Article Review: Autosomal Dominant Polycystic Kidney Disease: Renal Physiology Diagnosis, Treatment and Novel Therapies
DOI:
https://doi.org/10.31033/ijrasb.9.1.9Keywords:
Kidney Disease, Renal Physiology, Somatostatin, IgA nephropathyAbstract
In the case of Autosomal dominant polycystic kidney disease, patients are usually cured with Vasopressin (V2) receptor antagonists, which delay the ongoing growth of cyst formation and slow the pace of AD disease progression. Before we know more, it is uncertain if the increase in vasopressin amide levels that was detected during V2RAT treatment impacts the production of glucose in the intestines. Cell growth and fluid secretion are aided by high intracellular concentrations of adenosine 3',5;-cyclic monophosphate (cAMP), which leads to cyst development. SST, a hormone implicated in a variety of cell activities, has the potential to block the generation of intracellular cAMP. Nevertheless, since Somatostatin is quickly removed in vivo, it has little therapeutic promise. As a result, analogues with a longer half-life have been established, which might be potential medicines in the therapy of ADPKD. This review covers the complicated physiological consequences of Somatostatin, especially on the kidneys, as well as the possible therapeutic use of SST analogues in ADPKD.
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