Depressive disorders in children with chronic kidney disease treated conservatively.

BACKGROUND: Children with chronic kidney disease (CKD) experience a lot of mental and emotional stress, which can lead to the development of depressive disorders. The prevalence of depressive disorders in CKD children is estimated to be between 7% and 35%. OBJECTIVES: The aim of our study was to analyze the prevalence and characteristics of depression and depressive symptoms in children and adolescents with CKD treated conservatively. MATERIAL AND METHODS: The cross-sectional, multicenter study was conducted in 73 CKD children aged 8-18 and in 92 of their parents. To assess the mental wellbeing of CKD children, Kovacs's Children's Depression Inventory 2 (CDI2) was used as CDI2: Self-Report and CDI2: Parent Form. RESULTS: The majority of CKD children acquired medium scores in CDI2, 11% of participants reported symptoms suggesting depressive disorder, and among them 8.2% met the criteria for depression. A significant relationship was found between age and interpersonal problems, age at CKD diagnosis, and total score and ineffectiveness, CKD duration and total score/emotional problems. Depressive symptoms were associated with the stage of CKD, and they differed significantly between stages III and IV. We noticed the child-parent disagreement on reported depressive symptoms. Parents perceive their children's mental state as worse than the children themselves. CONCLUSIONS: There is a problem of depression in children with CKD treated conservatively. Variables associated with depressive symptoms in CKD children treated conservatively require further study. Key factors predisposing to the development of depression seem to be age at the time of diagnosis, disease duration, and progression of CKD from stage III to IV. Disparities between depressive symptoms self-reported by CKD children and their parents' assessment require further analysis. However, these disparaties indicate that the final diagnosis of the occurrence of depressive disorders should be based on a multidimensional assessment of the patient's situation.

[Urinary concentration of proinflammatory cytokines with regard to infected urinary tract region]. / Stezenie cytokin prozapalnych w moczu w zaleznosci od umiejscowienia zakazenia w drogach moczowych.

UNLABELLED: Uropathogenic bacteria stimulate epithelial cells of interstitial tissue and macrophages to secrete proinflammatory cytokines: interleukin I (IL-1beta), interleukin 6 (IL-6) and interleukin 8 (IL-8). The aim of the study was to check: 1) if the concentration of proinflammatory cytokines (IL-1beta, IL-6, IL-8) differs in dependence on region and clinical picture of urinary tract infection, 2) what is the influence of antibacterial treatment on their concentration. MATERIAL: We examined 67 children, aged 1-15 years, who were divided into 3 groups: 27 children with acute pyelonephritis (AP), caused by E. coli (group I), in whom the examination was carried out twice: A - before treatment, B - after 14 days of antibacterial treatment, 10 children with chronic urinary tract infection (UTI) associated with neurogenic bladder (group II) and 30 healthy children (group K). METHOD: Urinary concentration of examined cytokines was assessed using ELISA immunoenzymatic method and was expressed in pg/mg creatinine. Results showed that in group I before treatment the urinary concentration of examined cytokines was increased (p<0.05). After antibacterial treatment concentration of IL-1beta was normal and concentration of IL-6 and IL-8 decreased but was still higher than in control group (p<0.05). In group II before treatment the increase in concentration of IL-1beta and IL-8 was not so high (p<0.05) and the urinary concentration of IL-6 was normal (p>0.05). In examination A in children from group I and II a positive correlation between examined cytokines and C reactive protein was shown. We have also found a positive correlation between urinary concentration of IL-1beta a IL-8. CONCLUSIONS: 1. Urinary concentration of examined proinflammatory cytokines is different in children with AP and UTI associated with neurogenic bladder and correlates with concentration of C-reactive protein. 2. In most of children with AP after 14-days of antibacterial treatment the urinary concentration of proinflammatory cytokines has been increased.

[Assessment of oxalate concentration in serum and urine of children with renal stones]. / Ocena stezenia szczawianów w osoczu i moczu dzieci z kamica moczowa.

UNLABELLED: Oxalate crystals are the main component of renal stones and oxalate urolithiasis is the most common type both in adults and children. The aim of the work was the assessment of oxalate concentration in plasma and urine of children with renal stones. MATERIAL: The examined group (I) consisted of 29 children (12.0 +/- 3.87 years) with confirmed stones in caliceal-pelvic system. The control group (C) was composed of 30 healthy children. METHODS: The oxalate concentration in plasma and urine was measured using an enzymatic method after 3-4 days of hypooxalate diet. Children with congenital abnormalities of urinary tract were excluded. We found 1-5 stones, 0.35-1.5 in diameter. RESULTS: In I group mean plasma oxalate concentration (4.89 +/- 1.58 micromol/l) was higher than in control group (p<0,05). However urinary oxalate concentration exceeded 95 percentile of those obtained in healthy group only in 16 (55%) children, mainly with II and III degree of urolithiasis. In children with urolithiasis we also found hypercalciuria with normal serum calcium concentration. No correlation between plasma and urinary oxalate concentration was found. CONCLUSIONS: 1. Plasma oxalate concentration in children with renal stones is higher than in healthy children. 2. Hyperoxaluria was found in 16 (55%) children with first attack of nephrolithiasis.

Urinary levels of matrix metalloproteinases and their tissue inhibitors in nephrotic children.

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.

Expression of P-glycoprotein in lymphocytes of children with nephrotic syndrome treated with glucocorticoids.

INTRODUCTION: 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<0.01). During glucocorticoid treatment, CD3/P-gp increased significantly and was much higher than in the control group (p<0.01) and in the NS children before treatment (p<0.01). In remission, the P-gp expression decreased, but did not achieve the values of the controls (p<0.05). Fourteen out of eighteen (14/18) children still showed P-gp values above the cut-off level. We also found a positive correlation between the P-gp expression and total prednisone dose in the NS children in all examinations: A: (r=0.540, p<0.05); B: (r=0.630, p<0.01); C: (r=0.653, p<0.01). CONCLUSION: In conclusion, the overexpression of P-gp in remission, after finishing glucocorticoid treatment, may indicate that P-gp plays a role in the response to corticosteroids in nephrotic children.

Platelet-derived growth factor and platelet profiles in childhood nephrotic syndrome.

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 (P<0.01) and platelet distribution width (P<0.05) were elevated, the mean platelet volume (MPV) (P<0.05) was decreased and the plateletcrit (P>0.05) 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.

Transforming growth factor-beta1 in nephrotic syndrome treated with cyclosporine and ACE inhibitors.

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<0.01). These results indicate that the urinary TGF-beta1 level increases in proportion to proteinuria during relapse of NS. Treatment with CyA and ACEI also influences urinary TGF-beta1, which is still higher after 12 months of treatment than in healthy children.