BackgroundAltered regulation of the complement system is associated with multiple kidney diseases. CD35, CD55 and CD59 regulate the complement system, and changes in their expression have previously been linked with kidney disease. This study assessed whether changes in the expression levels of these proteins are associated specifically with chronic kidney disease (CKD) to understand its pathogenesis.Materials and methodsSixty CKD patients and 60 age-matched controls were enrolled and divided into two groups: Group I (n=30 pediatric patients and n=30 controls) and Group II (n=30 adult patients and n=30 controls). The expression of CD35, CD55 and CD59 on peripheral blood cells was evaluated by flow cytometry as the proportion of positive cells expressing the marker and mean fluorescence intensity (MFI), also the relation of these markers to the stage of CKD was also evaluated.ResultsPediatric and adult CKD patients had significantly lower proportion of erythrocytes expressing CD35, CD55 and CD59 than healthy controls (P<0.001). In pediatric CKD patients, there was no significant difference in the three studied markers on neutrophils, lymphocytes and monocytes. The changes in expression of CD35, CD55 and CD59 on leukocytes were more pronounced in adult patients, who had lower proportion of CD59-positive neutrophils, CD35- and CD59-positive lymphocytes, and CD59-positive monocytes, as well as lower expression of CD59 on neutrophils and monocytes than adult controls (P<0.001, P=0.019, P<0.001, P=0.026, P<0.001 and P=0.003, respectively). The eGFR directly correlated with the proportion of positivity of some of those markers on peripheral leukocytes while there was inverse correlation between the disease stage and the same markers.ConclusionThere are alterations in the patterns of expression of complement regulatory proteins CD35, CD55 and CD59 on peripheral blood cells of patients with CKD compared with healthy controls.
Background: Deep venous thrombosis (DVT) is associated with significant morbidity and mortality. Thus, there is a great need to demonstrate a more efficient biomarker that would confirm the diagnosis of DVT. Our work aimed to evaluate the role of platelet-derived growth factor-beta (PDGF-B) as a new marker of DVT and its correlation with other radiological and laboratory tools used for the diagnosis. Materials and Methods: A case–control study enrolled forty patients selected from our university hospital between April 2018 and August 2018, who divided into two groups: Group I ( n = 20) consisted of patients diagnosed with acute venous thrombosis and Group II ( n = 20) consisted of patients diagnosed with chronic venous thrombosis. Twenty samples were collected from age- and gender-matched apparently healthy controls to be used as a control. Venous duplex ultrasonography, routine laboratory investigations, D-dimer (DD), and protein expression of PDGF-B were performed on all patients. Results: There was a highly significant increase in a protein expression of PDFG-B in all cases of acute and chronic venous thrombosis compared to the control group with P < 0.001; furthermore, it was more specific than DD for the detection of DVT (specificity 95% and 90%, respectively). Conclusion: Our study submits a novel association of PDGF-B plasma levels with DVT, and PDGF-B is considered to be a more specific indicator for DVT than is DD.
Background Mature bone marrow T lymphocytes and NK may have a special relevance in the control of the malignant growth. Objective We aimed to assess the percentage of the residual BM T-cells, (T-helper –T-cytotoxic- NKT) and the NK cells of childhood precursor B-lymphoblastic leukemia (B-ALL) as an indicator of innate and adaptive immunity in these patients. Subjects and Methods This study was conducted on 40 B-ALL patients, and 40 apparently healthy matched children served as a control group. The flow cytometry was used to assess the percentage of the residual BM T-cells (T-helper, T-cytotoxic and NKT), and the NK cells. Results Compared with the control group, the percentage of the residual BM T-cells, its subtypes (T-helper, T-cytotoxic), and NKT cells in addition to the NK cells was significantly decreased in Group IA, and Group IB, but there was no significant difference between Group IA and Group IB in all studied parameters. In terms of the CD4/CD8 ratio, there was a significant increase in Group IA as compared to the control group (P < 0.026), but there were no significant statistical differences in CD4/CD8 ratio between Groups IB, and the control. Likewise, in CD4/CD8 ratio between groups IA, and Groups IB (P > 0.05). The percentage of NK, and NKT cells shows a significant increase in Hepatomegaly and Splenomegaly, as compared to non-Hepatomegaly and non-Splenomegaly patients of Groups IB (P < 0.05). However, there was a significant increase in statistical differences in the percentage of NKT cell between non-Splenomegaly, as compared to Splenomegaly patients of Group IA (P < 0.05). Additionally, there is a negative correlation between B.M Blast% to CD4/CD8 ratio and NK%, but there is no significant correlation between B.M Blast% to NK T% in the group 1 A.
Background: β-thalassaemia (β-Thal) is an inherited chronic haemolytic anaemia resulting from absent or low level of synthesis of β-globin chains of haemoglobin A in erythropoietic cells. The complement system is an important part of innate immune response that may be implicated in red blood cell (RBC) lysis. Mammalian cells are provided with surface bound complement regulatory proteins (MCRPs) that regulate the activation of complement cascade, thus protecting them from uncontrolled complement-mediated lysis. Objective is to evaluate the role of complement regulatory proteins (CD55, CD59, and CD35) on red blood cells, and to explain the pathogenesis of anaemia in β-thalassemia major. Methods: This case-control study enrolled 74 β thalassemia major patients who were compared with 40 age and sex matched controls. We performed expression of CD55, CD59, and CD35 on RBCs using flow cytometry. Results: CD55 levels of β-thalassemia major patients (79.78% ± 18.54%) were significantly decreased compared to healthy controls (99.45% ± 0.59%) (P < 0.001). CD59 levels of β-thalassemia major patients (97.76% ± 1.72%) were significantly lower than in the controls (99.75% ± 0.36%) (P < 0.001), also CD35 levels were significantly lower in the β-thalassemia major patients (4.30% ± 4.66%) than in the control group (19.40% ± 10.90%) (P < 0.001). Conclusion: β-thalassemia major patients suffer from increased haemolysis and a consequent increase in their demand for blood transfusion. Complement-mediated haemolysis was shown in our study by decreased expression of CD55, CD59, and CD35 in β-thalassemia major patients. This allows complement deposition on RBCs and enhances or accelerates their lysis.
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