Effective treatment of an orthologous model of autosomal dominant polycystic kidney disease

Vicente E. Torres; Xiaofang Wang; Qi Qian; Stefan Somlo; Peter C. Harris; Vincent H. Gattone

doi:10.1038/nm1004

Effective treatment of an orthologous model of autosomal dominant polycystic kidney disease

Vicente E. Torres, Xiaofang Wang, Qi Qian, Stefan Somlo, Peter C. Harris, Vincent H. Gattone

Nephrology and Hypertension

Research output: Contribution to journal › Article › peer-review

345 Scopus citations

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of end-stage renal disease. The vasopressin V2 receptor (VPV2R) antagonist OPC31260 has been effective in two animal models of PKD with pathologies that are probably related. Here we show, in a mouse model of ADPKD (Pkd2 ^-/tms1m), a similar cellular phenotype and response to OPC31260 treatment, with reduction of renal cyclic AMP (cAMP) levels, prevention of renal enlargement, marked inhibition of cystogenesis and protection of renal function.

Original language	English (US)
Pages (from-to)	363-364
Number of pages	2
Journal	Nature Medicine
Volume	10
Issue number	4
DOIs	https://doi.org/10.1038/nm1004
State	Published - Apr 2004

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

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title = "Effective treatment of an orthologous model of autosomal dominant polycystic kidney disease",

abstract = "Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of end-stage renal disease. The vasopressin V2 receptor (VPV2R) antagonist OPC31260 has been effective in two animal models of PKD with pathologies that are probably related. Here we show, in a mouse model of ADPKD (Pkd2 -/tms1m), a similar cellular phenotype and response to OPC31260 treatment, with reduction of renal cyclic AMP (cAMP) levels, prevention of renal enlargement, marked inhibition of cystogenesis and protection of renal function.",

author = "Torres, {Vicente E.} and Xiaofang Wang and Qi Qian and Stefan Somlo and Harris, {Peter C.} and Gattone, {Vincent H.}",

note = "Funding Information: This work was supported by National Institutes of Health grant DK44863 (V.E.T.) and by a grant from the Polycystic Kidney Disease Foundation (V.H.G.). OPC31260 was a gift from Otsuka Pharmaceutical. Technical assistance was provided by Ming Li.",

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AU - Torres, Vicente E.

AU - Wang, Xiaofang

AU - Qian, Qi

AU - Somlo, Stefan

AU - Harris, Peter C.

AU - Gattone, Vincent H.

N1 - Funding Information: This work was supported by National Institutes of Health grant DK44863 (V.E.T.) and by a grant from the Polycystic Kidney Disease Foundation (V.H.G.). OPC31260 was a gift from Otsuka Pharmaceutical. Technical assistance was provided by Ming Li.

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N2 - Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of end-stage renal disease. The vasopressin V2 receptor (VPV2R) antagonist OPC31260 has been effective in two animal models of PKD with pathologies that are probably related. Here we show, in a mouse model of ADPKD (Pkd2 -/tms1m), a similar cellular phenotype and response to OPC31260 treatment, with reduction of renal cyclic AMP (cAMP) levels, prevention of renal enlargement, marked inhibition of cystogenesis and protection of renal function.

AB - Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of end-stage renal disease. The vasopressin V2 receptor (VPV2R) antagonist OPC31260 has been effective in two animal models of PKD with pathologies that are probably related. Here we show, in a mouse model of ADPKD (Pkd2 -/tms1m), a similar cellular phenotype and response to OPC31260 treatment, with reduction of renal cyclic AMP (cAMP) levels, prevention of renal enlargement, marked inhibition of cystogenesis and protection of renal function.

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Effective treatment of an orthologous model of autosomal dominant polycystic kidney disease

Abstract

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