Somatostatin in renal physiology and autosomal dominant polycystic kidney disease

DIPAK Consortium Investigators, A Lianne Messchendorp*, Niek F Casteleijn, Esther Meijer, Ron T Gansevoort

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

8 Citations (Scopus)
236 Downloads (Pure)

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive cyst formation, leading to growth in kidney volume and renal function decline. Although therapies have emerged, there is still an important unmet need for slowing the rate of disease progression in ADPKD. High intracellular levels of adenosine 3 0,5 0-cyclic monophosphate (cAMP) are involved in cell proliferation and fluid secretion, resulting in cyst formation. Somatostatin (SST), a hormone that is involved in many cell processes, has the ability to inhibit intracellular cAMP production. However, SST itself has limited therapeutic potential since it is rapidly eliminated in vivo. Therefore analogues have been synthesized, which have a longer half-life and may be promising agents in the treatment of ADPKD. This review provides an overview of the complex physiological effects of SST, in particular renal, and the potential therapeutic role of SST analogues in ADPKD.

Original languageEnglish
Pages (from-to)1306-1316
Number of pages11
JournalNephrology, Dialysis, Transplantation
Volume35
Issue number8
Early online date27-Apr-2019
DOIs
Publication statusPublished - 1-Aug-2020

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