Asymmetric dimethylarginine is not a marker of arterial damage in children with glomerular kidney diseases.

INTRODUCTION: Asymmetric 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 METHODS: In 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. RESULTS: In 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 (ß = 0.536, 95% CI: 0.013-1.060, p = 0.045). CONCLUSIONS: 1. 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.

Complete blood count-derived inflammatory markers in adolescents with primary arterial hypertension: a preliminary report.

AIM OF THE STUDY: The aim of our study was to evaluate selected inflammatory markers in children with untreated primary hypertension and to establish the relation between inflammatory markers and 24-hour ambulatory blood pressure monitoring (ABPM) and clinical and biochemical parameters. MATERIAL AND METHODS: In 54 children (15.12 ±2.02 years) with untreated primary hypertension, with excluded overt inflammation, we evaluated: neutrophils (NEU; 1000/µl), lymphocytes (LYM; 1000/µl), platelets (PLT; 1000/µl), mean platelet volume (MPV; fl), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), ABPM (OSCAR 2 SUNTECH), and selected clinical and biochemical parameters. The control group consisted of 20 healthy children (15.55 ±2.27 years). RESULTS: Children with primary hypertension had (p < 0.01) higher 24-hour systolic, diastolic and mean blood pressure, systolic and diastolic blood pressure loads, and pulse pressure. Hypertensive children did not differ in inflammatory indicators (NEU, LYM, PLT, MPV, NLR, PLR) from the control group. In 54 hypertensive children we found the following correlations: between office systolic and diastolic blood pressure and MPV (r = 0.35, p = 0.011, r = 0.36, p = 0.008), between 24-hour ambulatory mean arterial pressure Z-score and NLR (r = 0.30, p = 0.030), 24-hour systolic blood pressure load and NLR (r = 0.38, p = 0.005), plasma renin activity and neutrophil count, NLR, PLR (r = 0.47, p = 0.016, r = 0.64, p < 0.001, r = 0.42, p = 0.033), urinary albumin loss and neutrophil count, NLR (r = 0.46, p = 0.001 and r = 0.42, p = 0.003). Multivariate analysis revealed that office SBP Z-score was related to MPV (ß = 0.35, p = 0.008) and albuminuria to neutrophil count (ß = 0.62, p = 0.018). CONCLUSIONS: In children with primary arterial hypertension there may be a relation between blood pressure, urinary albumin loss, and subclinical inflammation.

Renalase in Children with Glomerular Kidney Diseases.

Studies suggest that renalase, a renal catecholamine-inactivating enzyme, plays a major role in the pathogenesis of kidney and cardiovascular diseases in adults. This study seeks to determine the role of renalase in children with glomerular kidney diseases. We evaluated the serum renalase, arterial stiffness, intima-media thickness, blood pressure, and clinical and biochemical parameters in 78 children (11.9 ± 4.6 years of age) with glomerulopathies such as idiopathic nephrotic syndrome (40 cases), IgA nephropathy (12 cases), Henoch-Schönlein nephropathy (12 cases), and other glomerulopathies (14 cases). The control group consisted of 38 healthy children aged 11.8 ± 3.3 years. The mean renalase was 25.74 ± 8.94 µg/mL in the glomerulopathy group, which was not significantly different from the 27.22 ± 5.15 in the control group. The renalase level did not differ among various glomerulopathies either. However, proteinuric patients had a higher renalase level than those without proteinuria (28.43 ± 11.71 vs. 24.05 ± 6.23, respectively; p = 0.03). In proteinuric patients, renalase correlated with daily proteinuria. In the entire glomerulopathy group, renalase correlated with age, systolic central blood pressure (BP), diastolic peripheral and central BP, mean peripheral and central BP; peripheral diastolic BP Z-score, glomerular filtration rate, cholesterol, triglycerides, and pulse wave velocity. We conclude that in children with glomerulopathies renalase, although basically not enhanced, may underlie blood pressure elevation and arterial damage.

Benign acute childhood myositis complicating influenza B infection in a boy with idiopathic nephrotic syndrome.

INTRODUCTION: Benign acute childhood myositis (BACM) is an acute complication of an infection characterized by calf pain, limitation of lower limb mobility, an increase in serum creatine kinase, and a self-limiting course. No reports of BACM in children with idiopathic nephrotic syndrome (INS) can be found in the literature. CASE REPORT: A 5-year-old boy with steroid-sensitive INS presented with fever, leg pain, and problems with walking. Physical examination showed pharyngeal erythema, preserved movements in all joints, and weakness of leg muscles. Laboratory tests showed white blood cell count 3900/µl, albumin 2.3 g/dl, urea 25 mg/dl, creatinine 0.3 mg/dl, increased transaminases (AspAT 440 U/l, AlAT 100 U/l) and creatine kinase (10 817 U/l), and proteinuria 3500 mg/dl. The boy was diagnosed with an INS bout and BACM. Testing for infective causes of myositis showed evidence of an influenza B virus infection. Treatment included prednisone and oseltamivir. A rapid improvement of motor function was observed, with normalization of serum creatine kinase and transaminases, and resolution of proteinuria. CONCLUSIONS: 1. As influenza virus infection in a child with INS is a risk factor for complications and a disease bout, these patients should be vaccinated against influenza. 2. Differential diagnosis of leg pain and mobility limitation in a child with INS should include lower limb deep venous thrombosis, arthritis, post-infectious neurological complications (including Guillain-Barré syndrome), and BACM. 3. Serum creatine kinase level should be measured in all cases of motor disturbances in a child with symptoms of respiratory tract infection.