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BACKGROUND: The knowledge and attitudes of dialyzed patients toward the best method of renal replacement treatment (ie, kidney transplantation [KTx]) may be the main factor motivating them to apply and be put on the national kidney transplant waiting list, resulting in a better prognosis. OBJECTIVE: Assessment of the knowledge and attitudes of dialyzed patients toward KTx. METHODS: A pilot study is considered an introductory step before the nationwide project, which will cover dialysis centers in Poland from 2023 to 2024. The authorship 4-part questionnaire, including self-assessment knowledge, attitude dimension, pain and mental evaluation section, was made available to 30 patients with hemodialysis aged 30 to 75 years. RESULTS: The median age of the patients was 59 years. The primary cause of end-stage renal disease (ESRD) was glomerulonephritis (33%). Most of the patients stayed on hemodialysis for 2 years or less (57%); 43% of the patients declared insufficient knowledge in the field of KTx, 41% of the patients were not informed at the nephrology clinic that KTx remains one of the methods of renal replacement therapy, and 65% did not receive information about the possibility of preemptive or early transplantation from a relative donor. Only 34% of the patients considered KTx to be a much better treatment option than dialysis, but only 20% of those were on the national waiting list for KTx. CONCLUSIONS: The pilot study showed insufficient knowledge of patients with ESRD regarding kidney transplantation as a method of renal replacement therapy. There is a need to introduce an effective educational program.

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INTRODUCTION: Immunoglobulin A nephropathy (IgAN) may lead to end stage renal disease and severely affect patient functioning and wellbeing. The aim of the study was to evaluate health-related quality of life (HRQoL) in children and adolescents with IgAN, and compare HRQoL in relation to the disease course, social status and psychological factors, such as expressing anger and perceived personal competence. MATERIAL AND METHODS: The multicentre cross-sectional study included 51 patients ≥ 8 years from 7 paediatric nephrology centres in Poland. Psychometric analysis was performed using the Kidscreen-52 questionnaire to evaluate HRQoL, the Anger Expression Scale to evaluate the severity of anger and the Personal Competence Scale to measure general perception of personal competence. RESULTS: Mean age of patients was 14.54 ±3.69 years; duration since the diagnosis of IgAN was 4.98 ±3.9 years. Patients with IgAN rated their psychological wellbeing as significantly worse compared to healthy peers (p < 0.05). The presence of proteinuria was associated with significantly worse physical wellbeing (58.72 ±18.45 vs. 74.44 ±22.97; p < 0.05). Current therapy (steroids/immunosuppressive drugs) had no effect on HRQoL in the study group. Perceived personal competence was rated high by 49% of children in the study group. Children with IgAN were characterized by lower intensity of expressed anger (p < 0.001) and significantly higher intensity of suppressed anger (p < 0.01) compared to reference ranges. Severity of expressed anger correlated positively with the parent relations and school environment dimensions of HRQoL. CONCLUSIONS: We found lower HRQoL in regard to physical and psychological wellbeing in a group of Polish children with IgAN compared to healthy peers. HRQoL should be monitored in this patient group.

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BACKGROUND: Retinal gene expression pattern is severely altered after exposition to hyperoxia in mice with oxygen-induced retinopathy (OIR), a common model of retinopathy of prematurity. Gene ontology and signaling pathway analyses may add new insights into a better understanding of the pathogenesis of this disease. METHODS: Seven-day-old C57BL/6J mice (n = 60) were exposed to 75% oxygen for 5 days and then recovered in room air. The controls (n = 60) were kept in the normoxic conditions. Retinas were harvested immediately following hyperoxia, during the phase of maximal neovascularization, and at the time of neovascularization regression. The retinal RNA samples were evaluated for gene expression using mouse gene expression microarrays. DAVID annotation tools were used for gene ontology and pathway analyses. RESULTS: The most significantly enriched signaling pathways during the neovascularization phase of OIR were: focal adhesion; ECM-receptor interaction; PI3K-Akt; oxidative phosphorylation; and Alzheimer's, Parkinson's and Huntington's disease signaling pathways. Genes involved in apoptosis, cell proliferation, cell differentiation, and immune responses were associated with neovascularization regression. CONCLUSIONS: Performed analyses revealed the possible involvement of various signaling pathways in OIR pathomechanism, mostly specific to the OIR phase. Dysregulation of genes involved in oxidative phosphorylation may have an impact on neovascularization development.

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Objective: To examine the gene expression regarding pulmonary vascular disease in experimental bronchopulmonary dysplasia in young mice. Premature delivery puts babies at risk of severe complications. Bronchopulmonary dysplasia (BPD) is a common complication of premature birth leading to lifelong affection of pulmonary function. BPD is recognized as a disease of arrested alveolar development. The disease process is not fully described and no complete cure or prevention is known. The focus of interest in the search for treatment and prevention of BPD has traditionally been at airspace level; however, the pulmonary vasculature is increasingly acknowledged in the pathology of BPD. The aim of the investigation was to study the gene expression in lungs with BPD with regards to pulmonary vascular disease (PVD).Methods: We employed a murine model of hyperoxia-induced BPD and gene expression microarray technique to determine the mRNA expression in lung tissue from young mice. We combined gene expression pathway analysis and analyzed the biological function of multiple single gene transcripts from lung homogenate to study the PVD relevant gene expression.Results: There were n = 117 significantly differentially regulated genes related to PVD through down-regulation of contractile elements, up- and down-regulation of factors involved in vascular tone and tissue-specific genes. Several genes also allowed for pinpointing gene expression differences to the pulmonary vasculature. The gene Nppa coding for a natriuretic peptide, a potent vasodilator, was significantly down-regulated and there was a significant up-regulation of Pde1a (phosphodiesterase 1A), Ptger3 (prostaglandin e receptor 3), and Ptgs1 (prostaglandin-endoperoxide synthase one).Conclusion: The pulmonary vasculature is affected by the arrest of secondary alveolarization as seen by differentially regulated genes involved in vascular tone and pulmonary vasculature suggesting BPD is not purely an airspace disease. Clues to prevention and treatment may lie in the pulmonary vascular system.

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BACKGROUND: We aimed to identify global blood and retinal gene expression patterns in murine oxygen-induced retinopathy (OIR), a common model of retinopathy of prematurity, which may allow better understanding of the pathogenesis of this severe ocular prematurity complication and identification of potential blood biomarkers. METHODS: A total of 120 C57BL/6J mice were randomly divided into an OIR group, in which 7-day-old pups were maintained in 75% oxygen for 5 days, or a control group. RNA was extracted from the whole-blood mononuclear cells and retinal cells on days 12, 17, and 28. Gene expression in the RNA samples was evaluated with mouse gene expression microarrays. RESULTS: There were 38, 1370 and 111 genes, the expression of which differed between the OIR and control retinas on days 12, 17, and 28, respectively. Gene expression in the blood mononuclear cells was significantly altered only on day 17. Deptor and Nol4 genes showed reduced expression both in the blood and retinal cells on day 17. CONCLUSION: There are sustained marked changes in the global pattern of gene expression in the OIR mice retinas. An altered expression of Deptor and Nol4 genes in the blood mononuclear cells requires further investigation as they may indicate retinal neovascularization.

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BACKGROUND: Bronchopulmonary dysplasia (BPD) is a common cause of abrupted lung development after preterm birth. BPD may lead to increased rehospitalization, more severe and frequent respiratory infections, and life-long reduced lung function. The gene regulation in lungs with BPD is complex, with various genetic and epigenetic factors involved. OBJECTIVES: The aim of this study was to examine the regulatory relation between gene expression and the epigenome (DNA methylation) relevant for the immune system after hyperoxia followed by a recovery period in air using a mouse model of BPD. METHODS: Newborn mice pups were subjected to an immediate hyperoxic condition from birth and kept at 85% O2 levels for 14 days followed by a 14-day period in room air. Next, mice lung tissue was used for RNA and DNA extraction with subsequent microarray-based assessment of lung transcriptome and supplementary methylome analysis. RESULTS: The immune system-related transcriptomeregulation was affected in mouse lungs after hyperoxia. A high proportion of genes relevant in the immune system exhibited significant expression alterations, e.g., B cell-specific genes central to the cytokine-cytokine receptor interaction, the PI3K-AKT, and the B cell receptor signaling pathways. The findings were accompanied by significant DNA hypermethylation observed in the PI3K-AKT pathway and immune system-relevant genes. CONCLUSIONS: Oxygen damage could be partly responsible for the increased susceptibility and abnormal response to respiratory viruses and infections seen in premature babies with BPD through dysregulated genes.

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BACKGROUND: In this study, we aimed to analyze differences in plasma protein abundances between infants with and without bronchopulmonary dysplasia (BPD), to add new insights into a better understanding of the pathogenesis of this disease. METHODS: Cord and peripheral blood of neonates (≤ 30 weeks gestational age) was drawn at birth and at the 36th postmenstrual week (36 PMA), respectively. Blood samples were retrospectively subdivided into BPD(+) and BPD(-) groups, according to the development of BPD. RESULTS: Children with BPD were characterized by decreased afamin, gelsolin and carboxypeptidase N subunit 2 levels in cord blood, and decreased galectin-3 binding protein and hemoglobin subunit gamma-1 levels, as well as an increased serotransferrin abundance in plasma at the 36 PMA. CONCLUSIONS: BPD development is associated with the plasma proteome changes in preterm infants, adding further evidence for the possible involvement of disturbances in vitamin E availability and impaired immunological processes in the progression of prematurity pulmonary complications. Moreover, it also points to the differences in proteins related to infection resistance and maintaining an adequate level of hematocrit in infants diagnosed with BPD.

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Purpose: Retinopathy of prematurity (ROP) is a vision-threatening complication of a premature birth, in which the etiology still remains unclear. Importantly, the molecular processes that govern these effects can be investigated in a perturbed plasma proteome composition. Thus, plasma proteomics may add new insights into a better understanding of the pathogenesis of this disease. Methods: The cord and peripheral blood of neonates (≤30 weeks gestational age) was drawn at birth and at the 36th postmenstrual week (PMA), respectively. Blood samples were retrospectively subdivided into ROP(+) and ROP(-) groups, according to the development of ROP. Results: The quantitative analysis of plasma proteome at both time points revealed 30 protein abundance changes between ROP(+) and ROP(-) groups. After standardization to gestational age, children who developed ROP were characterized by an increased C3 complement component and fibrinogen level at both analyzed time points. Conclusions: Higher levels of the complement C3 component and fibrinogen, present in the cord blood and persistent to 36 PMA, may indicate a chronic low-grade systemic inflammation and hypercoagulable state that may play a role in the development of ROP.

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OBJECTIVE: In the presented study, we aimed to systematically analyze plasma proteomes in cord blood samples from preterm infants stratified by their gestational age to identify proteins and related malfunctioning pathways at birth, possibly contributing to the complications observed among preterm infants. STUDY DESIGN: Preterm newborns were enrolled of three subgroups with different gestation age: newborns born ≤26 (group 1), between 27 and 28 (group 2) and between 29 and 30 (group 3) weeks of gestation, respectively, and compared to the control group of healthy, full-term newborns in respect to their plasma proteome composition. RESULT: Preterm delivery is associated with multiple protein abundance changes in plasma related to a plethora of processes, including inflammation and immunomodulation, coagulation, and complement activation as some key features. CONCLUSION: Plasma proteome analysis revealed numerous gestation-age-dependent protein abundance differences between term and preterm infants, which highlight key dysregulated pathways and potential new protein treatment targets.

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BACKGROUND: In this study, we aimed to analyze time-resolved plasma proteome changes in preterm neonates stratified by their gestational age to detect malfunctioning pathways that derive from the systemic immaturity of the neonate and to highlight those that are differentially regulated during the early development. METHODS: Preterm newborns were enrolled in three subgroups with different gestational ages: before 26 weeks of gestation (group 1), between 27 and 28 weeks of gestation (group 2), and between 29 and 30 (group 3) weeks of gestation. Plasma protein abundances were assessed at two time points (at preterm delivery and at the 36th week of post-menstrual age) by quantitative proteomics. RESULT: The quantitative analysis of plasma proteome in preterm infants revealed a multitude of time-related differences in protein abundances between the studied groups. We report protein changes in several functional domains, including inflammatory domains, immunomodulatory factors, and coagulation regulators as key features, with important gestational age-dependent hemopexin induction. CONCLUSION: The global trend emerging from our data, which can collectively be interpreted as a progression toward recovery from the perinatal perturbations, highlights the profound impact of gestation duration on the ability to bridge the gap in systemic homeostasis after preterm labor.

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Although over 85% of osteogenesis imperfecta (OI) cases are associated with mutations in the procollagen type I genes (COL1A1 or COL1A2), no hot spots for the mutations were associated with particular clinical phenotypes. Eight patients that were studied here, diagnosed with OI by clinical standards, are from the Polish population with no ethnic background indicated. Previously unpublished mutations were found in six out of those eight patients. Genotypes for polymorphisms (Sp1 - rs1800012 and PvuII - rs412777), linked to bone formation and metabolism were determined. Mutations were found in exons 2, 22, 50 and in introns 13 and 51 of the COL1A1 gene. In COL1A2, one mutation was identified in exon 22. Deletion type mutations in COL1A1 that resulted in OI type I had no effect on collagen type I secretion, nor on its intracellular accumulation. Also, a single base substitution in I13 (c.904-9 G>T) was associated with the OI type I. The OI type III was associated with a single base change in I51 of COL1A1, possibly causing an exon skipping. Also, a missense mutation in COL1A2 changing Gly→Cys in the central part of the triple helical domain of the collagen type I molecule caused OI type III. It affected secretion of the heterotrimeric form of procollagen type I. However, no intracellular accumulation of procollagen chains could be detected. Mutation in COL1A2 affected its incorporation into procollagen type I. The results obtained shall help in genetic counseling of OI patients and provide a rational support for making informed, life important decisions by them and their families.

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OBJECTIVES: Evaluate the time dependent expression of genes in preterm neonates and verify the influence of ontogenic maturation and the environmental factors on the gene expression after birth. MATERIAL AND METHODS: The study was carried out on 20 full-term newborns and 62 preterm newborns (mean birth weight = 1002 [g] (SD: 247), mean gestational age = 27.2 weeks (SD: 1.9)). Blood samples were drawn from all the study participants at birth and at the 36th week postmenstrual age from the preterm group to assess whole genome expression in umbilical cord blood and in peripheral blood leukocytes, respectively. (SurePrint G3 Human Gene Expression v3, 8x60K Microarrays (Agilent)). RESULTS: A substantial number of genes was found to be expressed differentially at the time of birth and at 36 PMA in comparison to the term babies with more genes being down-regulated than up-regulated. However, the fold change in the majority of cases was < 2.0. Extremely preterm and very preterm infants were characterized by significantly down-regulated cytokine and chemokine related pathways. The number of down-regulated genes decreased and number of up-regulated genes increased at 36 PMA vs. cord blood. There were no specific gene expression pathway profiles found within the groups of different gestational ages. CONCLUSIONS: Preterm delivery is associated with a different gene expression profile in comparison to term delivery. The gene expression profile changes with the maturity of a newborn measured by the gestational age.

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INTRODUCTION: Development of obesity in childhood may be linked to an increased risk of hypertension. OBJECTIVES: This study aimed (a) to analyze the expression of genes associated with blood pressure (BP) in obese children, (b) to evaluate ambulatory blood pressure monitoring (ABPM) as a diagnostic tool in hypertension in children, and (c) to assess the prevalence of metabolic syndrome in children with obesity. PATIENTS AND METHODS: Office BP measurements and ABPM were performed in 49 children with obesity and 25 age-matched healthy children. Expressions of 12 monogenic hypertension genes and 45 genes variants associated with BP were assessed using the microarray technique. RESULTS: No significant differences in gene expression levels were found. Children with obesity had significantly higher (P<0.001) mean office systolic and diastolic BPs compared with the controls. The diagnosis of high normal BP and hypertension with ABPM was established in 27 and 33% of children, respectively. Nocturnal BP decrease less than 10% was found in 27% of children, whereas nocturnal BP decrease more than 20% was found in 13% of children. Nocturnal BP increase was found in 13% of patients. The diagnosis of metabolic syndrome was established in 29% of obese patients. CONCLUSION: The following can be concluded: (a) the prevalence of metabolic syndrome was found in nearly one-third of children with obesity. (b) ABPM is a useful and reliable tool in the diagnostics of pediatric hypertension. Abnormal BP can be observed in ∼50% of obese children.

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Myelomeningocele (MMC) results from a failure of normal neural tube fusion in early fetal development. Retrospective, observational study of medical data of 54 children treated in Pediatric Nephrology and Urology Clinics for five years was performed. The following data were analyzed: serum creatinine, eGFR, urine analysis, renal scintigraphy (RS), renal ultrasound, and urodynamics. Mean age of studied population: 12.3 years, median of eGFR at the beginning and at the end of survey was 110.25 and 116.5 mL/min/1.73 m² accordingly. Median of frequency of urinary tract infections (fUTI): 1.2 episodes/year. In 24 children: low-pressure, in 30 children: high-pressure bladder was noted. Vesicouretral reflux (VUR) was noted in 23 children (42.6%). fUTI were more common in high-grade VUR group. High-grade VURs were more common in group of patients with severe renal damage. At the end of the survey 11.1% children were qualified to higher stages of chronic kidney disease. Renal parenchyma damage progression in RS was noted in 22.2% children. Positive VUR history, febrile recurrent UTIs, bladder wall trabeculation, and older age of the patients constitute risk factors of abnormal renal scans. More than 2.0 febrile, symptomatic UTIs annually increase by 5.6-fold the risk of severe renal parenchyma damage after five years.

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BACKGROUND: Electrical bioimpedance analysis (BIA) is becoming more widely used in clinical practice as a method of body composition analysis. In healthy children blood pressure (BP) changes with age, body mass and height. Until now the relation between water compartments and BP in healthy children has not been evaluated. The aim of this study was to evaluate the relationship between body composition as well as water compartments (measured by electrical bioimpedance) and BP. METHODS: The study was performed in 72 children (32 girls and 40 boys) aged: 6-7 and 12-13 years. BIA measurements were taken using Nutriguard Data Input device with Bianostic electrodes and following parameters were calculated: total body water (TBW), lean body mass (LBM), fat mass (FM), intra- and extracellular water (ICW, ECW) and phase angle alpha. BP was measured twice using the oscillometric method. RESULTS: Elevated BP > 95th percentile for gender, age and height were observed in 9 children. A significant correlation between systolic (S)BP and TBW (R = 0.4023, p < 0.001), LBM (R = 0.3600, p = 0.002), FM (R = 0.4725, p < 0.001), ECW (R = 0.4598, p < 0.001) and body mass index (BMI) (R = 0.4089, p < 0.001) was found. Furthermore, diastolic (D)BP significantly correlated with TBW (R = 0.3056, p = 0.011), LBM (R = 0.2783, p = 0.021), FM (R = 0.3956, p < 0.001), ECW (R = 0.3869, p = 0.001) and BMI (R = 0.3550, p = 0.002). In the studied group malnutrition (weight < 3rd percentile) was found in 8 children and 2 had obesity (BMI > 95th percentile). Growth disorders were found in 6 children (5 of them being undernourished). CONCLUSIONS: In the studied children SBP and DBP correlated with water compartments, lean body and fat masses derived from BIA. The problem of unrecognized hypertension and malnutrition in children and adolescents is still underestimated in the Polish population.

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AIM: Estimation of eGFR in children with normal kidney function using the Schwartz equations results in underestimating real GFR. MATERIALS AND METHODS: We propose modification of three Schwartz equations - two based on creatinine concentration (eGFRScrBS bedside) and (eGFRScr) and one 3-marker based on creatinine, urea and cystatin C concentrations (eGFRS3M). The iohexol test (reference method) was performed 417 times in 353 children >2 years with mean GFR: 98 ± 31.6 ml/min/1.73m(2). The assessment included also the Filler and Zappitelli equations. The modification was performed using methods: (1) based on equation, eGFRcor = a [eGFR - T] + T, where T = 50, if eGFR > T, and a equals for: eGFRScrBS 1.4043, for eGFRScr 2.0048, for eGFRS3M 1.2951, and (2) based on correction of all coefficients of the original equation. RESULTS: For comparison of all the results and for children with GFR< 60, 60-90, 90-135 and > 135 ml/min/1.73m(2) the correlation coefficient, relative error (RE) and root mean square relative error (RMSRE) was employed and revealed improvement of RE from 25.9 to 6.8 and 3.9% (depending on the correction method) for eGFRScr; from 19 to 8.1 and 3.9% for eGFRScrBS and: from 11.6% to 2.0 and 2.3% for eGFRS3M (respectively). The RMSRE values changed from 30 to 21.3 and 19.8% for eGFRScr, from 25.1 to 21.6 and 19.8% for eGFRScrBS and from 19.1 to 15.8 and 15.3 % for eGFRS3M. CONCLUSIONS: Modifications of Schwartz equations at GFR > 60 ml/min/1.73m(2) significantly improves the accuracy of calculating eGFR. The 3-markers equation is more accurate and should be employed frequently.

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Cardiovascular diseases remain the most frequent cause of morbidity and mortality in patients with chronic kidney disease (CKD). The aim of the study was to assess the association between oxidative stress biomarkers and cardiovascular risk factors and left ventricular hypertrophy in children with CKD. Material and Methods. The studied group consisted of 65 patients aged 1.4-18.6 (mean 11.2) years with stages 1 to 5 CKD. Serum oxidized low-density lipoprotein (oxLDL), protein carbonyl group, creatinine, cystatin C, albumin, lipids, high-sensitivity C-reactive protein, intercellular adhesion molecule-1, insulin, plasma renin activity, and aldosterone levels were measured. Patients were divided into groups depending on CKD stage. Anthropometric measurements, ambulatory blood pressure (BP) measurements, and echocardiography with left ventricular mass (LVM) calculation were performed. Results. Serum oxLDL strongly correlated with creatinine (R = 0.246; p = 0.048), cystatin C (R = 0.346; p = 0.006), total cholesterol (R = 0.500; p < 0.001), triglycerides (R = 0.524; p < 0.001), low-density lipoprotein concentrations (R = 0.456; p < 0.001), and 24 hour BP values of systolic (R = 0.492; p = 0.002), diastolic (R = 0.515; p < 0.001), and mean arterial pressure (R = 0.537; p < 0.001). A significant correlation between oxLDL levels and LVM z-scores (R = 0.299; p = 0.016) was found. Conclusions. Hypertension and dyslipidemia correlated with lipid oxidation in children with CKD. oxLDLs seem to be valuable markers of oxidative stress in CKD patients, correlating with left ventricular hypertrophy.

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Immune reactions are among the most serious complications observed after hematopoietic stem cell transplantation (HSCT) in children. Microarray technique allows for simultaneous assessment of expression of nearly all human genes. The objective of the study was to compare the whole genome expression in children before and after HSCT. A total of 33 children referred for HSCT were enrolled in the study. In 70% of the patients HSCT was performed for the treatment of neoplasms. Blood samples were obtained before HSCT and six months after the procedure. Subsequently, the whole genome expression was assessed in leukocytes using GeneChip Human Gene 1.0 ST microarray. The analysis of genomic profiles before and after HSCT revealed altered expression of 124 genes. Pathway enrichment analysis revealed upregulation of five pathways after HSCT: allograft rejection, graft-versus-host disease, type I diabetes mellitus, autoimmune thyroid disease, and viral myocarditis. The activation of those pathways seems to be related to immune reactions commonly observed after HSCT. Our results contribute to better understanding of the genomic background of the immunologic complications of HSCT.

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Introduction: Hypertension (HT) is one of the major risk factors of chronic kidney disease (CKD) progression and cardiovascular complications. The aim of the study was to analyze blood pressure (BP) values and assess the usefulness of clinical measurements in BP monitoring in children with chronic kidney disease. Material and methods: The study was conducted in 62 children (40 boys and 22 girls) aged 4,2-18,6 years (median age 12.4 (9.1; 16.0) with CKD stages 1 + 2 (n = 9), 3 (n = 17), 4 (n = 15) and 5. Creatinine concentration was measured and glomerular filtration rate was calculated using the Schwartz formula. Each of the patients underwent clinical BP measurements and 24-hour ambulatory blood pressure monitoring (ABPM). Results: Based on clinical meaurements elevated BP values were found in 25 patients (40.3%): in stages 1 + 2 in 33.3%, in stage 3 in 41.2%, in stage 4 in 46.6% and in stage 5 in 38.1% patients. Hypertension was diagnosed with ABPM in 30 patients (48.4% of the studied population): in stages 1 + 2 - 3 patients (33.3%), in stage 3 - 8 patients (47, 1%), in stage 4 - 7 patients (46.7%) and stage 5 - 12 patients (57.1%). Only 12 patients (19.4%) had hypertension diagnosed in both clinical and ABPM measurements. White coat effect was found in 13 children (21.0%) and masked HT in 18 children (29.0%). In 24-hour BP monitoring the highest values of systolic, diastolic and mean BP values were found in children with masked HT. In children with masked HT higher values of 24-hour systolic (120 vs. 105.5 mmHg, p<0.001) and diastolic (75 vs. 65 mmHg, p<0.001) BP compared with clinical values were detected. Children with masked HT had significantly higher nighttime diastolic BP compared with children with HT (1.43 vs. 0.74 z-score, p<0.001). Conclusions: The large percentage of children with masked hypertension is an indication for frequent ABPM measurements in children with chronic kidney diseses. Office measurements are not sufficient to detect HT in children with CKD. The best diagnostic method to confirm and monitor hypertension in patients with CKD is 24-hour ambulatory blood pressure monitoring.

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AIM: To assess the relationship between stereoscopic vision, visual perception, and microstructure of the corpus callosum (CC) and occipital white matter, 61 children born with a mean birth weight of 1024 g (SD 270 g) were subjected to detailed ophthalmologic evaluation, Developmental Test of Visual Perception (DTVP-3), and diffusion tensor imaging (DTI) at the age of 4. RESULTS: Abnormal stereoscopic vision was detected in 16 children. Children with abnormal stereoscopic vision had smaller CC (CC length: 53 ± 6 mm versus 61 ± 4 mm; p < 0.01; estimated CC area: 314 ± 106 mm(2) versus 446 ± 79 mm(2); p < 0.01) and lower fractional anisotropy (FA) values in CC (FA value of rostrum/genu: 0.7 ± 0.09 versus 0.79 ± 0.07; p < 0.01; FA value of CC body: 0.74 ± 0.13 versus 0.82 ± 0.09; p = 0.03). We found a significant correlation between DTVP-3 scores, CC size, and FA values in rostrum and body. This correlation was unrelated to retinopathy of prematurity. CONCLUSIONS: Visual perceptive dysfunction in ex-preterm children without major sequelae of prematurity depends on more subtle changes in the brain microstructure, including CC. Role of interhemispheric connections in visual perception might be more complex than previously anticipated.

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