Dear Colleagues,

Thrombotic microangiopathy (TMA) is a pathological syndrome characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and organ damage, primarily of the kidney and brain. Several approaches have been proposed for classification of TMA, each taking into account various aspects, such as genetic predisposition and secondary causes, violations of complement function or von Willebrand factor metabolism, dependence on pregnancy, transplantation, oncological diseases, the influence of drugs, etc. The molecular mechanisms causing TMA are diverse and not fully understood. The pathogenesis of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are the most studied forms of TMA. There is less clarity regarding other forms of TMA. The key reason for the development of TMA is damage of the microvascular endothelium. However, the mechanisms of endotheliopathy remain poorly understood. The purpose of this Special Issue is to present, analyze and summarize the latest data on the molecular and cellular mechanisms of the development of various forms of TMA and thrombotic complications. Of interest are articles that will characterize the pathogenetic mechanisms of TMA associated with other comorbidities. Another objective of the Issue is to consider the effectiveness of new approaches to the treatment of TMA, based on the use of new drugs that affect the main pathogenetic links of this disease.

Dr. Pavel Avdonin
Dr. Galina A. Generalova
Dr. Vasily Nikolaevich Sukhorukov
Guest Editors

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• thrombotic mycroangiopathy
• von Willebrand factor
• endothelium
• complement
• hemolytic uremic syndrome
• drugs
• pathology
• cardiovascular diseases
• thrombotic complications
• comorbidities