Literature DB >> 20706133

Regression of superficial glomerular podocyte injury in type 2 diabetic rats with overt albuminuria: effect of angiotensin II blockade.

Genei Ihara1, Hideyasu Kiyomoto, Hiroyuki Kobori, Yukiko Nagai, Naro Ohashi, Hirofumi Hitomi, Daisuke Nakano, Nicolas Pelisch, Taiga Hara, Takefumi Mori, Sadayoshi Ito, Masakazu Kohno, Akira Nishiyama.   

Abstract

OBJECTIVE: Clinical studies indicate that the remission, regression or both of nephrotic-range albuminuria are exerted by angiotensin II receptor blockers (ARBs) in diabetes. The current study was performed to test the hypothesis that these effects of ARBs are associated with regression of glomerular podocyte injury.
METHODS: We examined the effects of an ARB, olmesartan, on glomerular podocyte injury in type 2 diabetic Otsuka-Long-Evans-Tokushima-Fatty rats with overt albuminuria.
RESULTS: At baseline (55-week-old), diabetic Otsuka-Long-Evans-Tokushima-Fatty rats showed severe albuminuria with desmin-positive areas (an index of podocyte injury) in both superficial and juxtamedullary glomeruli, and podocyte injury was much greater in juxtamedullary than in superficial glomeruli. At 75-week-old, Otsuka-Long-Evans-Tokushima-Fatty rats had developed more severe albuminuria and superficial glomerular podocyte injury, whereas juxtamedullary glomerular podocyte injury did not advance further. Olmesartan (10 mg/kg per day) decreased albuminuria and superficial glomerular desmin staining to levels that were lower than those at baseline, whereas advanced juxtamedullary glomerular podocyte injury was not changed.
CONCLUSION: The current study demonstrates for the first time that juxtamedullary glomerular podocyte injury reaches a severe condition at an earlier time than superficial glomerular podocyte injury during the progression of overt albuminuria in type 2 diabetic rats. Our data also support the hypothesis that the antialbuminuric effects of ARBs are associated with regression of superficial glomerular podocyte injury in type 2 diabetes with nephrotic-range albuminuria.

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Year:  2010        PMID: 20706133      PMCID: PMC2955758          DOI: 10.1097/HJH.0b013e32833dfcda

Source DB:  PubMed          Journal:  J Hypertens        ISSN: 0263-6352            Impact factor:   4.844


  39 in total

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3.  Global heterogeneity of glomerular volume distribution in early diabetic nephropathy.

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4.  Angiotensin II type 1 receptor-mediated augmentation of renal interstitial fluid angiotensin II in angiotensin II-induced hypertension.

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Journal:  J Hypertens       Date:  2003-10       Impact factor: 4.844

5.  Progression of nephropathy in type 2 diabetic patients.

Authors:  Kasper Rossing; Per K Christensen; Peter Hovind; Lise Tarnow; Peter Rossing; Hans-Henrik Parving
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  18 in total

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2.  Multiphoton imaging of the glomerular permeability of angiotensinogen.

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3.  Role of the renin angiotensin system in diabetic nephropathy.

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4.  Add-on aliskiren elicits stronger renoprotection than high-dose valsartan in type 2 diabetic KKAy mice that do not respond to low-dose valsartan.

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5.  Aberrant activation of the intrarenal renin-angiotensin system in the developing kidneys of type 2 diabetic rats.

Authors:  Y-Y Fan; H Kobori; D Nakano; H Hitomi; H Mori; T Masaki; Y-X Sun; N Zhi; L Zhang; W Huang; B Zhu; P Li; A Nishiyama
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6.  Angiotensin-converting enzyme inhibitor does not suppress renal angiotensin II levels in angiotensin I-infused rats.

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9.  Angiotensin receptor and tumor necrosis factor-α activation contributes to glucose intolerance independent of systolic blood pressure in obese rats.

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10.  Albuminuria indicates the pressure-associated injury of juxtamedullary nephrons and cerebral strain vessels in spontaneously hypertensive stroke-prone rats.

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