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 ( = 0.35, p = 0.008) and albuminuria to neutrophil count ( = 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.

Acute post-streptococcal glomerulonephritis (APSGN) is an immunological complication of infection with group A -hemolytic streptococcus (GAS). The disease manifests as microscopic or gross hematuria, arterial hypertension, edema, and acute kidney injury and has most commonly a self-limiting course. We report a very severe case of APSGN in a 5-year-old girl with superimposed generalized infection. The girl presented significant overhydration, a very low glomerular filtration rate (GFR) (11.2 ml/min/1.73 m2), hyperuricemia (12.7 mg/dl), nephrotic proteinuria, and gross hematuria. Her immunological tests allowed for the diagnosis of APSGN (elevated antistreptolysin O [ASO] titer, low C3, and normal C4 complement factors). She also showed very high inflammatory indicators suggestive of sepsis. She received supportive treatment together with ceftriaxone and a single dose of rasburicase. Her renal function recovered, and urinalysis normalized. Gallbladder deposits complicated the treatment. This article summarizes the existing knowledge on APSGN with particular emphasis on the immunological mechanisms of the disease. The proposed immunological pathway leading to glomerular injury is discussed. In children, APSGN has an excellent prognosis, including in cases with severe renal impairment in the early stages of the disease.

Introduction: Adhesion molecules: E-selectin and intercellular adhesion molecule 1 (ICAM-1) are well-established markers of endothelial injury. The aim of the study was to assess the relation between E-selectin and ICAM-1 and clinical and biochemical parameters in children and adolescents with primary hypertension (PH). Material and methods: In 77 patients with PH (15.04 ±2.62 years, 50 boys, 27 girls) we evaluated serum E-selectin, ICAM-1, and selected clinical and biochemical parameters including inflammatory indicators and ambulatory blood pressure monitoring (ABPM). Results: The E-selectin concentration was 55.63 ±26.49 ng/ml and the ICAM-1 concentration was 302.17 ±67.14 ng/ml. E-selectin and ICAM-1 correlated (p < 0.05) with BMI Z-score (r = 0.24, r = 0.29), ICAM-1 also with uric acid (r = 0.35), HDL-cholesterol (r = –0.28), platelet-to-lymphocyte ratio (r = 0.26), and systolic and mean blood pressure variability (r = 0.24, r = 0.24); in boys ICAM-1 correlated with mean platelet volume (r = 0.29). In multivariate analysis the only significant predictor of E-selectin was mean arterial pressure during 24 hours (β = 0.329, 95% CI: 0.012-0.646) and of ICAM-1 – uric acid (β = 0.430, 95% CI: 0.040-0.819). In 27 children with newly diagnosed PH E-selectin correlated negatively with diastolic blood pressure dipping (r = –0.54, p = 0.004) and positively with ambulatory arterial stiffness index (r = 0.51, p = 0.012). Conclusions: Elevated mean arterial pressure and hyperuricemia are risk factors of endothelial damage in paediatric patients with primary hypertension. In children with untreated primary hypertension there may be a relation between endothelial damage and disturbed circadian blood pressure profile.

Introduction: The immune system can trigger an inflammatory process leading to blood pressure elevation and arterial damage. The aim of the study was to assess the relation between subclinical inflammation and arterial damage in pediatric patients with primary hypertension (PH) and to establish the usefulness of neutrophil-to-lymphocyte (NLR) and platelet-to-lymphocyte (PLR) ratios, and mean platelet volume (MPV) as markers of arterial damage in these subjects. Material and methods: In 119 children with PH (14.94 ±2.76 years) and 45 healthy children (14.91 ±2.69 years) we analyzed markers of subclinical inflammation (NLR, PLR, MPV), clinical and biochemical parameters, office blood pressure, ambulatory blood pressure monitoring (ABPM), central blood pressure, aortic pulse wave velocity (aPWV), augmentation index corrected for heart rates 75 (AIx75HR), carotid intima media thickness (cIMT), and common carotid artery stiffness (E-tracking). Results: Children with PH were characterized by significantly higher neutrophil (3.9 ±1.7 vs. 3.0 ±1.0 [1000/µl], p < 0.001) and platelet counts (271.9 ±62.3 vs. 250.3 ±60.3 [1000/µl], p = 0.047), NLR (1.9 ±1.5 vs. 1.3 ±0.4, p = 0.010), PLR (131.4 ±41.9 vs. 114.7 ±37.6, p = 0.020), aPWV (5.36 ±0.88 vs. 4.88 ±0.92 m/s, p = 0.004), and cIMT (0.46 ±0.07 vs. 0.43 ±0.07 mm, p = 0.002) compared to healthy children. In PH children NLR correlated positively (p < 0.05) with: systolic, diastolic and mean blood pressure in ABPM (r = 0.243, r = 0.216, r = 0.251), aPWV [m/s] (r = 0.241), aPWV Z-score (r = 0.204), and common carotid artery PWVbeta [m/s] (r = 0.202). Conclusions: There is a link between arterial stiffness and subclinical inflammation in pediatric patients with primary hypertension. Neutrophil-to-lymphocyte ratio may serve as a promising marker of arterial stiffness in pediatric patients affected by primary hypertension.

Introduction: Numerous studies suggest that levamisole, an antihelmintic agent with an immunomodulatory effect, reduces the number of relapses in children with frequently relapsing and steroid-dependent nephrotic syndrome (FRNS/SDNS). The aim of the study was to present a single center’s experience in treatment of FRNS and SDNS with levamisole. Material and methods: Among 72 children with FRNS/SDNS treated in our department with leva­misole in the years 1984-2011 we studied in detail 53 patients (mean age: 6.5 ±3.0 years), in whom the medication was administered for at least 6 months. In these 53 patients we evaluated: the course of the disease before levamisole, the renal biopsy result, medications used, prednisone dose on levamisole initiation, duration of levamisole treatment, time to first relapse and number of relapses on levamisole, and levamisole side effects. Results: The duration of nephrotic syndrome was 3.4 ±2.9 years, and the number of relapses before levamisole treatment was 6.0 ±3.4. The dose of prednisone on initiation of levamisole treatment was 1.2 ±0.6 mg/kg/24 h, and the duration of levamisole treatment was 15.0 ±7.3 months. During levamisole treatment proteinuria relapsed in 34/53 (64.2%) children, and the time to first relapse was 8.8 ±8.1 months. During levamisole therapy relapses of the disease decreased significantly (2.7 ±2.0 vs. 1.8 ±2.1 relapses/year, p = 0.02). Time to first relapse correlated with total number of relapses (R = –0.59, p < 0.001) and number of relapses in one year during levamisole treatment (R = –0.60, p < 0.001). Conclusions: Levamisole is effective in reducing the number of relapses in children with frequently relapsing and steroid-dependent nephrotic syndrome. Early relapse of proteinuria on levamisole treatment in children with FRNS/SDNS suggests low efficacy of further treatment.