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      Evaluation of Renal Tubular Functions in Convalescent Phase of Hemorrhagic Fever with Renal Syndrome

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          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.

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          Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. The Hantavirus Study Group.

          In May 1993 an outbreak of severe respiratory illness occurred in the southwestern United States. A previously unknown hantavirus was identified as the cause. In Asia hantaviruses are associated with hemorrhagic fever and renal disease. They have not been known as a cause of human disease in North America. We analyzed clinical, laboratory, and autopsy data on the first 17 persons with confirmed infection from this newly recognized strain of hantavirus. The mean age of the patients was 32.2 years (range, 13 to 64); 61 percent were women, 72 percent were Native American, 22 percent white, and 6 percent Hispanic. The most common prodromal symptoms were fever and myalgia (100 percent), cough or dyspnea (76 percent), gastrointestinal symptoms (76 percent), and headache (71 percent). The most common physical findings were tachypnea (100 percent), tachycardia (94 percent), and hypotension (50 percent). The laboratory findings included leukocytosis (median peak cell count, 26,000 per cubic millimeter), often with myeloid precursors, an increased hematocrit, thrombocytopenia (median lowest platelet count, 64,000 per cubic millimeter), prolonged prothrombin and partial-thromboplastin times, an elevated serum lactate dehydrogenase concentration, decreased serum protein concentrations, and proteinuria. Rapidly progressive acute pulmonary edema developed in 15 of the 17 patients (88 percent), and 13 patients, all of whom had profound hypotension, died (case fatality rate, 76 percent). Increases in the hematocrit and partial-thromboplastin time were predictive of death. Infection with a newly described hantavirus causes the hantavirus pulmonary syndrome, which is characterized by a brief prodromal illness followed by rapidly progressive, noncardiogenic pulmonary edema.

            Author and article information

            Am J Nephrol
            American Journal of Nephrology
            S. Karger AG
            April 1998
            01 April 1998
            : 18
            : 2
            : 123-130
            a Department of Internal Medicine, Hallym University Hangang Sacred Heart Hospital, Seoul, b Division of Nephrology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, and c Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju, Korea
            13320 Am J Nephrol 1998;18:123–130
            © 1998 S. Karger AG, Basel

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            Page count
            Figures: 4, Tables: 5, References: 26, Pages: 8
            Self URI (application/pdf): https://www.karger.com/Article/Pdf/13320
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