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 30 ,50 -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.

ADPKD, cAMP, renal physiology, somatostatin, somatostatin analogues
dx.doi.org/10.1093/ndt/gfz054, hdl.handle.net/1765/133784
Nephrology, Dialysis, Transplantation
Department of Hematology

Messchendorp, AL, Casteleijn, NF, Meijer, E, Gansevoort, R.T, Drenth, J.P.H, de Fijter, J.W, … Zietse, R. (2020). Somatostatin in renal physiology and autosomal dominant polycystic kidney disease. Nephrology, Dialysis, Transplantation, 35(8), 1306–1316. doi:10.1093/ndt/gfz054