Sibel Ersan

Peritoneal fibrosis (PF) is a pathological change that occurs mostly long‐term peritoneal dialysis (PD) patients, as a result of triggering the inflammatory response. Plasminogen activator inhibitor‐1 (PAI‐1) is an important molecule featured in the development of fibrosis. It has been shown in literature that PAI‐1 gene alterations are associated with fibrosis in many tissues and organs. However, PAI‐1 gene alterations in long‐term PD patients have not yet been investigated. In this study, PAI‐1 4G/5G polymorphism was examined by reverse hybridization, and all coding exons of the PAI‐1 gene were examined by sequence analysis to provide treatment modification in patients with predisposition before fibrosis develops. The patients were divided into two groups according to ultrafiltration failure test and duration of PD treatment: those with suspected PF or a high probability of developing PF (36%) and those with a low probability of developing PF (64%). There was no significant difference between the two groups in findings such as peritoneal equilibration test (PET), Kt/V, the content of the PD solution used, peritonitis, and PAI‐1 4G/5G polymorphism (P > .05). A total of eight gene alterations (rs2227660, rs2227668, rs2854233, rs41281004, rs61553169, rs368413856, rs2227684) were detected by sequence analysis, one of which was exonic (rs6092). When the genotype distributions of these variants were examined, no significant difference was found between the two groups. PAI‐1 gene changes were not detected in patients with the probability of developing PF. There is a need for further studies involving other molecules responsible for predisposing to PF with larger patient populations in patients undergoing long‐term PD treatment.

Background: Therapeutic apheresis (TA) as primary or adjunctive therapy proved itself in a broad spectrum of diseases. This study aims to present TA practices in a tertiary center with an emphasis on the rate of the utility of TA on the new American Society for Apheresis (ASFA) indications. Methods: We conducted a retrospective analysis of data regarding TA applications through our electronic medical database from June 2016 to July 2018. The data included demographics, clinical indications, and procedural characteristics. We also searched for the rate of the utility of TA procedures on new ASFA indications by entering both the diagnostic and TA modality codes for these indications on the electronic database during the study interval. Results: A total of 720 TA procedures were performed on 96 patients (54 males, 42 females, with a mean age of 48.15 +/- 26.71 years). The procedures were 68.8 % therapeutic plasma exchange (TPE), 16.4 % leukocytapheresis, 11.5 % immunoadsorption (IA), 3.1 % double filtration plasmapheresis (DFPP), and 0.13 % erythrocyte exchange. The categorical indications included 60.41 % category I and category II, 28.12 % category III, and 1.04 % category IV. The most common indication was thrombotic thrombocytopenic purpura (TTP) (26.04 %). The procedure failure rate was 2.08 %. Patient-related adverse events were reported in 7.5 % of procedures. The case mortality rate was 16.66 %. TA utility rate was 0.98 % for the new indications in the ASFA 2016 guideline. Conclusion: Therapeutic apheresis is a progressively developing, safe, and effective treatment modality with add-on indications. Physicians should keep track of new developments on this modality to implement the appropriate indications into clinical practice.

Matrix metalloproteinases (MMPs) are zinc-containing proteinases that are involved in the degradation of extracellular matrix (ECM) and a number of cell surface proteins in order to maintain tissue homeostasis. They are involved in pathogenesis of several ischaemic organ injuries. In the present study, we aimed to determine the expression and level of MMP-2 and MMP-9 in renal ischaemia–reperfusion injury (IRI) model and the potential beneficial effect of nebivolol, a β₁-adrenergic receptor blocker, on both MMP-2 and -9 level and expression and tubular injury caused by IRI. Twenty Wistar albino rats were divided into three groups: sham-operated , ischaemia–reperfusion, and nebivolol-pretreated. IRI model was induced by bilateral clamping of renal arteries for 45 min followed by 24 h of reperfusion. The analysis of serum creatinine levels, quantity and expression of MMP-2 and MMP-9 were performed after 24 h of IRI. The effects of nebivolol on level and expression of MMP-2 and MMP-9 levels were investigated by enzyme-linked immunosorbent assay and immunohistochemistry, respectively. The pathological examinations were performed to score tubular damage by light microscopy. Creatinine levels increased significantly in the ischaemia–reperfusion group compared to the sham-operated group. Rats in the nebivolol-pretreated group showed significant decrease in expression and quantity of MMP-2 and MMP-9 during IRI. The pathological examinations demonstrated significantly low level of tubular injury score in nebivolol-pretreated group. Nebivolol attenuated IRI by decreasing the expression and level of MMP-2 and MMP-9.

Introduction. None of the classification systems in immunoglobulin A (IgA) nephropathy has been widely agreed or implemented by clinicians or pathologists. In order to meet this need, "Oxford Classification System", which is highly reproducible and predictive for clinical course, was developed in 2009. In the present study, we investigated clinical and pathological characteristics of patients with IgA nephropathy based on current classification and the predictivity of crescent presence on prognosis. Methods. The study comprised 40 patients with diagnosis of primary IgA nephropathy on renal biopsy. The biopsy findings and follow-up parameters of patients were retrospectively re-evaluated. Pathological findings were examined based on the Oxford classification system. The presence of crescent formation in the specimens was noted. Results. The presence of crescent formation was predictive of poor prognosis regarding the glomerular filtration rate (eGFR), the level of proteinuria, and mean arterial pressure (MAP). Conclusion: Considering the importance of crescent formation in prediction of the clinical course and need for immunosuppressive therapy, it is suggested that crescent presence can be included in this classification system.

Peritoneal fibrosis is almost uniform feature encountered in peritoneal dialysis patients. The transition of epithelial cells to mesenchymal phenotype, neovascularization, and consequently development of peritoneal fibrosis occur due to the involvement of peritoneal membrane by various insults such as uremia itself, peritonitis attacks, and exposure to bio-incompatible peritoneal dialysis fluids. Bevacizumab is a monoclonal antihuman antibody developed against vascular endothelial growth factor and can reduce fibrosis by preventing neovascularization. There has been no study so far that demonstrates the effect of bevacizumab on peritoneal fibrosis in a rat model. A total of 41 female Wistar albino rats were divided into six groups. The control group (C) received 0.9 % isotonic saline (2 ml/day) intraperitoneally (i.p) for 21 days. Chlorhexidine group (CH) received 15 % ethyl alcohol and 0.1 % chlorhexidine gluconate (CG) in saline (2 ml/day) i.p for 21 days. The resting group (R) received CG 2 ml/day i.p for 21 days. The bevacizumab-1 group (B1) received CG 2 ml/day i.p for 21 days and bevacizumab 2.5 mg/kg i.p as a single dose on day 21. The bevacizumab-2 group (B2) received CG 2 ml/day for 21 days and bevacizumab 2.5 mg/kg i.p on day 0 and day 21. The bevacizumab-3 group (B3) received bevacizumab 2.5 mg/kg i.p on day 0 and day 21. Peritoneal samples were taken from the left anterior abdominal wall. The thickness, vascularization, and fibrosis scores in the peritoneal samples were assessed using a light microscope. On histopathological evaluations, peritoneum thicknesses, vascularization scores, and fibrosis significantly decreased in bevacizumab groups B1 and B2. Histopathologically, bevacizumab was proven to attenuate fibrotic process in experimental peritoneal sclerosis model.