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Published ahead of print on June 1, 2005
J Am Soc Nephrol 16: 2456-2461, 2005
© 2005 American Society of Nephrology
doi: 10.1681/ASN.2005020179
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Epidemiology and Outcomes

Asymmetric Dimethylarginine and Progression of Chronic Kidney Disease: The Mild to Moderate Kidney Disease Study

Danilo Fliser*, Florian Kronenberg{dagger}, Jan T. Kielstein*, Christian Morath{ddagger}, Stefanie M. Bode-Böger§, Hermann Haller* and Eberhard Ritz{dagger}

* Department of Internal Medicine, Medical School Hannover, Hannover, Germany; {dagger} Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Innsbruck, Austria; {ddagger} Department of Internal Medicine, Ruperto-Carola University, Heidelberg, Germany; and § Institute for Clinical Pharmacology, Otto-von-Guericke University, Magdeburg, Germany

Address correspondence to: Dr. Danilo Fliser, Division of Nephrology, Department of Internal Medicine, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. Phone: 49-511-532-6319; Fax: 49-511-55-2366; fliser.danilo{at}mh-hannover.de

Received for publication February 17, 2005. Accepted for publication April 19, 2005.

Reduced bioavailability of nitric oxide (NO) is thought to play an important role in progression of renal damage. The hypothesis that the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) is involved in progression of kidney disease was tested. Plasma ADMA concentrations and other putative progression factors were assessed in 227 relatively young patients (45.7 ± 12.6 yr) with nondiabetic kidney diseases and mild to moderate renal failure. Progression assessed as doubling of serum creatinine and/or renal replacement therapy was evaluated prospectively. Baseline plasma ADMA concentrations in renal patients correlated significantly with serum creatinine (r = 0.595), GFR (r = –0.591), age (r = 0.281), and proteinuria (r = 0.184; all P < 0.01). Patients who reached an end point during follow-up were significantly older (P < 0.05) and had significantly higher creatinine, ADMA, and parathyroid hormone blood concentrations and protein excretion rates at baseline, whereas GFR and hemoglobin were significantly lower (all P < 0.01). Cox regression analysis revealed baseline serum creatinine (odds ratio 2.00; 95% confidence interval [CI] 1.61 to 2.49; P < 0.001) and ADMA (odds ratio 1.47; 95% CI 1.12 to 1.93 for an increment of 0.1 µmol/L; P < 0.006) as independent predictors of disease progression. In patients with ADMA levels above median, progression was significantly faster (P < 0.0001), and their mean follow-up time to a progression end point was 52.8 mo (95% CI 46.9 to 58.8) as compared with 71.6 mo (95% CI 66.2 to 76.9) in patients with ADMA levels below the median. The endogenous NO synthase inhibitor ADMA is significantly associated with progression of nondiabetic kidney diseases. Lowering plasma ADMA concentrations may be a novel therapeutic target to prevent progressive renal impairment.




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