Hyperuricemia in Preeclampsia as an Endothelin Effect

Abstract

Charles G. Coffey*

Although the etiology of the elevated serum uric acid levels observed in preeclampsia remains unknown, much is actually known of uric acid metabolism in general. One aspect of uric acid metabolism that may be relevant to understanding its involvement in preeclampsia is that, in the human, cells in only a few organs have been found to be actually capable of producing uric acid. These organs are: the liver (probably responsible for most of uric acid production), the small bowel, as well as (probably) the endothelium, the placenta, and lactating mammary epithelial cells. Cells of all other organs lack xanthine oxidase (which is an enzyme necessary for the conversion of xanthine to uric acid). Given that the liver, placenta, and endothelium are known to be involved in preeclampsia, it is plausible to assume that a process that increases purine catabolism in cells of these organs could explain the increased serum uric acid levels. In this paper, that are discussed mechanisms whereby activation of endothelin-1 receptors on cells of these organs (which are known to have endothelin-1 receptors) will tend to result in increased purine catabolism in them.