Terapevt Arkh
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This review devoted to the nephrotic syndrome (NS) subsequent thrombotic outcomes. The pathogenesis of hypercoagulation disorders that cause venous and arterial vascular system thrombosis are studied. Discussed procoagulant and anticoagulant mechanisms imbalance due to the anticoagulants natural urinal loss, affected by disfunction of the glomerular filter selective permeability, leading to high molecular weight liver-derived proteins (at least of the albumin size) leakage, fibrinolysis depression, excessive liver synthesis of plasma clotting cascade factors and platelet activation. ⋯ The most frequent adverse variants of arterial and venous thromboses are studied, specified their basic and general risk factors, as well as individual, varying in different patients. Indications and prophylactic anticoagulant therapy regimen and thrombosis treatment duration in patients with NS are discussed. It also stressed that the decision on time and method of anticoagulant therapy for a NS patients is still a challenge for healthcare providers.
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Neoangiogenesis is a basic factor for most physiological as well as pathological processes i.e. tumor metastases. The most important is vascular endothelium growth factor (VEGF) and its receptors (VEGFR1/2) in angiogenesis processes. Nowadays antiangiogenic agents (which inhibit VEGF like bevacizumab neither VEGFR2 like ramucirumab) are widely used in very different chemotherapeutic regimens in clinical oncology. ⋯ Appearance of antiangiogenic drugs led to adverse nephrotoxic effects: arterial hypertension, proteinuria, rarely nephrotic syndrome, and kidney dysfunction. Various hystological variants of nephropathy are described, however, in most cases, signs of thrombotic microangiopathy of the renal vessels are noted. This literature review discusses mechanisms, clinical and morphological aspects of nephropathy associated with antiangiogenic drugs.