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Previous Volume 353:529-530 August 4, 2005 Number 5 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: The elegant work presented by Feldman et al. (May 5 issue)¹ shows that point mutations in codon 137 of the V2 vasopressin receptor (V2R) can result in either a loss-of-function mutation (R137H, which is associated with congenital nephrogenic diabetes insipidus) or a gain-of-function mutation (R137C or R137L, which is associated with the congenital nephrogenic syndrome of inappropriate antidiuresis). In the Discussion section of the article, the authors mention the possibility of an activating mutation in aquaporin-2. Because the clinical data were also consistent with this differential diagnosis, how was this possibility ruled out so as to arrive . . . [Full Text of this Article]

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• Zuber, A. M., Singer, D., Penninger, J. M., Rossier, B. C., Firsov, D. (2007). Increased Renal Responsiveness to Vasopressin and Enhanced V2 Receptor Signaling in RGS2-/- Mice. J. Am. Soc. Nephrol. 18: 1672-1678 [Abstract] [Full Text]