Urinary tract infections activate both mucosal and systemic inflammatory responses reflected by elevation of cytokine concentrations in serum and urine. We determined urine and serum concentrations of tumour necrosis factor soluble receptors I and II (sTNFR I and sTNFR II) and interleukin-1 receptor antagonist (IL-1ra) in 41 women with acute pyelonephritis caused by Escherichia coli, 2 weeks after the infection, during a subsequent episode of cystitis or asymptomatic bacteriuria and also later when the same patients were free from bacteriuria. Concentrations of sTNFR I, sTNFR II and IL-1ra were related to the expression of five virulence markers of E. coli, glomerular filtration rate (GFR) and to the concentration of C-reactive protein (CRP) in serum. Patients with acute pyelonephritis had elevated serum concentrations of sTNFR I and sTNFR II compared to healthy women (P < 0.001 for both comparisons). The concentrations of sTNFR I and sTNFR II in urine were significantly higher in patients with acute pyelonephritis compared to controls (P < 0.001 in both cases). The concentration of sTNFR II in urine was higher in patients infected by E. coli producing haemolysin (P = 0.05) and in patients infected by E. coli expressing hydrophobic properties (P = 0.05) compared to patients infected by strains without these virulence traits. Patients who had high concentrations of sTNFR II in serum during acute pyelonephritis had lower GFR at follow-up (r = -0.48, P = 0.05). Patients who responded with a marked increase in CRP had higher sTNFR I and sTNFR II in urine (r = 0.58, P < 0.01 and r = 0.48, P < 0.01, respectively). The concentrations of sTNFR I and sTNFR II in serum and urine decreased during follow-up and were lower 2 weeks after the infection when all patients were free from bacteriuria. IL-1ra in serum was elevated during pyelonephritis (P < 0.001) while that in urine was significantly lower compared to controls (P < 0.001). It is concluded that the increased concentrations of TNF receptors may block the cytotoxic and inflammatory actions and reduce the sensibility of renal cells to TNF alpha-mediated effects.