Pathogenesis of nonoliguric acute renal failure.
| Project/Area Number |
63480188
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
HONDA Nishio Hamamatsu University School of Medicine Vice President, 医学部, 副学長 (00010231)
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| Co-Investigator(Kenkyū-buntansha) |
ARAI Takami Hamamatsu University School of Medicine Internal Medicine, Senior Resident, 医学部, 医員
IKEGAYA Naoki Hamamatsu University School of Medicine Internal Medicine, Senior Resident, 医学部, 医員
HISHIDA Akira Hamamatsu University School of Medicine Internal Medicine, Assistant Professor, 医学部, 講師 (70111812)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1989: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1988: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | nonoliguric acute renal failure / oliguric acute renal failure / glomerular filtering surface area / tubular necrosis / cast formation |
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| Research Abstract |
The role of glomerular alterations, tubular necrosis and cast formation in the maintenance of oliguric and nonoliguric acute renal failure was evaluated. Uranium-induced oliguric acute renal failure (OARF) or nonoligulic acute renal failure (NOARF) was induced by i.v.
injection of 2.0 or 0.9 mg/Kg of uranyl acetate in rabbits. Ischemic OARF or NOARF was induced by clamping left renal artery in rats with intact right kidney or in rats of which right kidney was removed.
Morphological studies done by scanning electron microscopy revealed that glometular alterations induced by renal ischemia or uranium injection included a flattening and spreading of podocyte cell bodies associated with loss of epithelial foot processes, and reduction in the diameter and density of endothelial fenestrae. There was no significant difference in these glomerular changes between OARF and.NOARF. Tubular alterations observed by light microscopy demonstrated that the number of necrotic tubules was larger in OARF than in NOARF and that there was no significant difference in the number of cast between OARF and NOARF.
We conclude from these observations that the difference of OARF and NOARF can not be ascribed to the glomerular alterations observed by scanning electron microscopy and to the cast formation. Back-leakage of filtrate through the necrotic tubules may play a role in maintaining oliguria in both ischemic and uranium-induced acute renal failure.
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Report
(3 results)
Research Products
(13 results)
