Literature DB >> 11508273

Podocyte foot process broadening in experimental diabetic nephropathy: amelioration with renin-angiotensin blockade.

S A Mifsud1, T J Allen, J F Bertram, U L Hulthen, D J Kelly, M E Cooper, J L Wilkinson-Berka, R E Gilbert.   

Abstract

AIMS/HYPOTHESIS: Changes in podocyte number and morphology have been implicated in the pathogenesis of proteinuria and the progression of human and experimental kidney disease. This study sought to examine podocyte foot process and slit pore architecture in experimental diabetic nephropathy and to determine whether such changes were modified with renoprotective intervention by blockade of the renin-angiotensin system.
METHODS: The number of filtration slits per 100 microm of glomerular basement membrane was assessed by transmission electron microscopy and quantitated histomorphometrically in control animals and in rats with 24 weeks of streptozotocin-induced diabetes. Diabetic rats were either untreated or received the angiotensin converting enzyme inhibitor ramipril, or the angiotensin II type 1 receptor antagonist, valsartan.
RESULTS: When compared with control animals, diabetes was associated with a decrease in the number of slit pores per unit length of glomerular basement membrane, indicative of podocyte foot process broadening. Both ramipril and valsartan attenuated these ultrastructural changes to a similar degree. These differences remained after correcting for glomerular volume as a possible confounding variable. CONCLUSION/
INTERPRETATION: Preservation of podocyte architecture could contribute to the renoprotective effects of renin-angiotensin system blockade in diabetic nephropathy.

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Year:  2001        PMID: 11508273     DOI: 10.1007/s001250100561

Source DB:  PubMed          Journal:  Diabetologia        ISSN: 0012-186X            Impact factor:   10.122


  31 in total

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Review 2.  Antiproteinuric effect of RAS blockade: new mechanisms.

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Review 3.  The renin-angiotensin system in glomerular podocytes: mediator of glomerulosclerosis and link to hypertensive nephropathy.

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Review 5.  Resistance to insulin and kidney disease in the cardiorenal metabolic syndrome; role for angiotensin II.

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Authors:  Z Li; J Xu; P Xu; S Liu; Z Yang
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7.  The renin inhibitor aliskiren attenuates high-glucose induced extracellular matrix synthesis and prevents apoptosis in cultured podocytes.

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8.  Bradykinin decreases podocyte permeability through ADAM17-dependent epidermal growth factor receptor activation and zonula occludens-1 rearrangement.

Authors:  Mamon Dey; Aleksander Baldys; Dezmond B Sumter; Pal Göoz; Louis M Luttrell; John R Raymond; Monika Göoz
Journal:  J Pharmacol Exp Ther       Date:  2010-06-21       Impact factor: 4.030

Review 9.  Clinical therapeutic strategies for early stage of diabetic kidney disease.

Authors:  Munehiro Kitada; Keizo Kanasaki; Daisuke Koya
Journal:  World J Diabetes       Date:  2014-06-15

10.  Glomerular type 1 angiotensin receptors augment kidney injury and inflammation in murine autoimmune nephritis.

Authors:  Steven D Crowley; Matthew P Vasievich; Phillip Ruiz; Samantha K Gould; Kelly K Parsons; A Kathy Pazmino; Carie Facemire; Benny J Chen; Hyung-Suk Kim; Trinh T Tran; David S Pisetsky; Laura Barisoni; Minolfa C Prieto-Carrasquero; Marie Jeansson; Mary H Foster; Thomas M Coffman
Journal:  J Clin Invest       Date:  2009-03-16       Impact factor: 14.808

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