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.
Acidosis, Renal Tubular/urine ; Acidosis, Renal Tubular/metabolism ; Hemorrhagic Fever with Renal Syndrome/urine ; Hemorrhagic Fever with Renal Syndrome/metabolism ; Human

OBJECTIVES: In order to evaluate the association between the Hantaan virus-induced cellular-immune response and clinical severity in patients with hemorrhagic fever with renal syndrome (HFRS). METHODS: We serially measured the serum (n = 16) and urine (n = 6) concentrations of soluble HLA class 1 antigen (sHLA-l) and clinical powameters in patients with HFRS. RESULTS: Serum sHLA-I concentrations in patients with HFRS were significantly higher than those in controls throughout all clinical phases (p < 0.01). The highly elevated Serum sHLA-I concentrations peaked in the oliguric phase and declined gradually through the phases of HFRS. Serum sHLA-l concentrations in patients with hypotensive episode were higher than in those without the episode (5,85 +/-2,184 vs. 2,389 +/- 860 ng/ml in oliguric phase, 4.11 +/- 1,952 vs. 1,502 +/- 592 ng/ml in diuretic phase, p < 0.05), and serum sHLA-l levels showed a significant correlation with blood WBC count (r = 0.75 in the febrile and hypotensive phase, p < 0.01) and serum creatinine concentrations (r = 0.64 in the oliguric phase, p< 0.01), respectively, Urine sHLA-I levels in the oliguric phase were significantly higher than those in the diuretic phase (390 +/- 155 vs. 214 +/- 45 ng/mg Cr, p < 0.05) and urine sHLA-I levels are associated with severe illness in patients with HFRS. The higher serum sHLA-I are associated with severe illness in patients with HFRS. The persistent elevation of serum sHLA-I during all phases of HFRS might be related to increased production due to prolonged cellular immunologic stimulation by the Hantaan virus rather than decreased excretion of sHLA-I through the kidney. CONCLUSION: We suggest that the serum and urine sHLA-I concentrations can be used as a stable and objective parameter for monitoring clinical severity and renal dysfunction in patients with HFRS.
Adult ; Enzyme-Linked Immunosorbent Assay ; HLA-A Antigens/urine* ; HLA-A Antigens/blood* ; Hemorrhagic Fever with Renal Syndrome/physiopathology ; Hemorrhagic Fever with Renal Syndrome/immunology* ; Human ; Male ; Sensitivity and Specificity ; Severity of Illness Index