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NDT Advance Access originally published online on December 13, 2006
Nephrology Dialysis Transplantation 2007 22(3):801-806; doi:10.1093/ndt/gfl719
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections

Carmine Zoccali1, Renke Maas2, Sebastiano Cutrupi1, Patrizia Pizzini1, Piero Finocchiaro1, Francesco Cambareri1, Vincenzo Panuccio1, Carmela Martorano1, Friedrich Schulze2, Giuseppe Enia1, Giovanni Tripepi1 and Rainer Boger2

1CNR-IBIM, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension & Renal Unit, Reggio Calabria, Italy and 2Clinical Pharmacology Unit, Department of Pharmacology, University Hospital Hamburg, Eppendorf, Germany

Correspondence and offprint requests to: Prof. Carmine Zoccali, CNR-IBIM, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, c/o Ki Point, Gransial SRL, Via Filippini n. 85, 89100 Reggio Calabria, Italy. Email: carmine.zoccali{at}tin.it



  Abstract

Background and methods. The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections.

Results. During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 ± 0.23 to 0.80 ± 0.18 µmol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation.

Conclusions. Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.

Keywords: asymmetrical dimethyl-arginine; C-reactive protein; inflammation; interleukin-6; procalcitonin

Received for publication: 28. 9.06
Accepted in revised form: 6.11.06


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