NDT Advance Access originally published online on May 16, 2006
Nephrology Dialysis Transplantation 2006 21(7):1752-1757; doi:10.1093/ndt/gfl246
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Editorial Comment
Therapeutic approaches in autosomal dominant polycystic kidney disease (ADPKD): is there light at the end of the tunnel?
Renal Division, Freiburg, Germany
Correspondence and offprint requests to: Gerd Walz, Renal Division, University Hospital Freiburg, Hugstetter Street. 55, 79106 Freiburg, Germany. Email: gerd.walz@uniklinik-freiburg.de
Keywords: mTOR inhibitors; polycystic kidney disease; tacrolimus; vasopressin-2 receptor antagonist
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| The new kids on the block |
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For more than three decades, autosomal dominant polycytic kidney disease (ADPKD) researchers around the globe, spurned by millions of affected patients, have tried to elucidate the mechanisms that lead to cyst formation and progression of renal failure in this heterogenetic disease. It was not until recently that realistic therapeutic interventions have come within reach. This editorial will briefly summarize the key findings that led the researchers to test vasopressin-2-receptor antagonists (V2RA) and mammalian targets of rapamycin (mTOR) inhibitors in animal models of polycystic kidney disease, and will highlight why these therapeutic avenues might be more promising and fortunate than their predecessors (Table 1).
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| Vasopressin-2-receptor antagonists (V2RA) |
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Modern ADPKD research started when epithelial cells lining the cysts in kidneys of ADPKD patients were successfully isolated and maintained in ex vivo
| (mTOR) inhibitors |
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| Other therapeutic approaches in ADPKD |
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| How to monitor the therapeutic efficacy in ADPKD? |
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| Is it too early to start clinical trials in ADPKD? |
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| Outlook |
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