Calcium, cyclic AMP, and MAP kinases: dysregulation in polycystic kidney disease
- PMID: 18195694
- DOI: 10.1038/sj.ki.5002695
Calcium, cyclic AMP, and MAP kinases: dysregulation in polycystic kidney disease
Abstract
Low intracellular calcium, present in untreated polycystic kidney epithelia, results in a proliferative response to cyclic adenosine monophosphate. Treatment with a calcium channel blocker (CCB) caused exacerbation of autosomal dominant polycystic kidney disease in rats. Data regarding use of CCBs in human polycystic kidney disease (PKD) are limited and mixed. Thus, it is premature to extrapolate these findings to human PKD.
Comment on
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Calcium channel inhibition accelerates polycystic kidney disease progression in the Cy/+ rat.Kidney Int. 2008 Feb;73(3):269-77. doi: 10.1038/sj.ki.5002629. Epub 2007 Oct 17. Kidney Int. 2008. PMID: 17943077
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