarbon exposure scores were significantly higher in group 1 than 2 (p < 0.001). Moreover, hydrocarbon exposure score since the diagnosis of glomerulonephritis was significantly higher in group 1 than 2 (p < 0.001). In group 1, 73% of patients continued to be exposed to hydrocarbons at their work site after the diagnosis of glomerulonephritis, compared to only 13% in group 2 (p < 0.001). At renal biopsy, group 1 had a significantly higher mean serum creatinine than group 2 but the degree of proteinuria and proportion of patients with hypertension were similar. During follow-up serum creatinine rose significantly in group 1 but not in group 2. In group 2, proteinuria fell significantly during follow-up but remained unchanged in group 1. A higher proportion of patients from group 1 developed hypertension requiring antihypertensive drugs (84% vs. 28%; p < 0.001). Urinary marker secretion data indicated a possible association between tubular damage and renal impairment. These results suggest that chronic hydrocarbon exposure and renal tubular damage are important additional risk factors in the progression of primary glomerulonephritis.
Yaqoob
M
M
Royal Liverpool University Hospital.
Stevenson
A
A
Mason
H
H
Bell
G M
GM
D000118:Acetylglucosaminidase / Q000652:urine; D000328:Adult; D003404:Creatinine / Q000097:blood; D005260:Female; D015432:Glomerulonephritis, Membranoproliferative / Q000139:chemically induced* / Q000652:urine; D015433:Glomerulonephritis, Membranous / Q000139:chemically induced* / Q000652:urine; D006801:Humans; D006838:Hydrocarbons / Q000009:adverse effects*; D006977:Hypertension, Renal / Q000209:etiology; D007668:Kidney / Q000187:drug effects; D007676:Kidney Failure, Chronic / Q000209:etiology; D007931:Leucyl Aminopeptidase / Q000652:urine; D008297:Male; D008875:Middle Aged; D016273:Occupational Exposure; D011507:Proteinuria / Q000150:complications; D013997:Time Factors
D006838:Hydrocarbons; D003404:Creatinine; D000118:Acetylglucosaminidase; D007931:Leucyl Aminopeptidase