Thromboembolism in Renal Diseases

Patients with renal diseases are prone to both thrombosis and bleeding, as they have profound changes in all three classic components of coagulation, defined approximately 150 years ago by Virchow: blood flow, vessel wall (endothelial injury), and coagulation properties of the blood (e.g., coagulation and fibrinolytic systems and platelets). The prothrombotic state in chronic kidney disease (CKD), glomerular diseases (including systemic lupus and vasculitis), and some less frequent conditions (idiopathic retroperitoneal fibrosis, antiphospholipid syndrome, hemolytic‐uremic syndrome, etc.) is associated with vascular endothelial damage, increase in certain coagulation and antifibrinolytic factors, decrease in anticoagulation proteins, dyslipidemia, hypoalbuminemia, changes in platelet membranes, hemo‐ and peritoneal dialysis and heparin treatment, increased microRNAs and circulating microparticles, antiphospholipid antibodies, nephrotic syndrome, anemia with high platelet count, and so on. Nevertheless, the same patients have substantially increased risk of bleeding due to platelet dysfunction and intake of certain medications (antiaggregants, heparin and low‐molecular weight heparins, and anemia). The aim of this review is to present the main thrombo‐embolic risk factors in a wide variety of patients with renal diseases, including chronic glomerulonephritis (primary and secondary), chronic renal disease, and idiopathic retroperitoneal fibrosis. We have evaluated the risk factors for arterial and venous thromboses in a wide variety of renal patients with both glomerular and non‐glomerular diseases, including the presence of nephrotic syndrome, inborn and acquired coagulation defects (i.e., factor V Leiden, MTHFR gene mutation, 20210 prothrombin gene mutation, and antiphospholipid antibodies), corticosteroid treatment, and dyslipidemia. We are describing the results of these investigations and suggesting prophylactic anticoagulant strategies in such patients. Multiple risk factors influence the coagulation system in renal disease leading to both hypercoagulation and hemorrhagic diathesis. Therefore, renal patients should be thoroughly investigated for coagulation abnormalities, especially if pathogenic (i.e., corticosteroid and immunosuppressive) and anticoagulation treatment is to be initiated. Moreover, the doses of anticoagulant/antiaggregant and hemostatic medications should be considered carefully, having in mind the underlying diseases and risk factors, renal function, and concomitant treatment

Viral load and lymphocyte subpopulations in newly diagnosed patients with chronic Hepatitis B

INTRODUCTION: The immune response against Hepatitis B virus (HBV) represents a key factor for infection outcome. However, the relation between viral replication and host immune reactivity is still a matter of investigation. AIM: To investigate whether the cellular immune response of newly diagnosed treatment naïve chronic hepatitis B (CHB) patients may be influenced by the replicative status of HBV.MATERIALS AND METHODS: A total of 45 (17 female and 28 male) newly diagnosed untreated CHB patients aged 42.48±13.19 years (19÷71 years) were enrolled in this study. The patients were divided in two groups according to the viral load: >0÷≤104 copies/ml (n=25) and >10 4÷<108 copies/ml (n=17). Flowcytometric immunophenotyping was performed for evaluation of the cellular immunity. Serum HBV DNA load was assessed by quantitative real-time polymerase chain reaction.RESULTS: Similar alterations were observed in both patients` groups in comparison with healthy controls which could be summarized as follows: decreased total T cells (CD3+) due to low helper-inducer (CD3+CD4+) and suppressor-cytotoxic (CD3+CD8+) subpopulations; reduced effector cytotoxic (CD8+CD11b-; CD8+CD28+) and activated (CD3+HLA-DR+, CD8+CD38+) T-cell subsets; increased CD57+CD8- cells; elevated percentage of B lymphocytes. No significant differences in the studied immune parameters were detected between both patients` groups except the significantly elevated CD4/CD8 ratio in individuals with higher in comparison to those with lower HBV DNA levels.CONCLUSION: Alterations in the cellular immune repertoire of CHB patients were observed resulting mainly in significantly decreased T-cell subpopulations, particularly those with effector cell immune phenotype regardless of the viral load

On Two Cases with Autosomal Dominant Hyper IgE Syndrome: Importance of Immunological Parameters for Clinical Course and Follow-Up

Autosomal dominant hyper-IgE syndrome (AD-HIES) is a rare disease described in 1966. It is characterized by severe dermatitis, a peculiar face, frequent infections, extremely high levels of serum IgE and eosinophilia, all resulting from a defect in the STAT3 gene. A variety of mutations in the SH2 and DNA-binding domain have been described, and several studies have searched for associations between the severity of the clinical symptoms, laboratory findings, and the type of genetic alteration. We present two children with AD-HIES–a girl with the most common STAT3 mutation (R382W) and a boy with a rare variant (G617E) in the same gene, previously reported in only one other patient. Herein, we discuss the clinical and immunological findings in our patients, focusing on their importance on disease course and management