ArticleCentral-European journal of immunology2019
Asymmetric dimethylarginine is not a marker of arterial damage in children with glomerular kidney diseases.
Article in Central-European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Circulating miR-16 as an Early Biomarker of Subclinical Myocardial Strain Impairment in Pediatric Primary Hypertension.International journal of molecular sciences · 2026Article
- ATHENA Study - The Role of Circulating Plasma MicroRNAs in Paediatric Patients with Untreated Primary Hypertension: Baseline Expression and Exercise-Induced Changes.Kidney & blood pressure research · 2026Observational
- MicroRNA-133a and MicroRNA-145 May Be Involved in the Development of Hypertension-Mediated Organ Damage in Children with Primary Hypertension-A Preliminary Study.Journal of clinical medicine · 2024Article
- Can Surrogate Markers Help Define Cardiovascular Disease in Youth?Current atherosclerosis reports · 2023Review
- Asymmetric Dimethylarginine (ADMA) in Pediatric Renal Diseases: From Pathophysiological Phenomenon to Clinical Biomarker and Beyond.Children (Basel, Switzerland) · 2021Review
- Serum Periostin as a Potential Biomarker in Pediatric Patients with Primary Hypertension.Journal of clinical medicine · 2021Article
- Arterial stiffness in children with primary hypertension is related to subclinical inflammation.Central-European journal of immunology · 2021Article
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7 authors at 1 institution in 1 country.
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Abstract
introductionAsymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, correlates with cardiovascular risk especially in patients with chronic kidney disease. The aim of our study was to establish significance of ADMA as a biomarker of arterial damage in children with glomerulopathies. MATERIAL AND
methodsIn 80 children with glomerulopathies (mean age, 11.33 ±4.25 years; 42 with idiopathic nephrotic syndrome [INS], 38 with IgA or Henoch-Schoenlein nephropathy [IgAN/HSN]), we analyzed serum ADMA [nmol/ml], peripheral and central blood pressure, arterial stiffness (augmentation index - AIx75HR, pulse wave velocity - PWV), common carotid artery intima media thickness (cIMT), and selected clinical and biochemical parameters.
resultsIn the study group, mean ADMA concentration was 1.66 ±1.19 [nmol/ml] and did not differ between INS and IgAN/HSN patients. We found no significant correlations between concentration of ADMA, cIMT [mm]/Z-score, PWV [m/s]/Z-score, and AIx75HR [%] in the whole group and in INS and IgAN/HSN patients. In the whole group of 80 children, ADMA correlated (p < 0.05) with BMI Z-score (r = -0.24), uric acid (r = -0.23), HDL-cholesterol (r = -0.25), and central mean arterial pressure (r = -0.25), in children with INS also with total protein (r = 0.37), albumin (r = 0.36), and total cholesterol (r = -0.40, p = 0.028). In multivariate analysis, serum albumin was the strongest determinant of ADMA in the whole group (β = 0.536, 95% CI: 0.013-1.060, p = 0.045).
conclusions1. In children with glomerulonephritis, measurement of asymmetric dimethylarginine cannot replace well established and validated methods of assessment of subclinical arterial damage. 2. In children with glomerular kidney diseases, ADMA concentration is related primarily to serum albumin concentration.
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