Evaluation of renal tubular functions in convalescent phase of hemorrhagic fever with renal syndrome.
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.
Kim
G H
GH
Department of Internal Medicine, Hallym University Hangang Sacred Heart Hospital, Seoul, Korea.
Han
J S
JS
Earm
J
J
Jeon
U S
US
Kim
Y S
YS
Ahn
C
C
Kim
S
S
Lee
J S
JS
D058186:Acute Kidney Injury / Q000097:blood / Q000503:physiopathology / Q000652:urine; D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000652:urine; D003289:Convalescence; D005260:Female; D006480:Hemorrhagic Fever with Renal Syndrome / Q000097:blood / Q000503:physiopathology* / Q000652:urine; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007677:Kidney Function Tests; D007684:Kidney Tubules / Q000503:physiopathology*; D008094:Lithium / Q000097:blood / Q000493:pharmacokinetics / Q000652:urine; D008297:Male; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D009994:Osmolar Concentration; D014556:Urine / Q000737:chemistry / Q000502:physiology
D015415:Biomarkers; D008094:Lithium