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UTI are common in renal Tx recipients and may significantly impact on the graft function. The aim of our study was to evaluate the prevalence, risk factors, and significance of UTI in Tx children. We performed a retrospective cross-sectional study of 76 Tx patients, median age at Tx was 13.4 yr. Twenty-one of 76 (28%) patients developed at least one UTI during the mean follow-up time of 3.3 +/- 2.0 yr post-Tx. The first UTI occurred at a median of 160 days post-Tx. The RR of having UTI was significantly higher in patients with the primary diagnosis of obstructive uropathy (RR = 2.6, 95th CI = 1.1-6.0, p = 0.032), history of PN pre Tx (RR = 2.7, 95th CI = 1.3-5.4, p = 0.009) and pre Tx VUR (RR = 2.2, 95th CI = 1.1-4.5, p = 0.045). These three factors also significantly decreased the infection-free survival time to the first UTI. Most UTI caused reversible acute allograft dysfunction, but the long-term graft function could not be reliably assessed with SCr. In conclusion, UTI occurred in 28% of pediatric Tx recipients, mostly during the first year post-Tx despite antibiotic prophylaxis. The diagnosis of obstructive uropathy, history of UTI and VUR prior to Tx were significant risk factors.

Background: Evaluation of acid-base disorders using the Stewart-Fencl principle is based on assessment of independent factors: strong ion difference (SID) and the total concentration of non-volatile weak acids (Atot). This approach allows for a more detailed evaluation of the cause of acid-base imbalance than the conventional bicarbonate-centered approach based on the Henderson-Hasselbalch principle, which is a necessary yet insufficient condition to describe the state of the system. The aim of our study was to assess acid-base disorders in peritoneal dialysis (PD) patients using both of these principles., Methods: A total of 17 patients with chronic renal failure (10 men), aged 60.7 (22-84) years, treated by PD for 25.7 (1-147) months were examined. A control group included 17 healthy volunteers (HV) (8 males), with a mean age of 42.7 (22-77) years and normal renal function. Patients were treated with a solution containing bicarbonate (25 mmol/L) and lactate (15 mmol/L) as buffers; eleven of them used, during the nighttime dwell, a solution with icodextrin buffered by lactate at a concentration of 40 mmol/L. The following equations were employed for calculations of acid-base parameters according to the Stewart-Fencl principle. The first is SID = [Na+] + [K+] + 2[Ca(2+)] + 2[Mg(2+)] - [Cl-] - [UA-], where SID is the strong ion difference and [UA-] is the concentration of undetermined anions. For practical calculation of SID, the second equation, SID = [HCO3-] + [Alb-] + [Pi-], was used, where [Alb-] and [Pi-] are the charges carried by albumin and phosphates. The third is Atot, the total concentration of weak non-volatile acids, albumin [Alb] and phosphates [Pi]., Results: The capillary blood pH in PD group was 7.41 (7.27-7.48), [HCO3-] levels 23.7 (17.6-29.5) mmol/L, SID 36.3 (29.5-41.3) mmol/L, sodium-chloride difference 39.0 (31.0-44.0) mmol/L, [Pi] 1.60 (0.83-2.54) mmol/L, and [Alb] 39.7 (28.8-43.4) g/L (median, min-max). Bicarbonate in blood correlated positively with SID (Rho = 0.823; p < 0.001), with the sodium-chloride difference (Rho = 0.649; p < 0.01) and pH (Rho = 0.754; p < 0.001), and negatively with residual renal function (Rho = -0.517; p < 0.05). Moreover, the sodium-chloride difference was also found to correlate with SID (Rho = 0.653; p < 0.01). While the groups of PD and HV patients did not differ in median bicarbonate levels, significantly lower median value of SID were observed in PD patients, 36.3 vs. 39.3 mmol/L (p < 0.01); additionally, PD patients were shown to have significantly lower mean value of serum sodium levels, 138 vs. 141 mmol/L (p < 0.01), and serum chlorides levels, 100 vs. 104 mmol/L (p < 0.001). Despite the higher [UA-] levels in PD patients, 9.1 vs. 5.4 mmol/L (p < 0.001), this parameter was not found to correlate with bicarbonate levels., Conclusions: The results suggest that the decreased bicarbonate in PD patients results from a combination of decreased sodium-chloride difference and mildly increased unmeasured anions.

Our understanding of the clinical aspects of IgA nephropathy (IgAN) has advanced since the 10th International Symposium on IgA Nephropathy in 2004. In this review we discuss new developments in areas of familial IgAN, the emerging field of biomarkers, and prognostic features. Familial disease continues to account for a significant number of newly diagnosed patients with IgAN. These patients have clinical manifestations and long-term outcomes similar to those of patients with sporadic disease. Characterization of the IgAN1 gene linked to IgAN in some Italian and American multiplex families has remained elusive. Other multiplex IgAN pedigrees have shown no linkage to any locus. With advances in technology to better measure and characterize polypeptides in small concentrations, the area of biomarkers has generated substantial interest since 2004. New potential disease-specific biomarkers of IgAN include the IgA1 neoepitope at the threonine228 and/or serine230IgA1 hinge-region residues, serum levels of galactose-deficient IgA, and urinary IgA-IgG immune complexes. Other investigators have used proteomic approaches to find panels of urinary polypeptides (many of which have not been sequenced) that discriminate patients with IgAN from normal healthy controls as well as patients with various other proteinuric renal diseases. These or other related findings may provide the necessary tools to better classify phenotypes in multiplex pedigrees and to improve monitoring of disease progression or response to therapy.

Characteristic features of IgA nephropathy (IgAN) include IgA1-containing immune complexes (IC) in the circulation, urine, and renal mesangium. IC contain IgA1 deficient in hinge region-associated galactose (Gal) and antibodies specific for antigenic determinants present on the hinge region. The biological effects of IC are primarily related to their molecular size and composition: when added to a culture of human mesangial cells, large IC exhibit a proliferative effect while small complexes are inhibitory. These activities have been observed using IC obtained from sera of IgAN patients or generated in vitro. Specifically, various preparations of human IgA1 with modified glycan moieties formed IC in vitro when incubated with sera from IgAN patients or healthy individuals, cord blood serum, or tissue culture supernatants of EBV-immortalized peripheral blood B cells secreting IgG. Interestingly, IgG antibodies specific for the IgA1 Gal-deficient hinge region are commonly found in sera of hominoid as well as non-hominoid primates and many other vertebrate species, and suggest the evolutionary uniqueness of the human IgA1 hinge region. Because of the molecular defect in IgA1 glycosylation and its subsequent recognition by naturally-occurring antibodies, experimental approaches that diminish or prevent formation of large immunostimulatory IC should be further explored.

Acid-base balance evaluation according to the Henderson-Hasselbalch equation enable us to assess the contribution of respiratory (pCO2) and/or non-respiratory (metabolic, HCO3(-)) components to the acid-base balance status. A new approach to acid-base balance evaluation according to Stewart-Fencl, which is based on a detailed physical-chemical analysis of body fluids shows that metabolic acid-base balance disorders are characterized not only by [HCO3(-)]. According to this concept independent variables must be taken into an account. The abnormality of concentration of one or more of the independent variable(s) determines the pH of a solution. The independent variables are: 1. strong ion difference (SID); 2. total concentration of nonvolatile weak acids [A(tot)]; 3. in agreement with the Henderson-Hasselbalch concept also pCO2. Traditional evaluation of acid-base balance disorders is based on the pH of body fluids (though pH may be within normal range if several acid-base balance disturbances are present). In order to maintain this view and simultaneously to respect the Stewart-Fencl principle, we invented a new equation, which uses only the independent variables to define the pH of body fluids. This analysis shows that for a given value of pCO2, the pH of body fluids is determined by a difference between SID and [A(tot)-]. pH = 6.1 + log((SID - [A(tot)-])/(0.03pCO2)) or in itemized form: pH = 6.1 + log((([Na+] + [K+] + [Ca2+] + [Mg2+] - [Cl-] - [UA-]) - (k1[Alb] + k2[P(i)]))/(0.03 x pCO2)). Evaluation of the individual components of this equation enables us to detect, which of the independent variable (or a combination of independent variables) deviates from the normal range and therefore which one or ones is a cause of the acid-base balance disorder. At the end of this paper we give examples of a practical application of this equation.