Impact Factor

Perspective ARTICLE

Front. Physiol., 29 July 2013 | http://dx.doi.org/10.3389/fphys.2013.00194

Purinergic signaling in inflammatory renal disease

Nishkantha Arulkumaran1,2*, Clare M. Turner1, Marije L. Sixma2, Mervyn Singer2, Robert Unwin3 and Frederick W. K. Tam1
  • 1Imperial College Kidney and Transplant Institute, Imperial College London, Hammersmith Hospital, London, UK
  • 2Division of Medicine, Bloomsbury Institute of Intensive Care Medicine, University College London, London, UK
  • 3Division of Medicine, UCL Centre for Nephrology, Royal Free Campus and Hospital, University College London, London, UK

Extracellular purines have a role in renal physiology and adaption to inflammation. However, inflammatory renal disease may be mediated by extracellular purines, resulting in renal injury. The role of purinergic signaling is dependent on the concentrations of extracellular purines. Low basal levels of purines are important in normal homeostasis and growth. Concentrations of extracellular purines are significantly elevated during inflammation and mediate either an adaptive role or propagate local inflammation. Adenosine signaling mediates alterations in regional renal blood flow by regulation of the renal microcirculation, tubulo-glomerular feedback, and tubular transport of sodium and water. Increased extracellular ATP and renal P2 receptor-mediated inflammation are associated with various renal diseases, including hypertension, diabetic nephropathy, and glomerulonephritis. Experimental data suggests P2 receptor deficiency or receptor antagonism is associated with amelioration of antibody-mediated nephritis, suggesting a pathogenic (rather than adaptive) role of purinergic signaling. We discuss the role of extracellular nucleotides in adaptation to ischemic renal injury and in the pathogenesis of inflammatory renal disease.

Keywords: purines, inflammation, renal circulation, ischemia, renal disease

Citation: Arulkumaran N, Turner CM, Sixma ML, Singer M, Unwin R and Tam FWK (2013) Purinergic signaling in inflammatory renal disease. Front. Physiol. 4:194. doi: 10.3389/fphys.2013.00194

Received: 21 May 2013; Accepted: 05 July 2013;
Published online: 29 July 2013.

Edited by:

Marcelo D. Carattino, University of Pittsburgh School of Medicine, USA

Reviewed by:

Shaohu Sheng, University of Pittsburgh, USA
Pablo D. Cabral, Case Western Reserve University, USA

Copyright © 2013 Arulkumaran, Turner, Sixma, Singer, Unwin and Tam. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

*Correspondence: Nishkantha Arulkumaran, Division of Medicine, Bloomsbury Institute of Intensive Care Medicine, University College London, Cruciform Building, Gower Street, London, UK e-mail: nish_arul@yahoo.com