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Renal Primary Cilia Lengthen after Acute Tubular Necrosis

Elizabeth Verghese^*, Sharon D. Ricardo^*, Raphael Weidenfeld^*, Junli Zhuang^*, Prudence A. Hill, Robyn G. Langham and James A. Deane^*

*Monash Immunology and Stem Cell Laboratories, Monash University, Melbourne, Victoria, Australia;
Department of Anatomical Pathology, St Vincent's Hospital, Melbourne, Victoria, Australia; and
Department of Nephrology, St Vincent's Hospital, Melbourne, Victoria, Australia

Correspondence: Dr. James A. Deane, Monash Medical Centre, Level 5/Block E246, Clayton Road, Clayton, Victoria 3168, Australia. Phone: +61-3-9594-5528; Fax: +61-3-9594-6495; E-mail: james.deane{at}med.monash.edu.au

Received for publication October 11, 2008. Accepted for publication May 20, 2009.

Renal primary cilia are sensory antennas required for the maintenance of normal epithelial differentiation and proliferation in the kidney, but they also have a potential role in epithelial differentiation during renal injury and repair. In mice, tubular damage causes an increase in the length of renal cilia, which may modify their sensory sensitivity during repair. Here, we investigated whether the alteration of renal cilium length during renal injury is clinically relevant. Using biopsies of human renal transplants that suffered acute tubular necrosis during transplantation, we compared the length of renal primary cilia with renal function. Serial biopsies showed that acute tubular necrosis resulted in more than a doubling of cilium length throughout the nephron and collecting duct approximately 1 wk after injury. Allografts displayed a trend toward normalization of cilium length in later biopsies, and this correlated with functional recovery. A mouse model of renal ischemia-reperfusion confirmed the increase and subsequent regression of cilium length during renal repair, displaying complete normalization of cilium length within 6 wk of injury. These findings demonstrate that the length of renal cilia is a clinically relevant indicator of renal injury and repair.

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Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673