Abstract
Renalase was described in 2005 as a new flavoprotein expressed mainly in the kidney that functions as a flavin adenine dinucleotide (FAD)- and nicotinamide adenine dinucleotide (NADH)-dependent amine oxidase. In contrast to other monoamine oxidases, renalase can be secreted into both plasma and urine where it has been suggested to metabolise catecholamines and contribute to blood pressure control.
Renalase was first reported to be undetectable in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD), suggesting a causal link between the reduced plasma renalase levels, increased plasma catecholamine, and heightened cardiovascular risk that are well documented in this population. Plasma renalase deficiency has been consistently reported in studies using animal models of CKD. However, in studies with 3/4 nephrectomised (3/4nx) rats, the reduced circulating renalase levels were accompanied by increased plasma renalase activity that appeared to be related to decreased inhibition of circulating enzyme. By contrast, a series of recent studies in human subjects provides evidence suggesting that plasma renalase levels are negatively correlated with renal function. Though, similar to that found in the rat remnant kidney, the increased plasma renalase activity in patients with ESRD was associated with decreased inhibition of the circulating enzyme.
Keywords: Chronic kidney disease, hypertension, plasmatic inhibitor, renalase.
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