L-Arginine, Symmetrical and Asymmetrical Dimethylarginine (SDMA/ADMA) in Acute Kidney Injury (AKI)

Acute Kidney Injury Clinical Trial

Official title: Regulation of L-Arginine Und Its Derivatives of Asymmetrical and Symmetrical Dimethylarginine and L-NG Monomethylarginine (ADMA/SDMA/L-NMMA) in Acute Kidney Injury and Correlation to Cardiac, Renal and Vascular Function and Mortality

Status Completed

Clinical Trial Summary

The purpose of the study is to determine the association between acute kidney injury and serum levels symmetrical and asymmetrical dimethylarginine (SDMA/ADMA) and their assumptive influence on mortality, renal function and on arterial stiffness.

Clinical Trial Description

Acute kidney injury (AKI) is a frequent complication with severe implications deteriorating overall prognosis. Nitric oxide (NO)-signal transduction plays an important role in mediating renal damage. NO is produced by NO-synthase (NOS) with L-arginine as its substrate. Endogenous L-Arginine derivatives, asymmetric and symmetric dimethylarginines (ADMA/SDMA), inhibit NO-production directly (AMDA) by blocking NOS activity or indirectly (SDMA) by blocking cellular L-Arginine uptake.

It is well known that SDMA and ADMA are markers of renal function (SDMA) and cardiovascular risk (ADMA/SDMA) in patients with chronic kidney disease (CKD). Moreover, ADMA and SDMA possibly even trigger cardiovascular risk in patients with CKD. However, there is only little information about the regulation and the influence of ADMA/SDMA in acute kidney injury. ;

Study Design

Observational Model: Cohort, Time Perspective: Prospective

Related Conditions & MeSH terms

• Acute Kidney Injury

• NCT number: NCT01552525
• Study type: Observational
• Source: Wuerzburg University Hospital
• Status: Completed
• Phase: N/A
• Start date: January 2011
• Completion date: March 2016