Skip Navigation


NDT Advance Access originally published online on February 19, 2004
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
19/5/1149    most recent
gfg622v1
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 (8)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Braden, G. L.
Right arrow Articles by Germain, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Braden, G. L.
Right arrow Articles by Germain, M. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2004) 19: 1149-1153
Nephrol Dial Transplant Vol. 19 No. 5 © ERA-EDTA 2004; all rights reserved

Original Article

Acute renal failure and hyperkalaemia associated with cyclooxygenase-2 inhibitors

Gregory L. Braden, Michael H. O'shea, Jeffrey G. Mulhern and Michael J. Germain

Department of Medicine and Renal Division, Baystate Medical Center, Springfield, MA and Tufts University School of Medicine, Boston, MA, USA

Correspondence and offprint requests to: Gregory L. Braden, MD, Chief, Renal Division, Baystate Medical Center, 759 Chestnut Street, Springfield, MA 01199, USA. Email: GBRAD6775{at}AOL.com

Background. The renal effects of cyclooxygenase-2 (COX-2) inhibitors have been incompletely elucidated, and acute renal failure (ARF) due to COX-2 inhibitors has been reported.

Methods. In order to determine the causes of ARF and hyperkalaemia in five patients during COX-2 inhibitor therapy, we carefully analysed case studies of consecutive in-patients or out-patients referred to our Renal Division over a 6-month period for ARF and hyperkalaemia who had recently received COX-2 inhibitors.

Results. ARF developed 2–3 weeks after COX-2 inhibitor therapy in five patients. The ARF was consistent with pre-renal azotaemia from renal hypoperfusion. Four patients were receiving the loop diuretic, furosemide. Four patients developed hyperkalaemia and decreased serum bicarbonate despite diuretic therapy, and one patient had changes in plasma renin activity and aldosterone levels consistent with reversible hyporeninaemic hypoaldosteronism. Renal failure was reversible after discontinuation of diuretics and COX-2 inhibitors.

Conclusions. COX-2 inhibitors may cause reversible ARF and hyperkalaemia in patients with oedematous conditions treated with low sodium diets and loop diuretics.

Keywords: acute renal failure; hyperkalaemia


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
 NEJMHome page
J. G. Abuelo
Normotensive Ischemic Acute Renal Failure
N. Engl. J. Med., August 23, 2007; 357(8): 797 - 805.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
S. Villanueva, C. Cespedes, A. A. Gonzalez, C. P. Vio, and V. Velarde
Effect of ischemic acute renal damage on the expression of COX-2 and oxidative stress-related elements in rat kidney
Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1364 - F1371.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.