Aspirin Impairs Transport of Protective Osmolytes in Renal Inner Medullary Collecting Duct Cells
Jeffrey S Bonner, Bailey M. Anderson, Joshua Blevins , Stephen A. Kempson*
Identifiers and Pagination:Year: 2009
First Page: 6
Last Page: 10
Publisher Id: TOUNJ-2-6
Article History:Received Date: 8/12/2008
Revision Received Date: 22/1/2009
Acceptance Date: 9/2/2009
Electronic publication date: 3/3/2009
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Non-steroidal anti-inflammatory drugs (NSAIDs) represent one of the most common classes of medications used worldwide for treatment of pain and inflammation, and their nephrotoxic effects have been well documented. This study is focused on aspirin action on the normal adaptive responses of cells in the hypertonic renal inner medulla, using a cultured cell model. Following adaptation to hypertonic conditions, further treatment of both MDCK and IMCD3 cells for 24h with 1.0 mM aspirin produced significant inhibition of the transport systems for the osmolytes betaine and taurine. Caspase 3 was not activated by this treatment, indicating that transport inhibition was not due to apoptotic events. Acetaminophen and caffeine, common in analgesic mixtures, had a similar inhibitory effect. We conclude that interference with osmolyte accumulation by medullary cells may help to explain in part the nephrotoxicity due to long-term use of NSAIDs and analgesic formulations.