Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Melin, J.
Right arrow Articles by Fellström, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Melin, J.
Right arrow Articles by Fellström, B.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2003) 18: 460-462
© 2003 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

Hyperglycaemia and renal ischaemia–reperfusion injury

Jan Melin, Olof Hellberg and Bengt Fellström

Department of Medical Sciences, Uppsala University, University Hospital, Uppsala, Sweden

Keywords: acute renal failure; diabetic nephropathy; hyperglycaemia; ischaemia–reperfusion injury; radiocontrast media; renal ischaemia

The first 10% of the full text of this article appears below.

Introduction

Hyperglycaemia is most probably a contributing factor in the development of ischaemic acute renal failure (ARF) in many patients. Both clinical and experimental data suggest that hyperglycaemia increases the risk of ARF [1–3]. Hyperglycaemia also worsens the outcome in renal transplantation [4,5]. Conversely, ischaemia–reperfusion (I/R) combined with hyperglycaemia could also be important in the development of diabetic nephropathy. Studies in our laboratory show that a brief renal ischaemia results in a progressive injury leading to end-stage renal failure in diabetic animals [6,7]. The mechanisms behind this increased sensitivity to renal I/R during hyperglycaemia are still poorly understood.

Experimental findings

An increased susceptibility to renal I/R injury in diabetic rats has been shown in several studies [1,3,6–9]. Furthermore, non-diabetic rats and dogs are more vulnerable . . . [Full Text of this Article]

Clinical observations

Critically ill patients
Kidney transplantation
Hyperglycaemia and radiocontrast media
Pathophysiology

Diabetic nephropathy

Prevention

Conclusion


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
K. J. Kelly, J. L. Burford, and J. H. Dominguez
Postischemic inflammatory syndrome: a critical mechanism of progression in diabetic nephropathy
Am J Physiol Renal Physiol, October 1, 2009; 297(4): F923 - F931.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
H. Shi, D. Patschan, T. Epstein, M. S. Goligorsky, and J. Winaver
Delayed recovery of renal regional blood flow in diabetic mice subjected to acute ischemic kidney injury
Am J Physiol Renal Physiol, November 1, 2007; 293(5): F1512 - F1517.
[Abstract] [Full Text] [PDF]