Literature DB >> 9148381

The renal hemodynamic basis of diabetic nephropathy.

G T O'Bryan1, T H Hostetter.   

Abstract

Diabetic nephropathy occurs in approximately one third of individuals with insulin-dependent diabetes mellitus (IDDM), recent studies suggest that a similar proportion of non-insulin-dependent diabetes mellitus (NIDDM) patients develop this serious complication as well. Of the many risk factors identified in the pathogenesis of nephropathy, hemodynamic alterations have been particularly well studied. Increases in glomerular filtration rate (GFR), largely driven by increases in plasma flow and glomerular capillary pressure, are apparent in early IDDM and NIDDM. Furthermore, the elevation in capillary pressure may be damaging to glomerular endothelial, epithelial and mesangial cells, thereby initiating and contributing to the progression of diabetic nephropathy. Numerous mediators of diabetic hyperfiltration have been proposed, and this phenomenon likely reflects a mutilfactorial etiology. The purpose of this article is to examine the hemodynamic alterations characteristic of diabetic nephropathy, their etiology, and their role in the development and progression of diabetic nephropathy.

Entities:  

Mesh:

Year:  1997        PMID: 9148381

Source DB:  PubMed          Journal:  Semin Nephrol        ISSN: 0270-9295            Impact factor:   5.299


  27 in total

1.  Hypertrophy and hyperfunction of the diabetic kidney.

Authors:  T H Hostetter
Journal:  J Clin Invest       Date:  2001-01       Impact factor: 14.808

Review 2.  Renal Effects of Incretin-Based Diabetes Therapies: Pre-clinical Predictions and Clinical Trial Outcomes.

Authors:  Scott C Thomson; Volker Vallon
Journal:  Curr Diab Rep       Date:  2018-04-13       Impact factor: 4.810

3.  Diabetes mellitus: Cardiovascular and renal benefits of SGLT2 inhibition: insights from CANVAS.

Authors:  Volker Vallon; Scott C Thomson
Journal:  Nat Rev Nephrol       Date:  2017-08-07       Impact factor: 28.314

Review 4.  A potential role for mechanical forces in the detachment of podocytes and the progression of CKD.

Authors:  Wilhelm Kriz; Kevin V Lemley
Journal:  J Am Soc Nephrol       Date:  2014-07-24       Impact factor: 10.121

5.  Enhanced hemodynamic responses to angiotensin II in diabetes are associated with increased expression and activity of AT1 receptors in the afferent arteriole.

Authors:  Jie Zhang; Helena Y Qu; Jiangping Song; Jin Wei; Shan Jiang; Lei Wang; Liqing Wang; Jacentha Buggs; Ruisheng Liu
Journal:  Physiol Genomics       Date:  2017-08-25       Impact factor: 3.107

Review 6.  Glomerular hyperfiltration: definitions, mechanisms and clinical implications.

Authors:  Imed Helal; Godela M Fick-Brosnahan; Berenice Reed-Gitomer; Robert W Schrier
Journal:  Nat Rev Nephrol       Date:  2012-02-21       Impact factor: 28.314

Review 7.  Appropriate drug therapy for improving outcomes in diabetic nephropathy.

Authors:  Robert D Toto
Journal:  Curr Diab Rep       Date:  2002-12       Impact factor: 4.810

8.  Ornithine decarboxylase, kidney size, and the tubular hypothesis of glomerular hyperfiltration in experimental diabetes.

Authors:  S C Thomson; A Deng; D Bao; J Satriano; R C Blantz; V Vallon
Journal:  J Clin Invest       Date:  2001-01       Impact factor: 14.808

9.  Human glomerular endothelium: interplay among glucose, free fatty acids, angiotensin II, and oxidative stress.

Authors:  Edgar A Jaimes; Ping Hua; Run-Xia Tian; Leopoldo Raij
Journal:  Am J Physiol Renal Physiol       Date:  2009-10-28

Review 10.  The tubular hypothesis of nephron filtration and diabetic kidney disease.

Authors:  Volker Vallon; Scott C Thomson
Journal:  Nat Rev Nephrol       Date:  2020-03-09       Impact factor: 28.314

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