To evaluate renal tubular functions and to investigate the causative factors of urinary-concentrating defects in the late stage of hemorrhagic fever with renal syndrome (HFRS), 11 HFRS patients in the convalescent phase were studied and compared with 8 acute renal failure (ARF) patients in convalescence (disease controls) and 9 healthy adults preparing for kidney donation (normal controls, NC). Minimal urine osmolality induced by water loading was higher (p < 0.05) in HFRS (89.5 ± 22.1 mosm/kg) and ARF patients (84.8 ± 14.7 mosm/kg) than in NC (47.8 ± 4.6 mosm/kg), but the solute-free water clearance of HFRS patients (9.0 ± 1.3%), measured at maximal diuresis, was not different from that of ARF patients (6.7 ± 1.2%) or NC (10.5 ± 1.4%). After 12-hour water deprivation + vasopressin stimulation, HFRS had lower urine osmolality (433.7 ± 31.1 versus 850.0 ± 35.1 mosm/kg; p < 0.05), urine-to-plasma osmolality ratio (1.47 ± 0.11 versus 2.91 ± 0.11; p < 0.05), and solute-free water reabsorption (0.53 ± 0.07 versus 0.91 ± 0.12%; p < 0.05) than NC. As compared with ARF patients (1.09 ± 0.16%) or NC (1.49 ± 0.16%), HFRS patients (0.43 ± 0.20%) had lower solute-free water reabsorption measured at maximal antidiuresis induced by water deprivation + vasopressin stimulation + hypertonic saline infusion (p < 0.05). In HFRS, the plasma vasopressin level and plasma vasopressin/osmolality ratio increased from 3.9 ± 0.8 to 6.1 ± 1.1 pg/ml and from 0.013 ± 0.003 to 0.020 ± 0.004 pg/ml/mosm/kg after 12-hour water deprivation, respectively (p < 0.01). However, neither basal nor stimulated values of the plasma vasopressin level or plasma vasopressin/osmolality ratio was different among the 3 groups. HFRS patients were not different from ARF patients or NC in lithium clearance, urinary-acidifying capacity, and fractional excretions of sodium, potassium and bicarbonate. We conclude that in the convalescent phase of HFRS, the urinary-acidifying ability is not disturbed, the urinary-diluting defect is mild, and the urinary-concentrating capacity is obviously impaired. This study suggests that the most important factor contributing to the urinary-concentrating defect in HFRS is the reduced collecting duct responsiveness to vasopressin.