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

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

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.

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.

Inclusion Criteria:

• acute kidney injury according to the definition of AKIN (Acute Kidney Injury Network)
• no started renal replacement therapy (e.g. dialysis)

Exclusion Criteria:

• dialysis or continuous venovenous hemofiltration before recruitment
• no recovery from kidney injury according to the definition of AKIN (Acute Kidney Injury Network)
• palliative care
• life expectancy is severely limited (< six months) due to preexisting malignancy or other disease