Determination of urine tumor necrosis factor, IL-6, IL-8, and serum IL-6 in patients with hemorrhagic fever with renal syndrome

OBJECTIVE: The aim of this study was to explore the role of cytokines in the pathogenesis of hemorrhagic fever with renal syndrome (HFRS). METHODS: Double-antibody sandwich ELISA was used to determine serum interleukin (IL)-6, urine tumor necrosis factor (TNF), IL-6, and IL-8 levels in 56 patients with HFRS. RESULTS: Serum IL-6, urine TNF, IL-6, and IL-8 concentrations in HFRS patients were significantly higher than those in the control group (p < 0.001). the concentrations increased at fever stage, then continued to increase during the hypotension stage and peaked at the oliguria stage. the concentrations of serum IL-6, urine TNF, IL-6, and IL-8 increased according to the severity of the disease, and differed greatly among different types of the disease. serum IL-6 had remarkable relationships with serum specific antibodies. it was positively related to serum 12-microglobulin (β-mg), blood ureanitrogen (bun), and creatinine (Cr). significant positive relationships were also found both between urine IL-6 and TNF, and between IL-6 and IL-8 (r = 0.5768, p < 0.05; r = 0.3760, p < 0.01). CONCLUSION: TNF, IL-6, and IL-8 were activated during the course of the disease. IL-6 was associated with the immunopathological lesions caused by the hyperfunction of the humoral immune response. IL-6, IL-8 and TNF were involved in renal immune impairment. determining them might, to a certain extent, be useful in predicting the prognosis and outcome of patients with hfrs.

Metabolic acidosis and urinary acidification defect during the course of hemorrhagic fever with renal syndrome

To evaluate urinary acidification defect and its contribution to metabolic acidosis (MA) during hemorrhagic fever with renal syndrome (HFRS), we serially analyzed acid-base balance and urinary acidification indices in 10 HFRS patients. Data of the patients were compared with those of 8 normal volunteers (NC). MA was observed in 6 of 8 patients in the oliguric phase, 5 of 7 in the early diuretic phase, 8 of 10 in the late diuretic phase and 2 of 9 in the convalescent phase. HFRS patients with MA had a higher plasma anion gap in the oliguric and early diuretic phases than NC and a higher plasma Cl/Na ratio in the late diuretic phase than NC. As compared with acid-loaded NC, HFRS patients had a higher urine pH in the oliguric, early diuretic and late diuretic phases, a higher urine anion gap (UAG) in the oliguric and early diuretic phases and a lower urinary NH4+ excretory rate in the oliguric, early diuretic and late diuretic phases. Overt distal acidification defect was observed in 6 of 8 patients in the oliguric phase, 3 of 7 in the early diuretic phase, 5 of 10 in the late diuretic phase and none of 9 in the convalescent phase. None of the convalescent patients had latent acidification defect. In conclusion, urinary acidification defect is marked in the oliguric and diuretic phases of severe HFRS and may play a role in the development of a high anion gap (AG) metabolic acidosis in the earlier phase and hyperchloremic MA in the later phase, but rapidly recovers in the convalescent phase.