ホスピタリティ研究における分析枠組みに関する一考察--ホスピタリティ認知概念を用いた研究方法の提案
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概要
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Six patients with acute hepatitis A who developed renal failure were studied in order to elucidate the pathogenesis of their renal dysfunction. The patients were admitted to our hospital on the 4-8th day (average, 5.6 days) since the onset of hepatitis symptoms. On admission, all of the patients were suffering from renal failure (serum creatinine 3.9∼19.0mg/dl, FENa 5.4∼13.9), although their hepatitis was nonfulminant except in one case. Bilirubinemia, uricacidemia and activation of the renin-angiotensin system were common to all patients, but none developed endotoxicemia or DIC. Immune complexes were not detected, and complements did not decrease except in 1 patient. Plasmapheresis was performed in 2 patients and daily hemodialysis in 4. Both hepatic and renal function in all patients recovered within about one month of admission. A kidney biopsy was performed in 5 patients on the 12∼38th hospital day (average, at 24.2 hospital days). Histological findings revealed slight glomerular changes without abnormal thickening of glomerular capillary walls. In contrast, changes were noted in renal tubules. All biopsy specimens demonstrated acute tubular necrosis or its recovery findings. Immunofluorescence study demonstrated no deposits of immunoglobulin, complements or fibrinogen in the biopsied renal tissues. Rapid aggravation and complete recovery of renal function in our patients suggests the clinical course of acute tubular necrosis rather than that of glomerulonephritis induced by immune complexes, Moreover, the results of our histological and immunological studies showed no evidence that immune complexes play a role in the development of renal failure. These results suggest that renal failure complicating hepatitis A infection may be caused by acute tubular necrosis in many cases.
- 日本ホスピタリティ・マネジメント学会の論文
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