EVALUATION OF RENAL TUBULAR FUNCTIONS IN CONVALESCENT PHASE OF HEMORRHAGIC-FEVER WITH RENAL SYNDROME

To evaluate renal tubular functions and to investigate the causative f actors of urinary-concentrating defects in the late stage of hemorrhag ic fever with renal syndrome(HFRS), 11 HFRS patients in the convalesce nt phase were studied and compared with 8 acute renal failure (ARF) pa tients in convalescence (disease controls) and 9 healthy adults prepar ing for kidney donation (normal controls, NC). Minimal urine osmolalit y 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-ho ur water deprivation + vasopressin stimulation, HFRS had lower urine o smolality (433.7 +/- 31.1 versus 850.0 +/- 35.1 mosm/kg; p < 0.05), ur ine-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 low er solute-free water reabsorption measured at maximal antidiuresis ind uced by water deprivation + vasopressin stimulation + hypertonic salin e infusion (p < 0.05). In HFRS, the plasma vasopressin level and plasm a 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 aft er 12-hour water deprivation, respectively (p < 0.01). However, neithe r basal nor stimulated values of the plasma vasopressin level or plasm a vasopressin/ osmolality ratio was different among the 3 groups. HFRS patients were not different from ARF patients or NC in lithium cleara nce, 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 ob viously impaired. This study suggests that the most important factor c ontributing to the urinary-concentrating defect in HFRS is the reduced collecting duct responsiveness to vasopressin.