In the present study, we found a positive correlation between proteinuria and CD8+T cells

In the present study, we found a positive correlation between proteinuria and CD8+T cells. were taken into 2 mL EDTA tube to evaluate peripheral NK SC-26196 cell subgroups according to CD56 and CD16 expression and CD3, CD4, CD 8 expression to determine subtypes T cells. These cells were evaluated by flow cytometry technique. Results Urinary density, fractional excretion of sodium, proteinuria, and metabolic acidosis are found to be higher in patients with CVID when compared to healthy controls. In the bivariate correlation analysis,?proteinuria?was positively correlated with age (r = 0.496, p = 0.001), CD8+T cells percentage (r = 0.427, p = 0.02). Albumin, CRP, and CD8+T cell percentage were found to be independent variables of?proteinuria. Conclusion Increased chronic ongoing inflammation was found to be associated with?proteinuria?in patients with CVID. Hence, in routine outpatient clinics, proteinuria should not be overlooked in this group of patients. strong class=”kwd-title” Keywords: Chronic inflammation, proteinuria, common variable immunodeficiency 1. Introduction Common variable immunune deficiency (CVID) refers to a group of heterogeneous disorders that are often due to inherited defects of the immune system. Patients with CVID are frequently susceptible to recurrent infections, autoimmunity, lymphoproliferation, and malignancy [1]. Because of the belief of CVID as rare congenital diseases, heterogeneity of diseases, and lack of awareness, delay in diagnosis is usually frequent. Partial elimination of problems in access to immune alternative therapy, effective treatment of infections with antibiotics, and introduction of targeted monoclonal antibodies have significantly reduced mortality SC-26196 in CVID patients. As a result, the management of the complications and the quality of life has become more important with increased life expectancy in CVID patients. Although recurrent and widespread upper and lower respiratory tract infections and increased autoimmunity, lymphoproliferation, and especially increased lymphomalignies are well-defined complications of immunodeficiencies, renal complications are relatively rare and overlooked in this group of patients [2]. Increased inflammatory markers such as C-reactive protein, interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-, interstitial cellular adhesion molecule-1, vascular cellular adhesion molecule-1, CD8+T cells, natural killer (NK) cells, and E-selectin are associated with the development of nephropathy in many chronic diseases [3]. Inflammation and inflammatory molecules are also thought to affect glomerular functions through alternations in vascular permeability, vasodilator, and vasoconstrictor mechanisms, extracellular matrix dynamics, and the proliferation of mesangial, endothelial, and vascular easy muscle cells, as well as the WNT-12 induction of cytotoxicity, apoptosis, and necrosis in the pathogenesis and progression of chronic kidney disease (CKD) [4]. Proteinuria is one of the most important prognostic factors causing progression in kidney disease. Proteinuria causes tubulotoxicity, activates inflammatory markers that cause fibrosis, and consequently nephropathy progression. Most studies have found that better renal outcomes are associated with brokers that lower proteinuria [5,6]. For this reason, depending on the underlying etiology, reduction of proteinuria, by the renin-angiotensin-aldosterone blockade, immunosuppressive treatment, and diet regimens, is one of the important parts of the treatment to slow the progression [7]. To date the data regarding the nephropathy SC-26196 in CVID is usually scant. Hence, we aimed to investigate the relation between the tubular dysfunction, proteinuria, and inflammatory SC-26196 cells including T and NK cells in patients with CVID. 2. Material and methods The study group included 27 patients with CVID (male (M): 12 (44.4%)/female (F): SC-26196 15 (55.6%), age: 39.88 13.47) who follow up at regular basis and 18 patients (F/M: 10/8, age: 33.83 7.97) as a control group. The study protocol was approved by the ethics committee of the university (sate: 16.11.2018; approval number: 2018/1574). Informed consent was obtained from study participants. The diagnosis of CVID was made according to the updated diagnostic criteria of ESID [2]. Demographic and clinical data were retrieved from individual medical files, which all recorded at the first visit of patients including, sex, age, diagnostic delay, detailed family history, and all other necessary information. Initial immunological workup and other diagnostic investigations to expose exact diagnosis and concurrent complications and/or disorders were also recorded. Venous blood samples for biochemical analyses were drawn after at least 10 h of fasting before taking any medication. All biochemical analyses were undertaken using an oxidase-based technique at Roche/Hitachi Modular System (Mannheim, Germany) in the Central Biochemistry Laboratory of the Necmettin Erbakan University Meram School of Medicine. Quantitative determination of serum immunoglobulins (IgG, IgM, IgA, and IgE) was made through particle-enhanced immunonephelometry using the Siemens BN II/BN ProSpec system (New York, USA). Blood samples obtained from the patients with.