Urinary Excretion of Aquaporin-2 in Humans: A Potential Marker of Collecting Duct Responsiveness to Vasopressin
|Title:||Urinary Excretion of Aquaporin-2 in Humans: A Potential Marker of Collecting Duct Responsiveness to Vasopressin|
|Authors:||Elliot, Sharon; Goldsmith, Paul K.; Knepper, Mark; Haughey, Mary; Olson, Beatriz|
|Publisher:||Journal of the American Society of Nephrology|
|Date Published:||March 01, 1996|
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This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
AQP2 is excreted in human urine, a fact which led Elliot, et al., to hypothesize that measurements of the AQP2 urinary excretion rate might be able to be used as an indicator of CD responsiveness to AVP. If so, the AQP2 excretion rate could prove useful in the clinical evaluation of various water-balance disorders.
To test their hypothesis, the authors developed a method of measuring the amount of AQP2 in urine, and they first measured the amount of AQP2 in the urine of healthy male and female volunteers over a 24 hour time period. Then they placed the volunteers in a hydrated state by restricting them from water for a period of time. And finally, they placed the volunteers in a water loaded state. The authors collected urine samples during these extremes of dehydration and of super hydration in order to see whether these short-term osmotic alterations resulted in corresponding changes in AQP2 urinary excretion. If they did, then it would suggest that AQP2 urinary excretion levels could be used as a marker of CD responsiveness to AVP.
The dehydrated state creates an osmotic condition that calls forth more AVP, which stimulates AQP2 to move to the CD cell apical membranes. The water-loaded state decreases osmolality, which suppresses AVP secretion. Thus, there is no AVP to stimulate AQP2s into action.
AQP2 urinary excretion was primarily detectable during water deprivation as compared with water-loaded conditions. Since the authors found that the short-term osmotic changes they induced in the volunteers produced extracellular fluid and AVP levels that corresponded with changes in AQP2 excretion (detectable urinary AQP2 during hydration, but not during water-loading), the authors suggest that measurement of urinary AQP2 may help clinicians assess the kidney CD response to AVP in different physiologic conditions.