Urinary renalase concentration in patients with preserved kidney function undergoing coronary angiography

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Contrast‐induced acute kidney injury (CI‐AKI) represents a frequent and clinically unpredictable complication of coronary angiography/percutaneous coronary interventions (CA/PCI), which has been linked to impaired prognosis in patients with different types of coronary artery disease.1 Due to late serum creatinine concentration (SCr) increase following renal injury, the diagnosis of CI‐AKI is frequently delayed or even missed and, thus, a search for early and reliable CI‐AKI diagnostic markers is currently under way.2 Renalase represents a flavin adenine dinucleotide‐dependent oxidase primarily expressed in proximal tubular cells and secreted into blood and urine.3 In line with its in vivo hypotensive properties, renalase was initially thought to be involved in the metabolism of circulating catecholamines.3 However, more recently these properties were disputed and renalase was demonstrated to have a primarily intracellular/metabolic activity related with the repair of aberrant α anomers of nicotinamide adenine dinucleotide (NAD)4 and 2‐ or 6‐dihydro‐nicotinamide adenine dinucleotide phosphate.5 Still, renalase was proved to act as a growth factor via PMCA4b extracellular receptor exhibiting anti‐apoptotic properties.6 In an animal model, renalase protected proximal tubular cells against ischaemic,7 cisplatin‐mediated8 and, most‐importantly, contrast‐induced acute kidney injury (AKI).9 In line with preliminary reports suggesting a decrease of urinary renalase level following ischemic injury,10 we have speculated that urinary renalase may represent a potential CI‐AKI biomarker. Thus, we sought to evaluate urinary renalase concentration before and after CA/PCI and verify its potential application as CI‐AKI early diagnostic marker.

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