Search

The aim of the study was to investigate urinary levels and clinical significance of osteopontin (uOPN) in children with different glomerular diseases according to histological diagnosis and degree of proteinuria.The examinations were conducted in 3 groups of children: I - 20 children with minimal change disease (MCD) examined twice: A - in relapse; B - in remission, group II - 17 children with focal segmental glomerulosclerosis (FSGS), III - 12 children with IgA nephropathy (IgAN). The control group (C) contained 20 healthy children. OPN was measured in the urine using ELISA commercial available kit (RD Quantikine) and was expressed in ng/ mg cr.The median uOPN/ cr. in MCD children in relapse (IA) was median 134.98 ng/ mg cr. and was higher when compared to controls (p0.01). In exam IB, when proteinuria subsided, OPN/ cr. increased to median 172.96 ng/ mg cr. and was higher in comparison to healthy subjects (p0.01) and MCD children in relapse (p0.05). Children from group II revealed higher uOPN/ cr. levels when compared to groups I, III and C (p0.01). UOPN/ cr. positively correlated with protein/ creatinine ratio in all examined groups of children (p0.01).We found significantly higher uOPN/ cr. in all the groups of children with glomerulonephritis. The highest uOPN/ cr. levels were found in patients with FSGS and correlated significantly with both interstitial changes and mesangial expansion found in kidney biopsy.

The aim of the study was to examine the urinary levels and clinical significance of monocyte chemoattractant protein-1 (uMCP-1) in children according to histological diagnosis and degree of proteinuria.Group I comprised 20 children with idiopathic nephrotic syndrome (INS), examined twice (A, during INS relapse; and B, after proteinuria subsided). Group II comprised 17 children with persistent proteinuria due to focal segmental glomerulosclerosis (FSGS). Group III included 12 children with immunoglobulin A nephropathy (IgAN). The control group (C) contained 22 healthy children. uMCP-1 was determined by enzyme-linked immunosorbent assay and expressed in pg/ml.The median uMCP-1/creatinine ratio (uMCP-1/cr) in children with minimal change disease in relapse (IA) was significantly higher than in controls (p0.05), but when controlling for cyclosporine A (CsA) treatment the median uMCP-1 in children with INS, who were not treated with CsA, was 12.01 pg/mg cr (range 1.82-261.56 pg/mg cr) and did not differ from healthy controls. In examination IB the uMCP-1/cr concentration decreased and did not differ from healthy controls (p0.05). Children from groups II and III also had higher uMCP-1/cr levels than groups I and C (p0.01). uMCP-1/cr positively correlated with serum total cholesterol, low-density lipoprotein and protein/creatinine ratio in relapse (IA), and with serum cholesterol level in group B. A positive correlation between uMCP-1/cr and protein/creatinine ratio was also confirmed in groups II and III.Increased uMCP-1 was found in children with IgAN and FSGS correlated with proteinuria. A slight increase in uMCP-1 in children with INS was probably associated with CsA treatment.

The Bonn Risk Index has been used to evaluate the risk of urinary calcium oxalate stone formation. According to the original method, risk should be determined based on 24-hour urine collection. We studied whether the Bonn Risk Index could be measured in spot urine samples and which part of the day is most suitable for this purpose.We collected total and fractionated 24-hour urine (in a 6-hour nocturnal portion and 9 consecutive 2-hour diurnal samples) in 42 children and adolescents with calcium oxalate urolithiasis and 46 controls. Bonn Risk Index values determined from each of the urine fractions were compared to those obtained from related 24-hour urine collections.Both groups exhibited similar circadian patterns of Bonn Risk Index values. Median Bonn Risk Index for the nighttime portion of urine in the stone group was 1.4 times higher than that obtained from the total 24-hour urine. The morning hours between 08:00 and 10:00 showed the peak lithogenic risk, and this fraction had the highest sensitivity and selectivity regarding discrimination between stone formers and healthy subjects. The afternoon hours demonstrated lower and less fluctuating crystallization risk. Despite diurnal fluctuations in Bonn Risk Index, there was still a well-defined cutoff between the groups.Bonn Risk Index determined from urine samples collected between 08:00 and 10:00 appears optimal in separating stone formers from healthy subjects, and appears as useful as the value determined from 24-hour urine collection. Investigation of this diurnal sample simplifies diagnosis in pediatric stone disease without loss of clinical information.

The purpose of the study was to investigate serum uric acid (SUA), high-sensitivity C-reactive protein (hs-CRP) and mean platelet volume (MPV) in pre-hypertensive (PH) and hypertensive (HT) children and adolescents. The study group consisted of 80 patients aged 10-19 years subdivided into PH and HT groups according to mean daytime or night-time systolic or diastolic blood pressure (BP) levels (90th percentile, but95th percentile andor = 95th percentile, respectively). The control group (C) contained 25 normotensive subjects. Serum hs-CRP level was determined by a nephelometric method (Behring); platelets (PLTs) were counted, and MPV was assessed by a Coulter Analyzer MAXM. SUA was measured with an Hitachi instrument. The median SUA and hs-CRP levels in PH and HT subjects were significantly higher than those of the controls (P0.01) and were higher in the HT group than in the PH group (P0.05). An increase in SUA above 5.5 mg/dl was associated with an increase in hs-CRP [odds ratio (OR) 4.8; confidence interval (CI) 1.3-17.4; P0.01]. MPV values in the PH group did not differ from those of the controls (P0.05), but it was significantly higher in HT patients (P0.01). Serum hs-CRP and MPV concentrations were positively correlated with all BP measurements except night-time diastolic blood pressure (DBP). We demonstrated that, in HT children and adolescents, increased SUA with a parallel increase in hs-CRP and PLTs with MPV is observed. Although large, multicentre, prospective studies are needed to confirm this observation, hyperuricaemia seems to be associated with an increase in hs-CRP in PH and HT patients.

Purpose: The Bonn Risk Index has been used to evaluate the risk of urinary calcium oxalate stone formation. According to the original method, risk should be determined based on a 200 ml urine sample taken from a 24-hour collection. We evaluated whether the Bonn Risk Index can also be effectively determined in small urine samples. Materials and Methods: We studied 190 children and adolescents with nocturia and calcium oxalate urolithiasis. Initially Bonn Risk Index was determined according to the original method of Laube. Subsequently Bonn Risk Index was calculated using a computer program controlling a specially designed system to define the time point of induced crystallization based on consecutive urine samples of 1.5, 2.0 and 3.0 ml. Results: No significant differences were found in Bonn Risk Index between values obtained from 200 ml samples and those based on the micromethod with urine samples of 2 and 3 ml. Conclusions: Assessment of risk of urinary calcium oxalate stone formation with Bonn Risk Index in small urine volumes, based on prototype equipment controlled by specialized computer software, is comparable to the original method. This finding facilitates the procedure and improves Bonn Risk Index determination in children.

The aim of the study was to assess urinary transforming growth factor beta1 (TGF beta1) level in children and adolescents with congenital solitary kidney (CSK), depending on estimated glomerular filtration rate (eGFR) and compensatory overgrowth of the kidney. The study group (I) consisted of 65 children and young adults, 0.5-22 years of age (median 10.0 years) with CSK and no other urinary defects. The control group (C) contained 44 healthy children and adolescents, 0.25-21 years old (median 10.3 years). We used an enzyme-linked immunosorbent assay (ELISA) to determine the urinary level of TGF beta1, the Jaffe method to assess creatinine concentration, and the Schwartz formula to estimate GFR. Kidney length was measured while the patient was in a supine position, and overgrowth (O%) was calculated with reference to the charts. Urinary TGF beta1 level in CSK patients was more than twice as high as that in controls (P < 0.05). Also, eGFR in patients with CSK exceeded the values in the control group (P < 0.01). Compensatory overgrowth of the solitary kidney was found (median 19.44%). Urinary TGF beta1 concentration was positively correlated with eGFR (r = 0.247, P < 0.05), uric acid concentration (r = 0.333, P < 0.01), and percentage of overgrowth (r = 0.338, P < 0.01) and body mass index (BMI) centile (r = 0.274, P < 0.05). We concluded that, although proteinuria and progressive renal insufficiency is not observed in patients with CSK during childhood, the renal haemodynamic changes are present and may be a risk factor for impairment of renal function and hypertension in future life.

The aim of this study was to determine the effects of cyclosporine A (CyA) on urinary levels of matrix metalloproteinase 2 and 9 (MMP2, MMP9) and their tissue inhibitors 1 and 2 (TIMP1, TIMP2) in steroid-dependent nephrotic syndrome (SDNS). The study group (1) consisted of 18 children SDNS aged 3.5–17.0 years treated with CyA. All NS children were examined three times: (A) at proteinuria relapse, before CyA treatment, (B) after 6 months, and (C) after 12 months of CyA administration. The control group (2) consisted of 18 healthy children. Serum CyA level was assessed by immunofluorescence. Enzyme-linked immunosorbent assay kits for total human MMP2 and 9 and TIMP1 and 2 were obtained from R&D Systems. Compared with healthy controls, urinary MMP9/Cr in NS children before CyA was on the same level and increased during CyA treatment, and urinary TIMP1/Cr was twice as high and increased significantly during CyA treatment. MMP9/TIMP1 in NS children treated with CyA increased, but the difference was not statistically significant. Urinary MMP2/Cr was similar, and urinary TIMP2/Cr was significantly higher in children treated with CyA (p < 0.01). The MMP2/TIMP2 ratio in NS children treated with CyA was significantly lower in comparison with healthy controls (p < 0.01). A negative correlation was noted between urinary MMP2/TIMP2 ratio and serum CyA in NS children (r = −0.541, p < 0.01). An imbalance within the MMP2 and TIMP2 and MMP9 and TIMP1 system may play a role in the pathogenesis CyA nephropathy.

Bonn Risk Index (BRI) is being used for the assessment of urinary calcium oxalate (CaOx) crystallization. There are no published data regarding BRI during growth. The objective of this study was to establish age- and sex-dependent BRI values in healthy children and adolescents. A total of 1,050 Caucasian subjects aged 3–18 years (525 males, 525 females) without a history of kidney stone disease were enrolled in the cross-sectional study. The study group was divided into 15 ranges according to age, each comprising 70 subjects. Urinary ionized calcium [Ca2+] was measured using a selective electrode while the onset of spontaneous crystallization was determined using a photometer and titrating with 40 mmol/L ammonium oxalate (Ox2−). The calculation of BRI value was based on the ratio of [Ca2+] to the required amount of ammonium oxalate added to 200 ml of urine to induce crystallization. The median BRI was 0.26 1/L and the values of the 5th and 95th percentiles were 0.06 1/L and 1.93 1/L, respectively. BRI correlated positively with body-area-related BRI (1/L × 1.73 m2) (R = 0.18; P

The aim of this study was to assess the serum concentration of high-sensitivity C-reactive protein (hs-CRP) in children with nephrotic syndrome (NS) treated with prednisone and cyclosporine A (CyA). Patients were divided into three groups: (I) 20 NS children (aged 4–14 years) in relapse and examined twice, (A) before treatment and (B) after proteinuria regression (a 3–4 week course of prednisone therapy); (II) 20 children with steroid-dependent or steroid-resistant NS, treated with CyA, also examined twice, (D) before treatment with CyA, (E) 6 months after therapy. A control group (C) consisted of 20 healthy children. Serum hs-CRP level was determined by a nephelometric method with a Behring Nephelometer 100 Analyzer, Dade Behring. The results showed that median hs-CRP concentration was the highest in children with relapsing steroid-sensitive NS before treatment (IA). After proteinuria regression (IB), the hs-CRP level had decreased and did not differ from that of healthy controls (C) (P > 0.05). In group II, before CyA administration (IID), the level of hs-CRP was normal, but it had increased after 6 months of treatment (IIE) up to a level six-times higher than that of the control group (P < 0.01). We concluded that, in children with steroid-sensitive nephrotic syndrome in relapse, the serum hs-CRP level is increased but returns to normal after 3–4 weeks of glucocorticoid treatment. In children chronically treated with CyA due to NS, serum hs-CRP level increases significantly during the therapy.

The aim of this study was to examine the expression of P-glycoprotein (P-gp) in CD3 lymphocytes of children with nephrotic syndrome (NS) in relation to their clinical response to glucocorticoid (GC) treatment. The examinations were performed on two groups. The study group (I) consisted of 88 children aged 2.0–20.0 years with NS, divided according to their clinical response to GC: NFR—non-frequent relapse NS; FR—frequent relapse NS; SD—steroid-dependent NS. The control group (II) consisted of 18 healthy children never treated with GC. We measured P-gp expression on CD3 lymphocytes of patients with NS using a flow cytometry assay. The CD3/P-gp was significantly higher than in controls. The difference was higher in SD (P=0.0001) and FR - (P=0.0002) group. The difference in NFR was smaller. Mean CD3/P-gp (in percent) was twice as high in SD children than in NFR, and the difference, as between FR and NFR, was statistically significant (P

Glucocorticoids are still the mainstay of therapy for nephrotic syndrome (NS) in children. Poor response to glucocorticoids may relate, in part, to the overexpression of P-glycoprotein (P-gp). The aim of the present study was to determine the expression of P-gp in lymphocytes (CD3) in the peripheral blood of children with steroid-sensitive nephrotic syndrome in the dynamics of the disease. The study group (I) consisted of 18 children, median age 5.75 years, with steroid-sensitive nephrotic syndrome, in whom the examinations were carried out three times: (A) before treatment, during relapse; (B) after 3–4 weeks of prednisone treatment; (C) 2 months after finishing prednisone treatment. The control group (II) consisted of 18 healthy children of the same age. P-gp expression in CD3 lymphocytes of peripheral blood was measured using flow cytometry. During NS relapse and prior to glucocorticoid administration, the CD3/P-gp level was higher (median 3.20%, range 0.80–7.80%) when compared to healthy controls (1.10%, range 0.30– 2.20%) (p

The aim of the study was to assess urinary transforming growth factor (TGF)-beta1 in children with steroid-dependent nephrotic syndrome (SDNS) treated with cyclosporine A (CyA) and ACE inhibitors (ACEI). The study involved 24 children (14 boys and 10 girls) with SDNS and signs of focal segmental glomerulosclerosis. The children were treated with prednisone, CyA, and ACEI. All children were examined four times: A during relapse of proteinuria, before treatment with CyA and ACEI, and B after 3 months, C 6 months, and D 12 months of treatment. The control group consisted of 20 healthy children of the same age. The urinary TGF-beta1 level was determined by ELISA (R and D Quantikine). The serum CyA level was measured by monoclonal antibody fluorescence polarization immunoassay. Prior to CyA treatment, the urinary TGF-beta1 level was the highest (135.61+/-38.31 pg/mg creatinine). During CyA treatment, TGF-beta1 was reduced to 117.96+/-81.57 after 3 months, to 80.26+/-49.52 after 6 months, and to 44.00+/-31.83 pg/mg creatinine after 12 months, but it was still higher than in the control group. At 3 months there was a positive linear correlation between urinary TGF-beta1 and proteinuria (r=0.654, P

The aim of the study was to investigate (1) whether there are any changes in release of platelet-derived growth factor AA (PDGF AA) in children with nephrotic syndrome without clinical thromboembolic symptoms 2; (2) whether serum PDGF AA correlates with the platelet count (PLT) and platelet indices; (3) whether prednisone therapy affects the serum PDGF AA and the PLT; (4) whether PDGF AA is a useful predictor of disease activity. The study involved two groups of children: 33 with nephrotic syndrome (I) who were evaluated twice (A during relapse and B after 2 weeks of prednisone treatment) and 34 healthy children (II). The serum concentration of PDGF was measured by ELISA. In group I/A the PLT (P0.01) and platelet distribution width (P0.05) were elevated, the mean platelet volume (MPV) (P0.05) was decreased and the plateletcrit (P0.05) was normal. In group I/B, the PLT was decreased and MPV increased. The concentration of PDGF AA was still increased and correlated negatively with the albumin concentration. Hence in children with nephrotic syndrome an increase in PLT, a decrease in MPV, and a higher concentration of PDGF were observed. Treatment of nephrotic syndrome with prednisone for 2 weeks is not sufficient to normalize platelet parameters. Further studies are necessary to confirm the role of PDGF AA in the hypercoagulation state in children with nephrotic syndrome.

Hyperhomocysteinemia is independent risk factor of cardiovascular diseases. Similarly to nephrotic syndrome (NS) predisposes to vein thrombosis.To evaluate serum and urinary total homocysteine (stHcy and utHcy) levels in children with the symptoms of SN, and to determine a correlation between its concentration and some parameters of hemostasis, as well as doses and the time of prednisone therapy and serum cortisol level.The examined group consisted of 18 children with NS, aged 7.64 +/- 5.1 years, divided on two groups: A--in time o proteinuria; B--during treatment with prednisone after regression of proteinuria. Control group (C) consisted of 20 children, aged 8.5 +/- 3.6 years. Serum and urinary tHcy levels were assayed by enzyme-linked immunosorbent assay method using the Axis-Shield set.Serum total Hcy concentration in groups A and B did not differ from the control group (p0.05). Urinary total Hcy concentration in groups A and B was significantly higher than that of control (p0.05). A positive correlation was observed between stHcy and serum albumin as well as cortisol levels, and between utHcy and serum AT III level.In children with steroid-dependent NS, subclinical disturbances in hemostasis were independent of serum tHcy concentration. There was no correlation between serum tHcy and cumulated doses, as well as time of prednisone treatment, however positive correlation was found with serum cortisone. Urinary excretion of Hcy significantly increases, in comparison to control, and correlates with serum AT III level.

The purpose of this cross-sectional study was to identify whether plasma symmetric dimethylarginine (pSDMA) is a useful marker of renal function in children.The study group consisted of 35 patients with chronic kidney disease (CKD) stages 1-5 (median age 11.5 years), classified on the basis of estimated glomerular filtration rate (eGFR) and divided into three groups: group A, patients with CKD stages 1 and 2; group B, CKD stage 3; and group C, CKD stages 4 and 5. A control group included 42 age-matched healthy children. Commercial enzyme-linked immunosorbent assay kits were used to measure pSDMA and serum cystatin C (sCysC) concentrations.The pSDMA and sCysC levels were significantly elevated in all CKD patients in comparison with healthy controls (p0.05). The pSDMA level in children was increased in the mild CKD (group A) (p0.01). There were also a significant difference in pSDMA concentration between groups A and B (p0.01). No differences in pSDMA levels were found between groups B and C. Receiver operating characteristics analyses showed that pSDMA was a better diagnostic tool than sCysC for identifying CKD stage among all the examined children and for detecting patients from group A (eGFR60 ml/min/1.73 m(2)).Increased pSDMA and sCysC levels were found in CKD children. Further studies are required to confirm potential applications of pSDMA and CysC as useful biomarkers for the diagnosis and progression of CKD.

Background: Although autistic spectrum disorders (ASD) are a strongly genetic condition certain metabolic disturbances may contribute to clinical features. Metabolism of oxalate in children with ASD has not yet been studied. Aim: The objective was to determine oxalate levels in plasma and urine in autistic children in relation to other urinary parameters. Method: In this cross-sectional study, plasma oxalate (using enzymatic method with oxalate oxidase) and spontaneous urinary calcium oxalate (CaOx) crystallization (based on the Bonn-Risk-Index, BRI) were determined in 36 children and adolescents with ASD (26 boys, 10 girls) aged 2e18 years and compared with 60 healthy non-autistic children matched by age, gender and anthropometric traits. Results: Children with ASD demonstrated 3-fold greater plasma oxalate levels [5.60 (5the95th percentile: 3.47e7.51)] compared with reference [(1.84 (5the95th percentile: 0.50e4.70) mmol/L ( p < 0.05)] and 2.5-fold greater urinary oxalate concentrations ( p < 0.05). No differences between the two groups were found in urinary pH, citraturia, calciuria or adjusted CaOx crystallization rates based on BRI. Despite significant hyperoxaluria no evidence of kidney stone disease or lithogenic risk was observed in these individuals. Conclusions: Hyperoxalemia and hyperoxaluria may be involved in the pathogenesis of ASD in children. Whether this is a result of impaired renal excretion or an extensive intestinal absorption, or both, or whether Ox may cross the blood brain barrier and disturb CNS function in the autistic children remains unclear. This appears to be the first report of plasma and urinary oxalate in childhood autism.

Vesicoureteral reflux (VUR) in children may lead to the renal fibrosis and scarring due to the overproduction and accumulation of extracellular matrix proteins (ECM) in interstitial tissue. Metalloproteinases produced in the kidneys are called biological markers of fibrosis. THE AIM OF THE STUDY was to assess if the presence of VUR in children disturb the balance between the serum and urinary concentrations of matrix metalloproteinases 2 and 9 and their tissue inhibitors 1 (TIMP-1) and 2 (TIMP-2) and predispose to excessive renal fibrosis. MATERIAL AND METHODS. The study was performed in 88 children, median aged 5.5 years (0.08-16 yrs) with VUR confirmed by voiding cystouretrography (VCUG). In 95% of estimated children the pyelonephritis indicated for VCUG performance. Control group consisted of 30 healthy children at similar age. Concentrations of MMP-2, MMP-9, TIMP-1 and TIMP-2 were estimated using immunoenzymatic ELISA method in urine of all examined children, additionally all the mentioned parameters in children with high (ll-V) grade of VUR were assessed in serum. RESULTS revealed that the urinary and serum concentrations of TIMP-1 and TIMP-2 were higher in healthy controls (p0.05). MMP-9 levels were higher only in the urine (p0.05) and MMP-2 in serum (p0.05). Increase in TIMP concentrations was connected with parallel increase in MMP levels in children with I-V grades of VUR, what was confirmed by the normal values of MMP-2/TIMP-2 and MMP-9/TIMP-1 ratios (p0.05). Only children with Ill-rd grade of VUR revealed reduced values of MMP/TIMP ratios (p0.05). Children's with Ill-V grade VUR revealed higher increase in serum concentrations of TIMP than in MMP, it was also seen in decrease in MMP/TIMP ratios (p0.05). No correlation was found between serum and urinary results of estimated parameters (p0.05).MMP-2 and MMP-9 and TIMP-1 and TIMP-2 play role in pathogenesis of VUR disturbances, what was confirmed by the change in their serum and urinary concentrations. In serum and urine of children with high (Ill-V) grade VUR the biggest disturbances were observed in MMPs: TIMPs system with the TIMP levels higher than MMP values, what indirectly indicated ECM degradation disturbances and increase in renal fibrosis.

UNLABELLED Most metabolic bone diseases are characterized by a disturbance in bone resorption, therefore biochemical markers concerning this process are of special interest. Recent investigations in bone biology identified the RANKL/ RANK/OPG system, the set of cytokines or cytokine receptors belonging to the tumor necrosis factor (TNF) family that are required for control of bone modeling and remodeling. The imbalance between OPG and RANKL was found not only in pathology of bone, but also in the control of the immune and vascular systems. However, clinical application of new bone markers in children may be difficult due to lack of reference data in relation to age, sex and physiological development. AIM To investigate the relationship of serum concentrations of OPG, RANKL and OPG/RANKL ratio in relation to age, sex and parameters of physical development in healthy children and adolescents. CHILDREN AND METHODS The study was performed on a group of 70 healthy children and adolescents, divided into subgroups according to sex and age. OPG and sRANKL serum concentrations were determined using ELISA. RESULTS Serum OPG did not differ between boys and girls or younger and older children. There was no correlation between OPG level and height, weight and BMI percentiles. The level of sRANKL was 3 times higher in males than in females (p < 0.01) and almost 3 times higher in older than younger children (p < 0.01). There was a positive correlation between sRANKL concentration and body weight percentile (r = 0.268, p < 0.05). There was no correlation between serum OPG and sRANKL levels. CONCLUSION In healthy children and adolescents the serum level of OPG is not influenced by age, sex or parameters of physical development, in contrast to sRANKL and sRANKL/OPG ratio, which are dependent on these factors. Age and sex reference data should be established.

Frasier syndrome is an uncommon genetic disorder featuring progressive glomerulopathy, male pseudohermaphroditism and gonadal dysgenesis. It is caused by mutations in intron 9 of the WT1 gene. Because of its rarity there is limited literature available on the diagnosis and treatment of this syndrome. The aim of the study was to present the clinicopathological findings and molecular analysis of phenotypically female adolescent presenting with severe proteinuria and primary amenorrhea. The significance of early recognition of Frasier syndrome and its differentiation from Denys-Drash syndrome was discussed. WT1 mutation analysis should be routinely done in females with steroid-resistant nephritic syndrome.

The aim of work was to investigate whether serum and urinary neutrophil gelatinase-associated lipocalin(sNGAL and uNGAL, respectively) are potential biomarkers of early cyclosporine A (CsA) nephrotoxicity in steroid-dependent nephrotic children (SDNS). The study group (I) consisted of 19 children with SDNS aged 9.46+/-5.52 years treated with CsA. The children were examined four times: at proteinuria relapse, prior to CsA treatment,then after 3, 6, and 12 months of CsA treatment. The control group (II) consisted of 18 healthy children aged 3-15 years. A commercial enzyme-linked immunosorbent assay method was used to measure NGAL concentration.The sNGAL level in SDNS children prior to the administration of CsA was similar to that in the healthy controls (p>0.05), but it increased significantly during the course of treatment (p

In small children, pyelonephritis (PN) is an important cause of scarring in the renal and disturbed in the production and degradation of extracellulare matrix proteins (ECM). Aim of the study was to assess the urinary levels metalloproteinases 2 and 9 (MMP-2 and MMP-9) and their inhibitors 1 and 2 (TIMP-1 and TIMP-2) in children with pyelonephritis (PN).Study group (I) consisted of 42 children with PN, aged 1-15 years, examined twice: A--prior to treatment (1-3 days of fever), B--after antibacterial treatment (10-14 days). The control group (K) consisted of 30 healthy children. Enzyme-linked immunosorbent assay kits were used for measurements of total human MMP-2, MMP-9, TIMP-1 and TIMP-2 in first morning urine.In children with PN (I) prior to treatment (A), urinary concentration of all parameters were increased as compared to the control (K) (p0.05). After treatment (B), only the levels of TIMP-1 was still elevated (p = 0.02). In PN before (A) and after (B) treatment MMP-9/TIMP-1 ratio. However MMP-2/TIMP-2 ratio was normal.In children with PN the balance MMP-9/TIMP-1 is disturbed, with the predominance of TIMP-1 production over MMP-9. It may lead to renal fibrosis.

Pyelonephritis (PN) is frequent bacterial infections in young infants and very important because may cause parenchymal scarring. Early confirmation of bacterial infection and application the appropriate treatment before obtaining result of urine culture, reduce probability of parenchymal scarring.To evaluate the useful of inflammatory and renal injury markers: serum procalcitonin (PCT), tumor necrosis factor alpha (TNF-alpha) and injury renal marker alpha1--microglobulin (A1M) measurement, in comparison with C-reactive protein concentration and abnormal urinary tract, in neonates and young infants with pyelonephritis.Investigation was performed in two groups: I group--23 children with PN (1 to 24 weeks of age), and K group--30 healthy children aged from 1 to 24 weeks. Serum concentration of CRP was measured by immunonephelometric assay, PCT by immunoluminometric assay, TNF alpha by ELISA method, and urinary A1M by nephelometric assay.In control group (K) medians of all investigated markers were below minimum of detection. PN patients (I) had the highest PCT TNF-alpha, A1M and CRP concentration before treatment and normal results after antibiotic treatment. Using a cut-off: of 0.5 mg/dl for CRP, 0.5 ng/ml for PCT 15 pg/ml for TNF-alpha and 10 mg/g cr for A1M, sensitivity and specificity in children with pyelonephritis were: for CRP 100% and 62.5%, for PCT 81.8% and 87.2%, for TNF alpha 77.1% and 93.1% and A1M 70.4% and 56.1%, respectively. A positive correlation between serum PCT and CRP and TNF alpha was found. Very high concentration all markers were in patients with vesicoureteral reflux and 1 patient with hydronephrosis.In early diagnostics of PN (before obtaining results of urine culture) in youngest children, determination of concentration PCT and TNF alpha, has higher value than determination of CRP, taking into concentration high sensitivity and specificity for bacterial infection.

The reason for our search was various investigations about urinary tract dysfunctions in enuretic children.The aim of our study was estimation of lover urinary tract function in children with monosymptomatic primary nocturnal enuresis without positive reaction for a long non pharmacological therapy.54 children after 9-12 months behavioral therapy and short pharmacological treatment (desmopresin) was undergoing urodynamic investigation (uroflowmetry and cystometry).Urodynamic disorders was found in 44/54 of estimated children. In 34 of children it was overactive bladder, in 6 patients we found detrusor-sphincter discoordination. Five children had decreased bladder capacity. Next to non pharmacological treatment we used anticholinergic or Baclofen depending on the results of urodynamic tests. The response to the treatment (non bedwetting at all) we observed in 34 children (in 9 of them after 3 months of therapy, in 16 after 6 months of therapy and in 12 after 12 months of therapy). The rest of children had decreased number of wet night per month.The pharmacological treatment of urodynamic disorders helps to children with monosymptomatic primary nocturnal enuresis to lost this symptom.

Idiopathic hypercalciuria is the most important predisposing risk factor for calcium oxalate (CaOx) renal stone formation. We assessed the associations between spontaneous CaOx crystallization based on the Bonn Risk Index (BRI), urinary pH, calciuria, oxaluria, and citraturia in 140 Caucasian patients with hypercalciuria, aged 4-17 years, and compared the findings with those in 210 normocalciuric controls. Of the 140 hypercalciuric patients, 58 had renal stones, and 82 had recurrent erythrocyturia, renal colic, or urinary obstructive symptoms-but without stones. Urinary ionized calcium ([Ca(2+)]) levels were measured using a selective electrode, while the onset of crystallization was determined using a photometer and titration with 40 mmol/L ammonium oxalate (Ox(2-)). The calculation of the BRI was based on the [Ca(2+)]:Ox(2-) ratio. The BRI values were 12-fold higher in hypercalciuric children than in healthy controls, but no differences were found in the BRI between subjects with urinary stones and those with urolithiasis-like symptoms. An increased BRI suggested an association with hypercalciuria, lower urinary pH, hypocitraturia, and hypooxaluria. These data indicate that hypercalciuria is an important factor associated with increased urinary CaOx crystallization, although the causal pathways need further investigation. Determination of the BRI in children with hypercalciuria may improve the risk assessment of kidney stones.

A small number of reports evaluating early effects of vesicoureteral reflux conservative therapy in children, based on antibacterial prophylaxis combined with correction of the of lower urinary tract function inspired us to perform the study. THE AIM OF THE STUDY was to assess the effects of vesicoureteral reflux (VUR) management in children according to grade, sex and way of treatment.The study group consisted of 108 children, who were treated in 2000-2007 due to VUR. There were 162 refluxing ureters (grades I-V) diagnosed by voiding cystourethrography (VCU). In 82 children cystometry and (or) uroflowmetry were additionally performed, which revealed lower urinary tract disorders in 41 (60 refluxing ureters), mostly detrusor hyperactivity or detrusor-sphincter dyscoordination. All children had conservative treatment, A - in 67 (102 refluxing ureters) only antibacterial prophylaxis, B - in 41 of children (60 refluxing ureters) in combination with pharmacological treatment of urodynamic abnormalities.The check-up VCU was performed after 23+/-15 months on average. VUR was observed to subside in 44/162 (28%) of refluxing ureters, including 22/108 (22%) of those treated managed with method A and 22/60 (37%) with method B. Fifty three of refluxing ureters were qualified for further conservative therapy and 65/162 (40%) for surgery (especially endoscopic). Following 2-3 years medical and surgical treatment, 87/162 (54%) refluxing ureters resolved.In the diagnostics of VUR in children we should take into consideration the assessment of lower urinary tract function, as treatment of these abnormalities increases the effects of VUR conservative management. However it should be confirmed on a larger group of patients.

Oxalate homeostasis is a derivative of absorption and transportation in the digestive system and renal/intestinal excretion of oxalate. The objective of this cross-sectional study was to determine normative values of plasma oxalate in relation to age, gender, and body size. A group of 1,260 healthy Caucasian children and adolescents aged 3 months to 18 years [mean +/- standard deviation (SD) 10.5 +/- 4.3] was studied. Each 1-year group comprised 70 subjects. Oxalate levels were assessed in blood plasma samples obtained from fasted individuals using the precipitation-enzymatic method with oxalate oxidase. Median oxalate levels in healthy infants was 3.20 micromol/L (5th-95th percentiles: 1.56-5.58) and was higher compared with older children [2.50 micromol/L (5th-95th percentiles: 0.95-5.74); p0.01]. No differences were found in plasma oxalate levels between boys and girls. There were no associations between plasma oxalate levels and anthropometric traits. In the healthy population aged 1-18 years, plasma oxalate concentration is independent of age, gender, and body size. Infants demonstrate higher plasma oxalate levels compared with older children, which suggests possible immature mechanisms of renal excretion. This study appears to be the first extensive report providing normative data for plasma oxalate in children and adolescents.

The variation in time required to obtain cessation of proteinuria in children with nephrotic syndrome (NS) represents one aspect of the variations shown by these children in response to glucocorticoid (GC) treatment. Polymorphism of the GC receptor gene (NR3C1) has been postulated as one factor that would partially explain differences in both the clinical presentation and the reaction to treatment in GC-treated diseases. We genotyped 118 children diagnosed with NS who initially responded to oral GC treatment [steroid-responsive nephrotic syndrome (SRNS) group] and 136 healthy children for three intron B single nucleotide polymorphisms of NR3C1, namely Bcl I (C/G), rs33389 (C/T) and rs33388 (A/T). In the SRNS group, we performed a three-marker haplotype analysis of NR3C1 in relation to the response to prednisone, represented as time to proteinuria resolution (TPR) as categorical and ordinal variable. Results: The distribution of individual polymorphisms and three-marker haplotypes was similar in healthy children and SRNS patients (all p values >0.05). The GTA haplotype was associated with a higher GC sensitivity, as determined by TPR, and was found to be more prevalent in early (response ≤7 days) than late (response >7 days) prednisone responders (27.7 vs. 14.5%, hap-score = −2.22, p = 0.05 adjusted for biopsy results). These results are in agreement with those reported earlier on an association of intron B haplotypes with GC sensitivity. The distribution of GC polymorphisms among the residents of north-eastern Poland was also determined.

High-grade vesicoureteric reflux (VUR) promotes the development of renal nephropathy (RN) due to scar formation. This process involves transforming growth factor beta-1 (TGF beta(1)), which stimulates production of the extracellular matrix proteins, including laminin (LN). The aim of the study was to assess LN and TGF beta(1) concentration according to VUR grade. The study group (1) consisted of 54 patients aged 6.23 +/- 4.15 years with VUR, including: A, 19 with grade II; B, 19 with grade III; and C, 16 with grades IV or V reflux. The control group (2) contained 27 healthy patients aged 6.76 +/- 4.02 years. LN and total TGF beta(1) concentrations in serum and urine were determined by the immunoenzymatic (EIA) method. To assess total serum TGF beta(1) levels, we used a solid-phase enzyme-linked immunosorbent assay (ELISA). Both serum and urinary levels of LN and TGF beta(1) in VUR patients were higher compared with controls (p < 0.05). The highest urinary concentration of LN and TGF beta(1) was found in subgroup C. A positive correlation was noted between urinary TGF beta(1) and LN. Increased TGF-beta(1) and LN levels in urine of high-grade VUR children suggests a potential role in fibrogenesis. Further trials are needed to investigate the role of serum and urinary LN level in VUR children.

The aim of work was the assessment of the length and function of the single kidney and arterial blood in children with renal agenesis (AN) treated in our Department in 2000-2003 years.The examinations were carried out: in 38 children (M--23, F--15) aged 1-16 years (mean 7.6 +/- 5.3) with unilateral AN, in whom in the ultrasound examination the picture of the single kidney was normal. The control group consisted of 40 healthy children aged 6.5 +/- 5.4 years. Ambulatory blood pressure (ABPM) was performed using ambulatory blood pressure monitor: BR--102 monitor f. Schiller. The renal length was assessed using ultrasound examination with 3.5 MHz or 5 MHz probe. Creatinine clearance was estimated by Schwartz method. Serum levels of creatinine was assayed by Jaffe method and urine protein by biuret method.Mean renal length was 93.9 +/- 18.33 mm. The degree of compensatory hypertrophia was 12.1 +/- 1.7%. Creatinine clearance and 24-hour proteinuria were normal. Mean systolic (RRs) and diastolic (RRr) blood pressure in children with AN was higher but did not exceed 95th centile by height. Nocturnal fall of RRs i RRr in children with single kidney (7.27 +/- 0.3% for RRs and 8.78 +/- 0.3 for RRr) was lower than in control group. We found a strong positive correlation between RRs and renal length (r = 0.725; p0.01).Renal agenesis (AN) does not cause impairment of the function of single kidney in childhood but leads to disturbances in 24-hour rhythm of arterial blood with the decrease of physiological nocturnal fall.

The aim of study was the analysis of cyclosporine A (CyA) treatment efficacy in children with steroid-dependent nephrotic syndrome (NS).The examined group consisted of 21 children (F--8, M--16) at the mean age 12.1 +/- 4.6 years with the relapses NS in the course of minimal change nephrotic syndrome (MCSN) in 9 (43%) and focal segmental glomerulosclerosis (FSGS) in 12 (57%) cases. All children were administrated CyA (Sandimun Neoral f. Novartis Pharma AG), together with prednisone (Encorton f. Polfa Pabianice) (0.2 - 0.5 mg/kg b.w./24 h) and ACE inhibitor (Enap f. Krka). The concentration of cyclospornine A in serum was measured by monoclonal antibody fluorescence polarization immunoassay. Serum concentration of creatinine, uric acid, albumin, cholesterol and creatinine clearance (Schwartz method) and proteinuria was analysed: A - before treatment, B--in 3rd day, C--in 3rd month, D--in 6th month, E--in 12th month of CyA treatment and F--after 3-6 months after finishing treatment. Blood pressure was measured by ABPM in examination A, D, E, and F.During administration of CyA the urinary protein excretion decreased successively and in 12th month of treatment was 4.5 +/- 3.9 mg/kg bw/24 h. The serum creatinine concentration increased by 33.9%, and uric acid by 52.8% in comparison to the initial level. Mean systolic blood pressure (RRs) in ambulatory blood pressure monitoring (ABPM) during 24 hours was 120.5 +/- 9.2 mmHg before treatment and increased by about 6% after 12 months of treatment. Respectively diastolic blood pressure (RRr) was 66.7 +/- 4.3 mmHg and increased to 71.0 +/- 2.5 mmHg at the end of 12 h month. The nocturnal fall of RRs before treatment was 14.2 +/- 2.8%, and RRr 14.9 +/- 2.1%. During treatment nocturnal fall of both RRs and RRr decreased to 9.2 +/- 2.7% for RRs and 9.8 +/- 2.7% for RRr after 6 months of treatment. After 12 months of treatment and in remission the nocturnal fall of blood pressure was still below 10%.CyA is an effective drug in children with relapses of steroid-dependent in the course of MCSN and FSGS. Side effects after CyA treatment, under the control of its concentration in serum and parameters of renal function are occasional and transient. Cyclosporine A disturbs the 24 hours rhythm of arterial blood pressure.

The study objective was to assess serum and urine fibronectin (FN) levels in children with vesicoureteral reflux (VUR) depending on reflux grade and urine osmolality. The study group (1) consisted of 54 VUR children, median age 4.28 (range 0.6–15) years: subgroup A, 19 children with grade II; subgroup B, 19 with grade III; and subgroup C, 16 with grade IV or V VUR. The control group (2) included 27 healthy children. The immunoenzymatic method enzyme immunoassay (EIA) was used to determine serum soluble and urine FN levels, with an osmometer to measure urinary osmolality. The median urine FN in VUR children was 224.1 (15.4–3537) ng/mg creatinine (Cr), compared with the control group: 137.9 (20.3–670.6) ng/mg Cr (p

Stone formation precedes long period, when the crystals are accumulated in basement membranes of renal tubules and intestinal tissue. Accumulated, inside of renal tubules crystals and stones in urinary tract cause urinary tract obstruction, what may lead to impairment of renal function. The aim of work was the assessment of serum cystatin C (cys C) concentration in children with urolithiasis, confirmed by the presence of renal stones in renal pelvis in comparison to serum creatinine concentration and creatinine clearance (Cr cl).Examined group (B) consisted of 30 children aged (13.08 +/- 4.14 years) with urolithiasis, which was divided into 3 subgroups (I, II, Ill) in dependence on stones' diameter (0.35-1.6cm). Control group (C) consisted of 26 healthy children at the same age. Nephelometric method was used to determine serum cystatin C level, Jaffe method to assess serum creatinine and the Schwartz formula to estimate glomerular filtration rate.In control group (C) serum cys C did not exceed 0.95 mg/l. In group B serum cystatin C and serum creatinine concentration and Cr cl was similar to the results of control group (p0.05). However in 16% of children with urolithiasis, in whom the stones of 0.8-1.6cm diameter were found in both renal pelvis, the concentration of serum cys C exceed 1.2 mg/l, and the value differed significantly from the results of control group (p0.05). A weak positive correlation between cys C and creatinine concentration and also between cys C and Cr cl was found. The serum cys C concentration in children with single stones of 0.35-0.8 diameter was normal.Serum cystatin C increases with increased degrees of urolithiasis assessed by stone size and their number in kidney.

Aim: The aim of the study was to assess plasma and urine concentrations of vascular endothelial growth factor (VEGF) in nephrotic syndrome children (NS) depending on the total dose of glucocorticoids (GC) and the percentage of lymphocytes with glucocorticoid receptor expression (CD3/GCR). Methods: We examined 51 children (2–15 years), allocated to three groups: group I: 13 children with the first NS onset, group II: 13 children with NS relapse, group C: 25 healthy children. The NS patients were examined: (A) before treatment and (B) 4–5 weeks after prednisone administration at a dose of 60 mg/m2/24 h. Plasma and urinary VEGF levels were determined using the immunoenzymatic ELISA method. Flow cytometry was applied to assess CD3/GCR expression. Results: Higher plasma and urinary VEGF concentrations were noted in NS children before treatment (A), as compared to control subjects (C). Following prednisone therapy (B), VEGF level was reduced but it was still higher than in the control group. Positive correlation was observed between VEGF and protein in the urine (group I r = 0.660, P

The study was aimed at investigating the association between MDR-1 genetic polymorphisms [C1236T, G2677T(A), C3435T] and parameters describing the clinical course and treatment response of childhood steroid-responsive nephrotic syndrome (SRNS). Three MDR-1 genetic markers were analyzed in 108 children diagnosed with SRNS and in 135 healthy controls with neither allergic nor renal disease. All subjects were genotyped by PCR-restriction fragment length polymorphism (RFLP) analysis, and an EM algorithm-based analysis was utilized to estimate haplotype frequencies. As expected, there was no difference in genotypic and allelic distribution between and among SRNS patients and healthy children. However, all individual polymorphisms were strongly associated with time to response to initial prednisone therapy. The frequencies of the mutated alleles were higher in late responders (time to remission: >7 days) to oral prednisone (0.53, 0.52,0.66) than in early responders (time to remission

The aim of this work was to determine the expression of P-glycoprotein (P-gp) on peripheral lymphocytes (CD3) in children with steroid-dependent nephrotic syndrome (SDNS) during cyclosporine A (CyA) and ACE-inhibitor (ACE-I) treatment. The study group (I) consisted of 20 children with SDNS aged 5–18 years, with a subsequent proteinuria relapse at the time of prednisone dose reduction. All nephrotic syndrome (NS) children were examined three times: A—at proteinuria relapse, before CyA treatment; B—after 3 months; C—after 12 months of CyA administration. The control group (II) consisted of 20 healthy children. CD3/P-gp was measured using a flow cytometry assay. The serum CyA level was assessed by means of the immunofluorescence method. The expression of CD3/P-gp in NS relapse, prior to CyA+ACE-I administration, was much higher (median 9.15%, range 1.50–13.50%) when compared to healthy controls (median 1.20%, range 0.30–5.70%). The absolute number of CD3/P-gp in this examination was almost five times higher when compared to healthy controls (p

The aim of work was the assessment of plasma anion oxalate (Ox) concentration in children during antibacterial treatment depending on way and time of antibiotic administration.The examinations were carried out in 80 children, without nephrolithiasis, aged 10.1 +/- 4.3 years with bronchopneumonia, treated with beta-lactame antibiotics. The children were divided in two groups: I--children treated with oral amoxicillin + clavulanic acid or cefuroxime axetil (n=40), II--children treated with the same antibiotics intravenously (n=40). The Ox concentration in plasma and urine was measured using an enzymatic method with oxalate oxidase, four times. (0)--before treatment, (a)--in third day and (b)--in last day of administration (10 to 14 day), (c)--3 weeks after finishing treatment with antibiotics.The result showed that in children before treatment (0) mean plasma Ox concentration was 2.439 +/- 0.645 micromol/l. In 3rd day (a) the Ox concentration increased to 7.848 +/- 0.999 micromol/l (p0.01), in last day of treatment (b) decreased to 5.681 +/- 0.871 micromol/l, and after 3 weeks (c) came back to initial values (p0.05). Intravenous antibiotics administration did not influence plasma Ox concentration.Plasma oxalate concentration increases during oral administration of beta-lactame antibiotics caused by increased intestinal absorption, as a result of saprophytic microflora deterioration. However intravewous administration of the same antibiotics does not change the concentration of plasma oxalate.

Background. It is estimated that 20–50% of adult patients start chronic dialysis therapy without prior contact with a nephrologist. The aim of this nationwide study was to assess clinical and metabolic status of children at the start of chronic dialysis in Poland with regard to the timing of the referral to a nephrologist. Methods. We studied data of 180 children (mean age 14±6 years) undergoing chronic dialysis in 13 (out of 14) dialysis pediatric centres in Poland. Patients were classified as early referrals (ERs) when they entered the dialysis programme at least 1 month after the first referral to a nephrologist or late referrals (LRs) when the dialysis was introduced within 1 month from the first visit. Results. Seventy-nine percent of pediatric patients were referred early (ER) to the dialysis centre and 21% were referred late (LR) and had to start dialysis within a month. When starting dialysis, LR patients had significantly higher levels of urea and phosphate as well as lower calcium and haemoglobin in comparison with ERs. Hypertension, pulmonary oedema, fluid overload, treatment in the intensive care unit (ICU) and body mass index (BMI) below 10th percentile turned out to be more frequent in the LR group. Peritoneal dialysis (PD) was used as the first method of dialysis in 59% of ERs and 46% of LRs. The majority of ER patients was treated in the predialysis period with calcitriol, phosphate binders and low protein diet (84%, 89%, 92% of all children, respectively), and 20% of them received epoetin. In the up to 3 years observation of our initial cohort, we also found that the patients who were referred late were less likely to receive kidney transplant (P ¼ 0.02). Conclusion. The results of the study indicate that the LR to a pediatric nephrologist was associated with poorer clinical and metabolic status of children entering chronic dialysis programmes.

Background. The aim of this nationwide analysis was to assess the incidence and current treatment profile of arterial hypertension in children undergoing chronic haemodialysis or peritoneal dialysis and attitudes of paediatric nephrologists towards the choice of antihypertensive drugs in their patients. Methods. The study group consisted of 134 children (89 males, 45 females, mean age 10.7 ± 5 years) from all 13 paediatric dialysis centres in Poland. The data were gathered through a questionnaire for each patient dialysed in November 2004. Results. The overall incidence of hypertension in the study group was 55% (74 of 134 patients; 47 males, 27 females). The incidence rate was similar in boys and girls (53 vs 60%) and in those on haemodialysis and peritoneal dialysis (56 vs 54%). Chronic glomerulonephritis as an underlying renal disease was significantly more frequent in the hypertensive than in the normotensive subjects (37 vs 10%, P= 0.004). Residual urine output was higher in normotensives (41 vs 10 ml/kg body weight; P < 0.001). Among those treated with antihypertensives: 32% were treated by monotherapy, 36% received two drugs, 22% received three drugs, while 7% received ≥4 drugs. The therapy was effective in only 57% of subjects. We observed no differences in biochemical and clinical parameters between those who responded to the therapy and those who failed to do so. Calcium channel blockers constituted the most frequently administered class of drugs [73% of children; in 43 out of 48 (90%) combined with other drugs, but in 11 out of 24 (46%) as a monotherapy]. In monotherapy, angiotensin-converting enzyme inhibitors and calcium channel blockers were administered most frequently. Conclusion. We conclude that the incidence of hypertension in dialysis children in Poland is high (55%). The effectiveness of antihypertensive treatment is rather low (58%) and the choice of drugs is limited.

The aim of the study was to assess serum cystatin C level in children with a congenital solitary kidney, depending on their age and compensatory overgrowth of the kidney. The study group (I) consisted of 36 children, 3-21 years of age (median 10.8 years), with a congenital solitary kidney and no other urinary defects. The control group (C) contained 36 healthy children, 5-21 years old (median 10.9 years). Nephelometric methods were used to determine serum cystatin C level, the Jaffe method to assess creatinine concentration and the Schwartz formula to estimate glomerular filtration rate. Kidney length was measured with the patient in a supine position, and overgrowth was estimated (O%) in comparison with the respective kidney in the control group. Serum cystatin C level in group I was higher than that in the control group (P0.05). Increased values, above 0.95 mg/l, were found in 16/36 (44%) children aged 12-21 years. Glomerular filtration rate (GFR, estimated by the Schwartz formula) and creatinine level in group I were similar to those of the control group (P0.05). Increased kidney length was found (median 18.2%). Cystatin C concentration was positively correlated with O% (r=0.406, P0.01) and kidney length to child height ratio (L/H) (r=0.376, P0.05). We conclude that Increased serum cystatin C concentration in patients with a unilateral congenital solitary kidney occurs after 12 years of age and correlates with compensatory overgrowth of the kidney.

Enhanced platelet reactivity may play a significant role in the hypercoagulable state of nephrotic syndrome (NS). Thrombocytosis with platelet aggregation cause the release of some cytokines, among them interleukin-7 (IL-7). The aim of the study was to evaluate serum IL-7 levels in children with the symptoms of NS and to determine a correlation between its concentration and platelet count, other hemostatic factors, and NS intensity.The study was performed in two groups. I--the examined group of 26 children with NS (12 boys, 14 girls) aged 6.8 +/- 2.1 years, subjected to two examinations: A--before treatment, B--during treatment with prednisone (60 mg/kg 24 h after albuminuria regression); and II--the control group (C) of 20 healthy children. Serum IL-7 level was assayed by enzyme-linked immunosorbent assay method using a RD Quantikine set.In group I, IL-7 level in examination A (33.33 +/- 33.24 pg/mL) was higher than in the control subjects (P0.01). In examination B, IL-7 concentration was reduced to the level of 10.86 +/- 5.22 pg/mL and did not differ from the controls (P0.05). A positive correlation was observed between IL-7 and platelet count and serum fibrinogen level. A negative correlation was noted with antithrombin III concentration. No correlation was found with serum levels of albumin and cholesterol or urine protein.In children with NS, serum IL-7 level increases proportionally to the elevated platelet count and other hemostatic components, but shows no correlation with serum albumin or urine protein.

To assess functional day-time bladder capacity (DBC) and urine osmolality in children with primary monosymptomatic nocturnal enuresis (PMNE) according to age and sex.A total of 263 children with PMNE were divided into two groups: Group I, 160 children (63 girls, 97 boys) aged 5-9 years (mean age 7.14+/-1.47 years); and Group II, 103 children (25 girls, 78 boys) aged 10-15 years (mean age 12.26+/-1.52 years). DBC (milliliters) was the largest void of the day measured over four 24-h periods, irrespective of the diet applied. Urine osmolality was determined three times: in the evening before bed-time; at night, 2-4 h after falling asleep; and in the morning in the nocturnal void.DBC was smaller in Group I than in Group II (151.27 vs 199.46 ml; p0.05). No statistically significant differences were found in relation to sex (p0.05). The mean osmolality of the nocturnal void in the morning was 854.15 and 909.22 mOsmol/kg H(2)O in Groups I and II, respectively (p0.05). Differences between boys and girls were not statistically significant (p0.05). No correlation was found between DBC and urine osmolality (p0.05). A detailed analysis of the results revealed DBC below the 5th percentile or above the 95th percentile in 23/263 cases (8.7%), reduced osmolality (800 mOsmol/kg H(2)O) in 76/263 (28.8%), a familial nature of nocturnal enuresis in 124/263 (47.1%) and difficulty waking in 86/263 (32.7%).In children with PMNE aged 5-15 years, functional DBC increases with age and does not differ between the sexes; the mean nocturnal urine osmolality is neither age- nor sex-dependent.

The aim of the work was to prepare the percentile curves for blood pressure measured by 24-hour ambulatory blood pressure monitoring (ABPM) in children by height.ABPM was performed in 852 healthy children aged 7-17 years (433 girls, 419 boys). Systolic (SBP) and diastolic (DBP) blood pressure was measured for 24 h, including the period of activity and rest, using BR-102 Schiller Poland LTD monitor and Quiet Tycos ABPM, USA. The mean number of readings over the 24-hour period was 58.4+/-4.The mean SBP in the group of girls with height 120-172 cm increased from 102.2+/-5.5 to 121.0+-7.8 mmHg, and in the group of boys with height 120-180 cm and over from 103.7+/-5.7 to 123.7+/-6.2 mmHg. A strong positive correlation between the height and SBP and weak with DBP was noted. The percentile charts for blood pressure in children aged 7-17 by height were prepared.The mean systolic blood pressure decreased at night more than diastolic blood pressure, independently of height. Systolic blood pressure was stronger correlated with the height than with the age.

Objective: To evaluate the expression of glucocorticoid receptors (GCR) in lymphocytes (CD3/ GCR) and monocytes (CD14/GCR) in children with nephrotic syndrome (NS). Patients: The patients were divided into two groups: group I: 17 children with the first NS attack, and group II: 17 children with a subsequent NS event. In both groups, examinations were carried out before treatment (A) and after albuminuria disappearance during prednisone treatment (B). The control group (C) consisted of 23 healthy children, never treated with glucocorticosteroids. Methods: Flow cytometry was employed twice to determine the number of CD3+ lymphocytes and CD14+ monocytes and the percentage of CD3/GCR+ and CD14/GCR+ cells. Results: In group I, the expression of CD3/GCR before treatment (A) decreased during prednisone therapy (B) (p

Literature data point to the relationship between leptin concentration and certain markers of the metabolic syndrome, including cholesterol, triglycerides and apolipoproteins. A substantial lipid metabolism disturbance occurs in children with idiopathic nephrotic syndrome (NS). The aim of the study was to find out whether in NS children, serum and urine leptin levels change proportionally to lipid metabolism disturbances. The study was performed on two groups: (I) 30 children with NS (A) before, (B) during, prednisone therapy after proteinuria regression; (II) 25 healthy children. Serum and urine leptin levels were determined by the immunoenzymatic ELISA method. Serum leptin level in NS children before and after treatment was similar to that in the control group (p>0.05). Leptin urinary excretion in group A was approximately 60 times and in group B 24 times higher than in the controls (p

We assessed the excretion of fructose-1,6-bisphosphatase (FBP) and N-acetyl-beta-D-glucosaminidase (NAG) in 52 children (aged 4.1 +/- 2.3): group I--26 children with acute pyelonephritis (APN), in whom the examination were carried out twice: A--before treatment, B--after 14-21 days of antibacterial treatment, group II--21 healthy children. Activity of FBP in urine was found in 80% children from group I and II, and activity of NAG was found in all children from both groups. In examination A mean excretion of FBP and NAG was higher than in healthy children (p0.05). After antibacterial treatment excretion of both enzymes decreased to values, which did not differ from control group (p0.05). High correlation between FBP and NAG (r = 0.9355; p = 0.00001) was shown only in 14 children, in whom the course of acute pyelonephritis was serious (CRP20 mg%, leucocytosis10 x 10(9), and renal swelling in ultrasonography).Increased excretion of FBP in urine is found mainly in children with severe course of acute pyelonephritis, in whom the correlation between NAG and FBP is observed.

The concentration of transforming growth factor-beta 1 (TGF-beta 1) in serum was performed by immunoenzymatic method in serum of children with nephrotic syndrome in following groups: group I--9 children (5-15 years) with focal segmental glomerulosclerosis (FSG), before Cyclosporine A treatment (CyA) (examination A) and after 3-6 months of Cyclosporine A treatment during remission (examination B), group II--13 children (5-14 years) with minimal change nephrotic syndrome (MCNS) during relapse (examination A) and after 7-20 days of prednisone (Encorton) treatment in dose 60 mg/m2, without the proteinuria (examination B), group III--15 healthy children (5-15 years). The aim of the work was to demonstrate any differences in concentration of TGF-beta 1 in serum of examined children and to show the influence of prednisone and Cyclosporine A on the concentration of TGF-beta 1. The results showed that before treatment increased concentration of TGF-beta 1 was shown only in children with MCSN (p0.05) and it was reverse proportional to albuminemia. However in children without proteinuria (B), the concentration of cytokines decreased in children with MCSN and increased in children with FSG treated with Cyclosporine A.The concentration of TGF-beta 1 in serum increases in children with nephrotic syndrome during gross proteinuria and hypoalbuminemia and after Cyclosporine A treatment.

Coulter flow cytometry was used to determine glucocorticoid receptors (GCR) in the peripheral blood cells of patients with nephrotic syndrome. The expression of GCR in the lymphocytes (CD3/GCR) and monocytes (CD14/GCR) of peripheral blood of 23 (age 4.9+/-2.7 years) children with steroid-sensitive nephrotic syndrome was assessed before treatment (proteinuria50 mg/kg per 24 h), after 4-6 weeks of prednisone treatment, without proteinuria, and in remission, without proteinuria and without any treatment. Before treatment the expression of CD3/GCR was 61.8+/-18.3% and CD14/GCR 43.6.8+/-20.3%; this did not differ from the results of the normal control group ( P0.05). However, after treatment GCR expression in lymphocytes was 50% ( P0.001) and in monocytes about 20% lower ( P0.05). In remission, the GCR expression increased and did not differ from the results before treatment ( P0.05). A positive correlation between the serum cortisol concentration and the expression of CD3/GCR was found ( r=0.504, P=0.02). In summary, we report that in children with steroid-sensitive nephrotic syndrome, prednisone treatment causes the temporary decrease of the expression of GCR in lymphocytes. A positive correlation between GCR expression and serum cortisol was found. A decrease in GCR expression in monocytes did not correlate with cortisol concentration.