Acute kidney injury induced by thrombotic microangiopathy in two cases of Bothrops envenomation

Clinical assessment and pathophysiology of Bothrops venom-related acute kidney injury: a scoping review

“…Few studies reported the occurrence of thrombotic microangiopathy (TMA) in patients following Bothrops snakebite with thrombocytopenia, anemia with blood films showing fragmented red cells, haptoglobin consumption, increase in serum lactate dehydrogenase and a progressive increase of serum creatinine [ 104 , 105 ]. Torrez et al [ 107 ] reported the association between AKI and prolonged thrombocytopenia in a 37-year-old man admitted to a hospital after snakebite due to Bothriopsis bilineata in the Brazilian Amazon, presenting oliguria, dark-colored urine, incoagulability and thrombocytopenia.…”

“…These studies reported the abnormal activated partial thromboplastin time (aPTT), bleeding symptoms and abnormal LDH level which are factors associated with AKI development [5,14,66]. The increase of LDH levels was observed in recent case reports about thrombotic microangiopathy in Bothrops envenoming and expressed the high cellular turnover and necrosis following the increase of creatinine levels [90,91].…”

“…This is the most likely pathway in AKI due to Bothrops snakes: the association between AKI and abnormal coagulation, including abnormal aPTT, hypofibrinogenemia and hemorrhagic symptoms, as soon as the increase of LDH is reported [5,14,66]. Snakebite induces thrombotic microangiopathy, characterized by the triad of AKI, thrombocytopenia, microangiopathic and haemolytic anaemia, which could lead to renal cortical necrosis [103][104][105]. Hemorrhagins contained in venoms of some snakes such as Bothrops spp.…”

Liver gene regulation of hemostasis-related factors is altered by experimental snake envenomation in mice

“…Hemostatic abnormalities evoked by B. jararaca snakebites include direct proteolytic activity of snake venom enzymes on fibrinogen, prothrombin, and factors X, VIII and V, in a mechanistic process that is distinct from the extrinsic and intrinsic coagulation pathways, and by a feedback mechanism of these activated factors, especially meizothrombin or thrombin, which ultimately leads to activation and consumption of coagulation factors in circulation, as well as exacerbated secondary fibrinolysis [12,[20][21][22][23]. Thrombocytopenia and platelet dysfunction are also observed during B. jararaca envenomation [16,22,24], but they are independent of coagulation activation [21,25]. Gradual fibrinogen consumption during snakebite envenomation causes hypofibrinogenemia or afibrinogenemia, leading to a prolongation of whole blood coagulation time (WBCT)-which is a sign of snake envenomation [26].…”

Complement in Secondary Thrombotic Microangiopathy

“…reviewed and are listed below: • Shigatoxin (STEC-HUS) producing enterobacteria: E. coli is the most common, the others include Shigella dysenteriae, Campylobacter jejuni, Moraxella osloensis • Viral infections: cytomegalovirus, Epstein-Barr virus, varicella zoster virus, parvovirus B19, human immunodeficiency virus, influenza virus • Respiratory tract infection agents: Bordetella pertussis, Streptococcus pneumoniae(16), Mycoplasma pneumoniae(93).• Protozoa: Toxoplasma gondii.• Rare agents: erlichiosis(94), Capnacytophaga canimorsus(95,96), Plasmodium vivax (malaria)(97), snakebites (Bothrops jararaca)(98), dengue fever(99)(100)(101), West Nile virus(102); Chikungunya Fever(103,104).• Severe Acute Respiratory Syndrome Coronavirus type 2 (SARS-CoV-2) Mechanisms of TMA-associated with infectious diseases are complex and include direct endothelial injury, development of ADAMTS13 inhibitors and complement activation inJ o u r n a l P r e -p r o o f different levels and magnitude. As an illustration, putative mechanisms of TMA in influenza infection are production of neuraminidase (although lower than seen with Streptococcus pneumoniae), direct infection of endothelial cells leading to apoptosis, activation of platelets and generation of thrombin.…”