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Common congenital defect a prickly problem for the kidney

Date:
February 21, 2011
Source:
Journal of Clinical Investigation
Summary:
One of the most common congenital defects in humans is a kidney abnormality known as hydronephrosis. Hydronephrosis arises because the flow of urine from the kidney to the bladder is impeded. By studying kidney development in mice, researchers have now identified a new cellular mechanism underlying hydronephrosis, something that they hope might lead to better therapeutics for the condition and improved diagnosis of its severity.

One of the most common congenital defects in humans -- it is detected in approximately 0.5% of fetuses analyzed by routine antenatal sonography -- is a kidney abnormality known as hydronephrosis. Hydronephrosis arises because the flow of urine from the kidney to the bladder is impeded.

By studying kidney development in mice, Norman Rosenblum and colleagues, at the Hospital for Sick Children, Toronto, have identified a new cellular mechanism underlying hydronephrosis, something that they hope might lead to better therapeutics for the condition and improved diagnosis of its severity.

Rosenblum and colleagues found that the Hedgehog signaling pathway controls the development of two populations of cells required for the initiation and transmission of coordinated contractions of the tract that links the kidney and the bladder (the ureter). Thus, genetic mutations in mice that disrupted the Hedgehog signaling pathway impaired urine flow from the kidney to the bladder, causing hydronephrosis.

As noted by both the authors and Doris Herzlinger, in an accompanying commentary, these data have the potential to lead to the development of novel therapeutics for the treatment of hydronephrosis. Further, they suggest that it might be possible to develop genetic tests that discriminate between cases of hydronephrosis that spontaneously resolve (as approximately 70-80% of cases do) and those that do not.


Story Source:

The above story is based on materials provided by Journal of Clinical Investigation. Note: Materials may be edited for content and length.


Journal Reference:

  1. Jason E. Cain, Epshita Islam, Fiona Haxho, Joshua Blake and Norman D. Rosenblum. GLI3 repressor controls functional development of the mouse ureter. J Clin Invest., February 21, 2011 DOI: 10.1172/JCI45523

Cite This Page:

Journal of Clinical Investigation. "Common congenital defect a prickly problem for the kidney." ScienceDaily. ScienceDaily, 21 February 2011. <www.sciencedaily.com/releases/2011/02/110221120947.htm>.
Journal of Clinical Investigation. (2011, February 21). Common congenital defect a prickly problem for the kidney. ScienceDaily. Retrieved September 16, 2014 from www.sciencedaily.com/releases/2011/02/110221120947.htm
Journal of Clinical Investigation. "Common congenital defect a prickly problem for the kidney." ScienceDaily. www.sciencedaily.com/releases/2011/02/110221120947.htm (accessed September 16, 2014).

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