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Introduction: Nocturnal enuresis can be diagnosed in a child older than 5 years of age who involuntarily discharges urine in the wrong time, i.e. at night, and in the wrong place, i.e. in bed. Aim: The aim of the study was to analyse the profile of patients who consult the specialist physician with monosymptomatic primary nocturnal enuresis. Material and methods: The data were collected from a questionnaire completed by guardians of children during the first nephrological consultation. The questions concerned the following: family history of nocturnal enuresis, bedwetting intensity, other urinary tract symptoms, a voiding chart and fluid intake record, number of nocturnal enuresis incidents in 14 days, episodes of nocturia, nocturnal diuresis volume, urinary urgency volume and constipation. Moreover, basic anthropometric measurements were taken. The data were analysed and the following values were calculated: average voided volumes, maximum voided volumes, voided volumes before 5 p.m. and 24-hour diuresis. An analogous analysis was conducted with respect to fluid intake. Results: Most patients were males. The family history of nocturnal enuresis was positive in ⅓ of patients. Approximately ⅓ of patients tended to drink fluids directly before bedtime. The number of patients with sporadic nocturnal enuresis (23–45%) was comparable to the number of patients with frequent nocturnal enuresis (28–55%). Nocturnal diuresis suggested nocturnal polyuria in 11 patients (21.6%). Decreased functional bladder capacity was found in almost ¼ of patients (12–23.5%). Conclusions: Monosymptomatic nocturnal enuresis is more common in boys. The family history was positive in ⅓ of patients. Patients and their guardians are not aware of fluid intake restrictions at bedtime. The frequency of nocturnal polyuria and decreased functional bladder capacity is comparable in the investigated patients.

BackgroundThis study aimed to evaluate outcome of children on chronic peritoneal dialysis (PD) with a concurrent colostomy.MethodsPatients were identified through the International Pediatric Peritoneal Dialysis Network (IPPN) registry. Matched controls were randomly selected from the registry. Data were collected through the IPPN database and a survey disseminated to all participating sites.ResultsFifteen centers reported 20 children who received chronic PD with a co-existing colostomy. The most common cause of end stage kidney disease was congenital anomalies of the kidney and urinary tract (n = 16, 80%). The main reason for colostomy placement was anorectal malformation (n = 13, 65%). The median age at colostomy creation and PD catheter (PDC) insertion were 0.1 (IQR, 0–2.2) and 2.8 (IQR 0.2–18.8) months, respectively. The colostomies and PDCs were present together for a median 18 (IQR, 4.9–35.8) months. The median age at PDC placement in 46 controls was 3.4 (IQR, 0.2–7.4) months of age. Fourteen patients (70%) developed 39 episodes of peritonitis. The annualized peritonitis rate was significantly higher in the colostomy group (1.13 vs. 0.70 episodes per patient year; p = 0.02). Predominant causative microorganisms were Staphylococcus aureus (15%) and Pseudomonas aeruginosa (13%). There were 12 exit site infection (ESI) episodes reported exclusively in colostomy patients. Seven colostomy children (35%) died during their course of PD, in two cases due to peritonitis.ConclusionAlthough feasible in children with a colostomy, chronic PD is associated with an increased risk of peritonitis and mortality. Continued efforts to reduce infection risk for this complex patient population are essential.

Wstęp: Choć czynniki stymulujące erytropoezę (ESA) są stosowane od wielu lat w leczeniu niedokrwistości nerkopochodnej u chorych ze schyłkową niewydolnością nerek, niewiele jest badań oceniających skuteczność takiego leczenia u dzieci. Celem pracy była ocena skuteczności leczenia ESA u dzieci z przewlekłą chorobą nerek w Polsce, zarówno w okresie przeddializacyjnym, jak i dializacyjnym. Materiał i metoda: Badanie prospektywne, prowadzone od 1.11.2008 do 30.04.2009 r., ankietowe. Ankiety rozesłano do 12 ośrodków prowadzących leczenie dzieci z PChN zarówno dializami, jak i w okresie przeddializacyjnym. Pytania dotyczyły mię- dzy innymi podstawowych danych chorego, przyczyny choroby nerek, wieku rozpoczęcia leczenia dializacyjnego, rodzaju stosowanej erytropoetyny, suplementacji żelaza, stężenia hemoglobiny. Wyniki: Analizą objęto 117 dzieci leczonych dializami i 35 w okresie przeddializacyjnym. W obu grupach stosowano głównie erytropoetynę beta (odpowiednio 74% i 77%) – mediana odpowiednio 99 (62‑142) i 77 (43‑98) IU/kg/tydzień. Średnie stężenie hemoglobiny wynosiło 10,9±1,6 g/dl u dzieci dializowanych i 11,2±1,1 g/dl w predializie. W grupie dializowanych 48% osiągnęło zalecane wartości hemoglobiny, w grupie leczonych zachowawczo – 71%. Wnioski: Badanie wykazało niedostateczną skuteczność leczenia niedokrwistości nerkopochodnej u dializowanych dzieci w Polsce. Obecność zakażenia, zaawansowanie niedokrwistości na początku leczenia oraz niedostatecznie wysoka dawka erytropoetyny były czynnikami ryzyka niepowodzenia leczenia.

T cells are involved in the pathogenesis of nephrotic syndrome (NS). The aim of the study was to determine whether the activity of T-helper-1 (Th1) and T-helper-2 (Th2) cells and the distribution of the lymphocyte subsets, namely CD45RA+CD4+ (\"naive\" helper T cells, suppressor-inducer), CD45RA+CD8+ (\"naive\" suppressor T cells, suppressor-effector), CD45RO+CD4+ (\"memory\" helper T cells), are predictive for steroid sensitivity in children with primary NS. These parameters were assessed at the onset of disease, before initiation of steroid therapy. Two groups of NS children were retrospectively formed according to steroid sensitivity (SS) or resistance (SR). The activity of Th1 and Th2 cells was defined by the production of interleukin-2 (IL-2), interferon-gamma, IL-4, and IL-10 in the supernatants of CD4+ T cell cultures activated with autologous monocytes presenting tetanus toxoid (TT). Peripheral lymphocyte subsets were determined using double- or triple-color flow cytometry. In SS children with NS we found a decreased proliferative response of CD4+ T cells to TT stimulation, cytokine synthesis indicating the predominance of Th2 activity, and an increased percentage of activated suppressor-inducer (CD45RA+ CD4+CD25+, 5.18+/-0.8, P<0.001) and suppressor-effector (CD45RA+CD8+CD25+, 2.05+/-0.6, P<0.01) cells, with the concomitant reduction of activated memory cells (CD45RO+CD4+CD25+, 0.2+/-0.1, P<0.001). In children with SRNS we found an increased proliferative response of CD4+ T cells to TT, a rise in activated memory (CD45RO+CD4+CD25+, 3.82+/-0.7, P<0.01) and suppressor-inducer peripheral T cells (CD45RA+ CD4+CD25+, 3.85+/-0.6, P<0.01), but a low percentage of activated suppressor-effector (CD45RA+CD8+ CD25+, 0.5+/-0.2, P<0.05) T cells. We conclude that prior to treatment the distribution of lymphocyte subpopulations in peripheral blood together with Th1 and Th2 cell activity provides a useful tool for evaluating the likelihood of steroid sensitivity in patients with primary NS.

Background/Aim: End-stage renal disease (ESRD) induces a clinical state of immunodeficiency with a higher incidence of infections and higher mortality due to infectious complications compared with the normal population. The definite mechanism responsible for the host defense alterations is not well understood. The aim of the study was to investigate intracellularly the relationship between cytokine synthesis and oxidative stress in peripheral blood lymphocytes in children with ESRD. Methods: Twenty-one children (age 11.7 ± 5.8 years) with ESRD treated with hemodialysis (HD; n = 10) and peritoneal dialysis (PD; n = 11) were studied. Nine healthy children of comparable age formed the control group. To determine intracellular oxidative stress we used dihydrorhodamine-123 (DHR), which after oxidation to rhodamine-123 (RHO) emitted a bright fluorescent signal. Intracellular oxidation of DHR in T lymphocytes reflected intracellular oxidative stress. The intracellular synthesis of cytokines (IL-2, IFN-γ, IL-4, IL-6) was also measured. Both parameters were detected at a single-cell level by flow cytometry. Lymphocyte subsets were evaluated using the monoclonal antibodies conjugated with fluorochromes. Results: We found that in T lymphocytes the mean fluorescence intensity (MFI), which reflected intracellular oxidative stress, was increased in ESRD patients compared to the controls (CD3+: 34.77 ± 11.55 vs. 22.55 ± 4.97, p < 0.01; CD3+CD8+: 34.31 ± 12.17 vs. 20.77 ± 4.89, p < 0.01; CD3+CD4+: 36.06 ± 6.98 vs. 24.44 ± 7.68, p < 0.001). HD patients showed slightly higher MFI compared to PD patients in CD3+ cells (39.32 ± 11.70 vs. 30.63 ± 10.20, NS), in CD3+CD8+ cells (37.90 ± 14.32 vs. 31.06 ± 9.34, NS) and in CD3+CD4+ cells (40.10 ± 2.28 vs. 29.33 ± 7.06, p < 0.001). The intracellular synthesis of IL-2 was higher in ESRD patients compared to the controls, both in CD3+ cells (31.34 ± 9.80 vs. 20.49 ± 15.26%, p < 0.05) and in CD3+CD4+ cells (36.10 ± 8.69 vs. 24.03 ± 16.95%, p < 0.05). The intracellular synthesis of IFN-γ, IL-4 and IL-6 was significantly lower in the ESRD group compared to the controls. Interestingly, in patients treated with HD, negative correlations between the degree of intracellular oxidative stress and intracellular cytokine synthesis in CD3+ lymphocytes were found. Conclusion: Our results show that patients with ESRD, especially those treated with HD, present increased oxidative stress in T lymphocytes, which may lead to decreased cytokine synthesis and abnormal immune response. Copyright © 2005 S. Karger AG, Basel