Idiopathic membranous glomerulonephritis (iMGN) has previously been shown to be associated with urinary excretion of terminal complement complexes while increased urinary levels of cytokines have been reported in mesangial proliferative glomerulonephritis. In the present cross-sectional study urinary excretion of IL-1βTNF-α, IL-6;, and soluble C5b-9 (SC5b-9) was examined for 23 patients with iMGN, 16 patients with diabetic nephropathy (DNP), and 17 healthy subjects. IL-1βexcretion (pg/mg crea) was significantly higher in iMGN patients (375, range 162–11 000) than in DNP patients (39, range 22–59,P57 pg/mg crea) was detected in 4/5 patients with progression but in none of the stable patients (P<0.001). Seventy-seven per cent of the iMGN patients and 94of DNP patients, but none of the healthy subjects had detectable SC5b-9 excretion. In DNP patients the urinary SC5b-9 levels correlated with proteinuria whereas in iMGN the SC5b-9 excretion could not be accounted for by proteinuria alone. Urinary excretion of SC5b-9 correlated with decreased renal function and had a relationship to urinary IL-1/βand TNF-αexcretion in iMGN patients. Moreover the median excretion rate of SC5b-9 was higher in patients with than in those without progression of iMGN. The results suggest that increased urinary IL-1β, TNF-α, and SC5b-9 excretion are detected in patients having iMGN. They may be indicators of a pro
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