Literature DB >> 17418688

Histopathology of diabetic nephropathy.

Paola Fioretto1, Michael Mauer.   

Abstract

The clinical manifestations of diabetic nephropathy, proteinuria, increased blood pressure, and decreased glomerular filtration rate, are similar in type 1 and type 2 diabetes; however, the renal lesions underlying renal dysfunction in the 2 conditions may differ. Indeed, although tubular, interstitial, and arteriolar lesions are ultimately present in type 1 diabetes, as the disease progresses, the most important structural changes involve the glomerulus. In contrast, a substantial subset of type 2 diabetic patients, despite the presence of microalbuminuria or proteinuria, have normal glomerular structure with or without tubulointerstitial and/or arteriolar abnormalities. The clinical manifestations of diabetic nephropathy are strongly related with the structural changes, especially with the degree of mesangial expansion in both type 1 and type 2 diabetes. However, several other important structural changes are involved. Previous studies, using light and electron microscopic morphometric analysis, have described the renal structural changes and the structural-functional relationships of diabetic nephropathy. This review focuses on these topics, emphasizing the contribution of research kidney biopsy studies to the understanding of the pathogenesis of diabetic nephropathy and the identification of patients with a higher risk of progression to end-stage renal disease. Finally, evidence is presented that the reversal of established lesions of diabetic nephropathy is possible.

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Year:  2007        PMID: 17418688      PMCID: PMC2746982          DOI: 10.1016/j.semnephrol.2007.01.012

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


  70 in total

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2.  Podocyte number predicts long-term urinary albumin excretion in Pima Indians with Type II diabetes and microalbuminuria.

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Journal:  Diabetologia       Date:  1999-11       Impact factor: 10.122

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4.  Glomerular cell number in normal subjects and in type 1 diabetic patients.

Authors:  M W Steffes; D Schmidt; R McCrery; J M Basgen
Journal:  Kidney Int       Date:  2001-06       Impact factor: 10.612

5.  Course of renal function in type 2 diabetic patients with abnormalities of albumin excretion rate.

Authors:  R Nosadini; M Velussi; E Brocco; M Bruseghin; C Abaterusso; A Saller; M Dalla Vestra; A Carraro; E Bortoloso; M Sambataro; I Barzon; F Frigato; B Muollo; M Chiesura-Corona; G Pacini; B Baggio; F Piarulli; A Sfriso; P Fioretto
Journal:  Diabetes       Date:  2000-03       Impact factor: 9.461

6.  Familial factors determine the development of diabetic nephropathy in patients with IDDM.

Authors:  M Quinn; M C Angelico; J H Warram; A S Krolewski
Journal:  Diabetologia       Date:  1996-08       Impact factor: 10.122

7.  Sequential renal biopsies in insulin-dependent diabetic patients: structural factors associated with clinical progression.

Authors:  P Fioretto; M W Steffes; D E Sutherland; M Mauer
Journal:  Kidney Int       Date:  1995-12       Impact factor: 10.612

8.  Glomerular structure in nonproteinuric IDDM patients with various levels of albuminuria.

Authors:  P Fioretto; M W Steffes; M Mauer
Journal:  Diabetes       Date:  1994-11       Impact factor: 9.461

9.  Cyclosporine associated lesions in native kidneys of diabetic pancreas transplant recipients.

Authors:  P Fioretto; M W Steffes; M J Mihatsch; E H Strøm; D E Sutherland; M Mauer
Journal:  Kidney Int       Date:  1995-08       Impact factor: 10.612

10.  Familial predisposition to nephropathy in African-Americans with non-insulin-dependent diabetes mellitus.

Authors:  B I Freedman; A B Tuttle; B J Spray
Journal:  Am J Kidney Dis       Date:  1995-05       Impact factor: 8.860

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  125 in total

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Journal:  J Endocrinol       Date:  2013-09-06       Impact factor: 4.286

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Journal:  Int J Clin Exp Med       Date:  2015-02-15

6.  Implication of dysregulation of the canonical wingless-type MMTV integration site (WNT) pathway in diabetic nephropathy.

Authors:  T Zhou; X He; R Cheng; B Zhang; R R Zhang; Y Chen; Y Takahashi; A R Murray; K Lee; G Gao; J-X Ma
Journal:  Diabetologia       Date:  2011-10-21       Impact factor: 10.122

7.  Sustained Klotho delivery reduces serum phosphate in a model of diabetic nephropathy.

Authors:  Julia M Hum; Linda M O'Bryan; Arun K Tatiparthi; Erica L Clinkenbeard; Pu Ni; Martin S Cramer; Manoj Bhaskaran; Robert L Johnson; Jonathan M Wilson; Rosamund C Smith; Kenneth E White
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Review 8.  Can we target tubular damage to prevent renal function decline in diabetes?

Authors:  Joseph V Bonventre
Journal:  Semin Nephrol       Date:  2012-09       Impact factor: 5.299

9.  Effects of increased renal tubular vascular endothelial growth factor (VEGF) on fibrosis, cyst formation, and glomerular disease.

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Journal:  Am J Pathol       Date:  2009-10-15       Impact factor: 4.307

10.  Connective tissue growth factor(CCN2), a pathogenic factor in diabetic nephropathy. What does it do? How does it do it?

Authors:  Roger M Mason
Journal:  J Cell Commun Signal       Date:  2009-02-14       Impact factor: 5.782

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