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Diagnostic Approach to Acute Kidney Injury in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Sonali Gupta, Divyansh Bajaj, Sana Idrees, Joseph Mattana
Thrombotic microangiopathies are rare causes of AKI and require prompt recognition and treatment. Well-described etiologies include thrombotic thrombocytopenic purpura, hemolytic uremic syndrome (which can be subdivided into typical and atypical forms), disseminated intravascular coagulation, malignant hypertension (referred to now as hypertensive emergency), scleroderma renal crisis, and drug toxicity such as can occur with calcineurin inhibitors. The pathogenesis includes thrombosis of capillaries and arterioles due to endothelial damage. Determining the cause of the thrombotic microangiopathy is essential, as this will guide the appropriate therapy [31].
Blood Coagulation and Fibrinolysis in TTP and HUS
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Juan Monteagudo, Arturo Pereira
Remuzzi et al. observed in 1978 a deficiency in the endothelial cell bioavailability of PGI2, which possesses powerful vasodilating and platelet antiaggregating actions, during the acute phase of the disease, possibly owing to a hypothetical defect in PGI2 release or lack of a synthesis stimulating factor in plasma.40 Other investigators attributed the PGI2 deficiency to either impaired stabilization in the circulation or to its accelerated degradation.41,42 Even though the endothelial cell seems to exhibit a deficiency in the production of PGI2 in the thrombotic microangiopathies, thus favoring platelet aggregation, the pathogenetic role for such an abnormality in TTP/HUS is not firmly established. In addition, although several authors have found decreased 6-keto-PGFjOC in the plasma of patients,43,44 others have reported normal45 or even higher levels.46,47 Furthermore, PGI2 infusion in HUS patients has failed to produce noticeable clinical improvement in most of them.48,49
Development of palliative medicine in the United Kingdom and Ireland
Published in Eduardo Bruera, Irene Higginson, Charles F von Gunten, Tatsuya Morita, Textbook of Palliative Medicine and Supportive Care, 2015
5 Moake JL. Thrombotic microangiopathies. The New England Journal of Medicine. 2002; 347(8):589-600. 6 Ludwig H, Van Belle S, Barrett-Lee P, Birgegard G, Bokemeyer C Gascon P et al. The European Cancer Anaemia Survey (ECAS): A large, multinational, prospective survey defining the prevalence, incidence, and treatment of anaemia in cancer patients. European Journal of Cancer (Oxford, England: 1990). 2004;40(15):2293-2306.
Cobalamin and folic acid deficiencies presenting with features of a thrombotic microangiopathy: a case series
Published in Acta Clinica Belgica, 2022
Britt Ceuleers, Sofie Stappers, Jan Lemmens, Lynn Rutsaert
‘Microangiopathic hemolytic anemia’ is a term used to describe any Coombs-negative hemolytic anemia resulting from red cell fragmentation in the small vessels, identified as schistocytes and fragmentocytes on peripheral blood smears. When these abnormalities are accompanied by thrombocytopenia, one should be aware of thrombotic microangiopathies. This group of related disorders, including thrombotic thrombocytopenia and hemolytic-uremic syndrome, is characterized by thrombosis in the microvasculature due to an endothelial injury, resulting in the aforementioned nonimmune hemolytic anemia and associated end-organ damage [1–3]. Here, we introduce three cases of vitamin B12 and/or folic acid deficiencies, presenting with features of a thrombotic microangiopathy. In this manner, we aim to make the reader aware of this notorious but rare manifestation of these nutritional deficiencies, hopefully leading to an earlier recognition of these pseudo-thrombotic microangiopathies (pseudo-TMA). Hence, unnecessary and expensive treatment, such as plasmapheresis, should be avoided or at least shortened in duration.
Introduction to a review series “Biomarkers of Platelet Activation”
Published in Platelets, 2022
Jianlin Qiao, Elizabeth E. Gardiner
Thrombotic microangiopathies (TMA), including thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS), are life-threatening disorders bearing the features of thrombosis, thrombocytopenia, and hemolytic anemia with strong likelihood of damage to multiple organs. The TMAs are difficult to differentially diagnose, and this is critical because different treatment options are selected based on that diagnosis. Patients with TMAs present with enhanced platelet activation, degranulation, and adhesion, with microparticles release as well as arterial thrombus formation, indicating the crucial role of platelet activation in the pathogenesis and development of TMAs. Al-Tamimi, Qiao, and Gardiner summarize what is known about platelet activation in TMA with an emphasis on the platelet activation biomarkers such as P-selectin, CD40L, GPIbα, GPVI, C-type lectin-like receptor (CLEC) 2, PF4, β-thromboglobulin, platelet-leukocyte aggregates, and platelet-derived microparticles [8]. These markers have been reported to closely correlate with disease severity of TMAs, and their levels are normalized after treatment, indicating the potential value of these biomarkers in the diagnosis and prognosis of TMAs.
Novel antiplatelet strategies targeting VWF and GPIb
Published in Platelets, 2021
Nithya Prasannan, Marie Scully
VWF is vital for normal hemostasis. Its role in thrombotic microangiopathies, vascular inflammation, and atherothrombotic events has been studied. Drugs that target the VWF-GPIb axis are therefore attractive options. Not all of these studied agents have proven their efficacy in these settings. However, one such agent that has been practice changing is caplacizumab and this has been demonstrated through TITAN and HERCULES trials in TTP patients. It does not alter the underlying pathophysiology of TTP but is an important adjunct to standard of care in iTTP.Further theoretical and early phase studies, utilizing the VWF-Platelet axis is being investigated, which may provide accompanying effective therapeutic compounds for other cardio or cerebrovascular conditions. Improved understanding of these diseases and its pathophysiology through continued research, development of new targeted drugs, and clinical experience is vital.