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Cardio-renal syndrome is a clinical condition that has recently been well defined. In acute kidney disease, this interaction might trigger chronic processes determining the onset of cardiovascular events and the progression of chronic kidney disease. Moreover, the high mortality rate of acute kidney injury (AKI) is also linked to the fact that this condition is often complicated by dysfunctions of other organs such as lungs or heart, or is associated with septic episodes. In this context the role and the potential link between bone, heart and kidney is becoming an important topic of research. The aim of this review is to describe the cardiac alterations in the presence of AKI (cardiorenal syndrome type 3) and explore how bone can interact with heart and kidney in determining and influencing the trend of AKI in the short and long term. The main anomalies of mineral metabolism in patients with AKI will be reported, with specific reference to the alterations of fibroblast growth factor 23 and Klotho as a link between the bone-kidney-heart axis., Competing Interests: J.B. is member of the CKJ editorial board. The other authors declare no conflict of interest., (© The Author(s) 2023. Published by Oxford University Press on behalf of the ERA.)

The problem of frailty in kidney transplantation is an increasingly discussed topic in the transplant field, partially also generated by the multiple comorbidities by which these patients are affected. The criteria currently used to establish the presence and degree of frailty can be rapidly assessed in clinical practice, even in patients with chronic kidney disease (CKD). The main objectives of this work are: (i) to describe the method of evaluation and the impact that frailty has in patients affected by CKD, (ii) to explore how frailty should be studied in the pre-transplant evaluation, (iii) how frailty changes after a transplant and (iv) the impact frailty has over the long term on the survival of renal transplant patients., (© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)

Chronic metabolic acidosis (CMA) is a common complication of the more advanced stages of chronic kidney diseases (CKD), and is associated with morbidity and mortality of CKD patients and possibly with the progression of renal disease. Nevertheless, there is limited evidence or information on the prevalence, the potential causal factors, the clinical impact and the effects of correction of CMA in kidney transplant recipients. In this review, we briefly look at the more relevant, though scanty, studies which have, over time, addressed the above-mentioned points, with the hope that in the future the interest of transplant nephrologists and surgeons will grow towards this unreasonably neglected issue., (© The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

The incidence and prevalence of chronic kidney disease represents an important problem for public health. In renal diseases, the main histologic alterations derive from the development of renal fibrosis which results from the loss of the balance between pro- and anti-fibrotic factors. Tyrosine kinase receptors (RTKs) and matricellular proteins (MPs) are nowadays studied as potential modulators of renal injury. RTKs regulate cell cycle, migration, metabolism and cellular differentiation. Discoidin domain receptor-1 (DDR-1) is an RTK that has been extensively studied in cancer, and lung and renal diseases. It modulates inflammatory recruitment, extracellular matrix deposition and fibrosis; in renal diseases, it appears to act independently of the underlying disease. MPs regulate cell-matrix interactions and matrix accumulation, cellular adhesion and migration, and expression of inflammatory cells. Periostin is an MP, mainly studied in bone, heart, lung and cancer. Several studies demonstrated that it mediates cell-matrix interactions, migration of inflammatory cells and development of fibrosis. Recently, it has been reported in several nephropathies. In this review, we discuss the potential pathological roles of DDR-1 and periostin focussing on the kidney in both experimental models and human diseases., (© The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

Epstein-Barr virus (EBV) early-antigen (EA) serologic profile was examined in conjunction with peripheral blood EBV DNA load, to assess its value in evaluating the risk of developing posttransplantation lymphoproliferative disease (PTLD). The cohort included 26 pediatric recipients of solid-organ transplants, 6 of whom developed PTLD. All 6 patients had high peripheral blood EBV DNA loads. Of the remaining 20 patients who did not develop PTLD, 14 had high EBV DNA loads, and 6 had low EBV DNA loads. None of the patients who developed PTLD had significant EA immunoglobulin G (IgG) titers. However, all 14 patients with high EBV DNA loads and without PTLD had high EA IgG titers, either at the time of initial high EBV DNA load or during the ensuing weeks. Here, we report that EBV DNA load analysis, combined with EA serologic analysis, is a potentially useful prognostic marker for evaluating the risk of developing PTLD.

To determine whether Epstein-Barr virus (EBV) constitutes a contributing factor in AIDS and, conversely, whether the human immunodeficiency virus (HIV) alters the course of primary EBV infection in a pediatric population, 62 children born to HIV-infected mothers and prospectively followed were evaluated. EBV infection was documented by EBV-specific serology and polymerase chain reaction and by clinical history. HIV infection status was determined according to the Centers for Disease Control and Prevention pediatric classification system. Demographics from HIV-infected and HIV-uninfected children were comparable. The data suggest that HIV-infected children may acquire primary EBV infection earlier in life. The incidence of accompanying splenomegaly or hepatomegaly (or both) around the time of EBV seroconversion was higher among HIV-infected children than among HIV-uninfected children. In contrast, HIV disease progression and HIV-1 RNA load did not seem to be influenced by primary EBV infection.

The Epstein-Barr virus (EBV) genome encodes a protein in its BamHI C restriction fragment rightward open-reading frame-1 (designated BCRF1 or viral interleukin-10 [vIL-10]) that shares protein homology and biologic properties with human IL-10. Several EBV disorders are characterized by prolonged active EBV infection. Because continued EBV replication could allow for increased vIL-10, ELISA and immunoprecipitation were used to determine whether vIL-10 expression during chronic active EBV infection resulted in vIL-10 and IL-10 antibodies. IL-10 antibodies were assayed in patients diagnosed with chronic and acute infectious mononucleosis (CIM, AIM), nasopharyngeal carcinoma (NPC), and EBV-associated lymphoproliferative disease (LPD), as well as from healthy organ transplant patients and EBV-negative or EBV-positive persons. Whether anti-IL-10 antibodies could inhibit IL-10 biologic activity was determined. vIL-10 antibodies were found in CIM, NPC, and LPD patients and antibodies reactive to IL-10 were found in CIM patients. One CIM patient had IL-10 antibodies that neutralized IL-10 bioactivity in vitro.

Antibody-dependent cellular cytotoxicity (ADCC) is an important antiviral effector mechanism. ADCC to the protein encoded by the Epstein-Barr virus (EBV) BamHI A rightward open-reading frame-1 (BARF1) was studied by transducing Raji-tk- cells with the BARF1 gene using a retroviral expression vector. The transduced Raji cells expressed BARF1 on the cell surface, as determined by flow cytometry. Sera from chronic and acute infectious mononucleosis and nasopharyngeal carcinoma patients were found to contain antibodies that react with the BARF1 protein. When BARF1-expressing Raji cells were used as targets for ADCC, sera from several nasopharyngeal carcinoma patients demonstrated significant ADCC reactivity, whereas sera from healthy EBV-seronegative and -seropositive persons lacked such reactivity. BARF1-specific ADCC activity could be competitively inhibited with recombinant BARF1 protein. The level of anti-BARF1 antibody activity in sera of patients with EBV-associated diseases suggests that the BARF1 protein may serve as a target on EBV-infected cells for ADCC.

A variety of antibody response patterns to the latent Epstein-Barr nuclear antigen (EBNA) family have been described in different groups of subjects infected with Epstein-Barr virus (EBV). The purpose of this study was to characterize the immune response to two EBNA proteins, EBNA-1 and EBNA-2, in a population of children who were born to mothers infected with HIV and who underwent EBV seroconversion. Serial serum specimens from 33 children (nine were infected with HIV, and 24 were not infected) were evaluated for the presence of antibodies to EBNA-1 and EBNA-2 by anticomplement immunofluorescence. All the EBNA serology profiles observed for children in our study who were not infected with HIV were consistent with those described for immunocompetent hosts with acute EBV infection, i.e., development of antibodies to EBNA-1, often preceded by the appearance of a humoral immune response to EBNA-2. In contrast, following EBV primary infection in HIV-infected children, antibodies to EBNA-2 arose after antibodies to EBNA-1 and tended to persist. Further studies are needed to investigate the role of EBNA-2 serology as a prognostic marker in HIV-infected children.