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From June 1985 to December 1998, 173 pediatric renal transplants were carried out in 170 patients at our center. From this pool, 73 patients (34 males and 39 females) with a follow‐up of 48 months were examined. In all patients, ureteroneocystostomy was performed according to the Lich‐Grégoire procedure. All patients were treated with cyclosporin A (CsA)‐based immunosuppression, including prednisone and sometimes azathioprine (AZA). Six months after transplantation, voiding cystography (VCU) was performed in all patients and reflux was classified from Grade I to Grade IV. The patients were divided into two groups: those with reflux (Group A: 25 patients) and those without (Group B: 48 patients). Grade I reflux was found in four patients, Grade II in seven patients, Grade III in seven patients, and Grade IV in seven patients. All the patients with severe reflux (Grade IV) underwent a corrective surgical procedure. Both groups were examined for immunologic and non‐immunologic risk factors and no significant differences were found. Analysis of patient and graft survival rates revealed no statistical differences (NS) between Groups A and B. Mean serum creatinine (mg/dL) was 1.06 ± 0.28 and 1.12 ± 0.41 at 4 yr in Groups A and B, respectively (NS). Mean calculated creatinine clearance (cCrC; ml/min) was 76.74 ± 15.92 and 77.96 ± 15.66 in Groups A and B, respectively (NS). The analysis was further extended by considering the grade of reflux (I to IV). Again, no significant differences in the above parameters emerged between the reflux sub‐groups; only in the Grade IV sub‐group was a slight decrease in cCrC detected, although this difference was not statistically significant when compared with the other sub‐groups. In conclusion, vesico‐ureteral reflux (VUR) does not seem to negatively affect graft function. However, as all severe reflux patients (Grade IV) were surgically corrected, no... [ABSTRACT FROM AUTHOR]

Background.The nephronophthisis-medullary cystic disease (NPH/MCD) complex represents a heterogeneous group of hereditary tubulointerstitial nephritis. The most common variant is juvenile recessive NPH, for which a gene locus (NPH1) has been mapped on chromosome 2q13. MCD is a less common dominant condition usually recognized later in life, which resembles NPH in many aspects, still presenting remarkable clinical differences. Nothing is known about the chromosome locus of MCD. [ABSTRACT FROM PUBLISHER]

Peritoneal fibrosis in patients on peritoneal dialysis is the result of interstitial collagen accumulation within the peritoneal membrane and in mural spaces. Hypothetically, collagen expression by target cells may be regulated by specific endoperitoneal factors, though the existence of such factors has not yet been demonstrated.We evaluated the effects of cell-free peritoneal effluents obtained from six children undergoing peritoneal dialysis on several mesothelial cell functions in vitro. Human peritoneal mesothelial cells (MC) were obtained from the omental tissue of six uraemic children who were undergoing surgery for insertion of a peritoneal catheter. Cells at confluence were utilized to determine cytotoxicity (LDH release), viability (trypan blue), proliferation (3H-thymidine incorporation), collagen expression (3H-proline incorporation, SDS-Page) and mRNA (dot-blot). A preliminary series of experiments, was undertaken to define which of the successive fluid collections during a dialytic procedure induces the greatest changes; this revealed maximal effects of the effluent from the long stasis period. Exposure to peritoneal effluents obtained from four patients with acute peritonitis induced marked changes in cell morphology, stimulated by (3H)-thymi-dine incorporation into DNA by 300% and upregulated the expression and transcription of type III collagen (6-fold increment in COL3Al mRNA). Qualitatively but not quantitatively comparable changes in cell proliferation (+100%) and collagen expression were induced by peritoneal effluents from patients without peritonitis. In an effort to reproduce the effect of peritoneal effluents in vitro, we exposed mesothelial cells to various cytokines putatively present in infected peritoneal effluents, namely IL-2, TGFβ and TNFα; in no case did we find stimulation of cell proliferation. Finally TGFβ but not TNFα or IL2 upregulated collagen synthesis by these cells.These findings demonstrate a direct influence of cell-free peritoneal effluents on mesothelial cell functions, including stimulation of interstitial collagen expression.All these changes were more evident upon exposure to effluents collected during acute peritonitis, which suggests a link between recurrent peritoneal infection and collagen deposition, the most typical precursor of peritoneal fibrosis. [ABSTRACT FROM PUBLISHER]

Nutritional status, assessed by anthropometric and biochemical methods, protein and amino-acid (AA) composition and muscle water were evaluated in 11 kidney transplanted children and in a control group of 10 children with normal renal function who were undergoing elective surgery. Samples of the rectus abdominis muscle were taken when surgery was performed in the control children and when the peritoneal catheter was removed in the transplanted children. The mean time from the transplantation to the study time was 97 ± 14 days (range 72–114 days). Height was reduced in the transplanted children compared to the controls but skinfold thickness, arm muscle circumference and serum proteins (total protein, albumin, transferrin, pseudocholinesterase) were normal. The body mass index was over the 50° percent ile in nine of the eleven children. The muscle contents of total, extracellular, and intracellular water, alkali-soluble protein (ASP), DNA and the ASP/DNA ratio were not significantly different in transplanted children from those in the controls. Plasma leucine and taunine levels were significantly decreased, whereas plasma citrulline and alanine levels and the glycine/serine ratio were increased. Muscle threonine, alanine+taurine, glycine and aspartic acid levels as well as the glycine/senine ratio were increased in the transplanted children. Transplanted children show an almost normal muscle AA profile and a plasma AA pattern that seems to be related to the prednisone therapy. [ABSTRACT FROM PUBLISHER]

Mesothelial cells (MC) from human peritoneal omentum fragments obtained during surgical insertion of peritotical catheters for continuous peritoneal dialysis in end stage renal failure (ESRF) patients were cultured in vitro. MC exhibited a phenotype different from macrophages, but MHC class II molecules were well expressed. Therefore MC lines were tested for antigen presenting capacity by pulsing with soluble antigens (tetanus toxoid and purified protein derivative (PPD)) or with a corpusculate antigen (Candida albicans bodies). Autologous peripheral blood mononuclear cells (PBMC) depleted of adherent monocytes and cloned T cells generated from an individual matched for the MHC class II antigen DR2 were used to test antigen-presenting function. MC effectively presented the soluble and corpusculate antigens to autologous and MHC-compatible allogeneic lymphocytes, indicating that they are endowed with both endocytic/phagocytic activity and with processing/presenting capacity. Preincubation of MC with human recombinant interferon-gamma (IFN-γ) up-regulated MHC class II and intercellular adhesion molecuIe-1 (lCAM-1) expression, but the effect on antigen-presenting function was not consistent. Since MC are an important component of the peritoneal environment, they may participate, along with macrophages. in activation of specific T cells and in the generation of local cell-mediated immunity to various pathogens. [ABSTRACT FROM AUTHOR]

Alfa-1-antitrypsin (alpha 1AT) was purified by pseudoligand chromatography and preparative electrophoresis from the serum of a patient with alpha 1AT deficiency. The combination of the two techniques yielded a high grade batch of alpha 1AT monomer and this was successfully used to purify the protein from the serum of PiMIM1, PiMIM2, and PiZZ phenotype subjects. This procedure should facilitate structural studies of alpha 1AT variants susceptible to intracellular accumulation. [ABSTRACT FROM PUBLISHER]

Presents abstracts on two studies involving kidney diseases. Use of apolipoproteins to prevent glomelular albumin permeability alterations induced by serum from patients with chronic renal failure caused by focal segmental glumerulosclerosis; Description of the function of the most commen congenital nephrotic syndrome gene mutations.

Apolipoprotein A1 (apoA1) is a component of the high density lipoproteins (HDL) that regulates the transport of cholesterol between the liver and peripheral cells and modulates the removal of any excess of cholesterol from membranes. Any variation in apoA1 composition may modify the plasma lipid profile and be involved in atherogenesis. We investigated apoA1 composition in plasma of 6 children with nephrotic syndrome, a condition characterized by high levels of cholesterol in plasma and by a high risk to develop atherosclerosis. Non-denaturing two-dimensional electrophoresis (Nat/SDS-PAGE), mass spectrometry, western blot and pull down experiments were done to characterize proteins and define putative interactions. ApoA1 was resolved in 12 variants, 6 of which had a slightly lower molecular weight (18-19 KDa) and migrated on the same axes of the β chain of haptoglobin (Hp). Low molecular weight apoA1 were observed in carriers of different Hp haplotypes (including one homozygous for the rare ββα1α1) ruling out any contaminant effect of co-migration of apoA1 with Hp α2 chain. Overall, apoA1 isoforms were much more present in plasma of nephrotic patients compared to a normal profile. These findings show that apoA1 plasma in nephrotic syndrome is heterogeneous in terms of molecular weight. Low molecular weight fragments lack internal structural domains and likely form macro-aggregates with Hp. Fragmentation and transport of apoA1 may be involved in the general disorder of lipid metabolism that characterizes nephrotic syndrome.

Unlabelled: Acute stress responses of women are typically more reactive than that of men. Women, compared to men, may be more vulnerable to posttraumatic stress disorder (PTSD). Whether there are differences between women and men with PTSD in levels of the stress hormone, cortisol, was investigated in a pilot study., Methods: women (n=6) and men (n=3) motor vehicle accident (MVA) survivors, with PTSD, had saliva collected at 1400 h, 1800 h, and 2200 h. Cortisol levels in saliva were measured by radioimmunoassay. An interaction between gender and time of sample collection was observed due to women's cortisol levels being lower and decreasing over time, whereas men's levels were higher and increased across time of day of collection. Results of this pilot study suggest a difference in the pattern of disruption of glucocorticoid secretion among women and men with PTSD. Women had greater suppression of their basal cortisol levels than did men; however, the diurnal pattern for cortisol levels to decline throughout the day was observed among the women but not the men., (2009 Elsevier Inc. All rights reserved.)

In humans, an increased synthesis of reactive oxygen species (ROS) may be a relevant cause of amplification of physiologic processes resulting in inflammatory organ damage or neoplasia. Efficient anti-oxidative systems targeting oxidative stress are thus essential to prevent tissue damage. In plasma, proteins proved to be the first line of defence against ROS and albumin, the highest concentration plasma protein, has a key role in this antioxidant function. Recent studies have clearly documented that albumin oxido-redox potential changes upon oxidation by different oxidants thus becoming a deputy biomarker of this process. ROS react primarily with the free (34)Cysteine ((34)Cys) residue of albumin to form two reversible intermediate derivatives, sulfenic-(SOH-alb) and sulfinic acid (SO(2)H-alb), resulting in sulfonic acid (SO(3)H-alb), the final stable product of the reaction. Upon stable oxidation (SO(3)H-alb), albumin properties are altered: the protein becomes more susceptible to trypsin digestion and is degraded faster compared to the non-oxidized counterpart. The present review focuses on the characterization of albumin chemical changes induced by ROS, their relevance in human pathology and the most recent advances in the approach to oxidation adduct analysis.