scholarly journals FP739PREECLAMPSIA, HELLP-SYNDROME AND THROMBOTIC MICROANGIOPATHY(TMA)-SIGNS DURING PREGNANCY AFTER KIDNEY TRANSPLANTATION

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i295-i295
Author(s):  
Tatyana Kirsanova ◽  
Maria Vinogradova ◽  
Alina Kolyvanova ◽  
Natalia Kravchenko ◽  
Tatyana Fedorova
2016 ◽  
Vol 48 (9) ◽  
pp. 3106-3108 ◽  
Author(s):  
J. Merola ◽  
P.S. Yoo ◽  
J. Schaub ◽  
J.D. Smith ◽  
M.I. Rodriguez-Davalos ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Shravya Govindappagari ◽  
Michelle Nguyen ◽  
Megha Gupta ◽  
Ramy M. Hanna ◽  
Richard M. Burwick

Severe vitamin B12 deficiency may present with hematologic abnormalities that mimic thrombotic microangiopathy disorders such as hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We report a patient diagnosed with severe vitamin B12 deficiency, following termination of pregnancy for suspected preeclampsia and HELLP syndrome at 21 weeks’ gestation. When hemolysis and thrombocytopenia persisted after delivery, testing was performed to rule out other etiologies of thrombotic microangiopathy, including atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and vitamin B12 deficiency. This work-up revealed undetectable vitamin B12 levels and presence of intrinsic factor antibodies, consistent with pernicious anemia. Parenteral B12 supplementation was initiated, with subsequent improvement in hematologic parameters. Our case emphasizes the importance of screening for B12 deficiency in pregnancy, especially in at-risk women with unexplained anemia or thrombocytopenia. Moreover, providers should consider B12 deficiency and pernicious anemia in the differential diagnosis of pregnancy-associated thrombotic microangiopathy.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3190-3190
Author(s):  
Wolf Ramackers ◽  
Lars Friedrich ◽  
Wolfgang Schüttler ◽  
Sabine Bergmann ◽  
Arnold Ganser ◽  
...  

Abstract Early rejection of xenogenic organs is associated with thrombotic microangiopathy and changes of coagulation resembling disseminated intravascular coagulation (DIC). Here, we used an ex vivo perfusion circuit as a model of pig-to-human kidney transplantation to study the nature and treatment of this pathology. Porcine kidneys were obtained following in situ cold perfusion with HTK organ preservation solution and immediately connected to a perfusion circuit containing porcine (“autologous”) or human (“xenogenic”) AB blood supplemented with complement component C1 inhibitor (1 U/ml) and heparin (1 U/ml). Perfusion of porcine kidneys with autologous blood was feasible for >240 min in all experiments. In contrast, perfusion of porcine kidneys with xenogenic human blood was limited by a dramatic increase of flow resistance after 30 to 240 min. Increased concentrations of C3a as a marker for complement activation were associated with early perfusion failure. In addition, a dramatic increase of thrombin-antithrombin complex (TAT) and D Dimer (DD) was observed together with consumption of platelets, fibrinogen and antithrombin (AT). Histological examination demonstrated extensive thrombotic microangiopathy. Supplementation recombinant human activated protein C (rhAPC, 300 ug/l*h, n=3) or recombinant human antithrombin (rhAT, 3 U/ml, n=3) abolished the increase of flow resistance and allowed for a xenogenic kidney survival of >240 min in all experiments. Increase of DD was abolished and the consumption of fibrinogen was abrogated by both treatments as compared to control, whereas the increase of TAT was abolished only by rhAPC. Histological examination revealed no evidence of thrombotic microangiopathy for both treatments as compared to control. In conclusion, the perfusion model introduced here is a suitable tool for studying coagulopathy during early rejection in xenotransplantation. Thrombotic microangiopathy and DIC-like activation of coagulation is associated with an increased flow resistance and failure of perfusion in this model. Pharmacological intervention such as the supplementation of rhAPC or rhAT can be studied using this model and has been shown to prevent coagulopathy and thrombotic microangiopathy.


2017 ◽  
Vol 16 (6) ◽  
pp. 89-92
Author(s):  
A.N. Strizhakov ◽  
◽  
E.V. Timokhina ◽  
I.V. Ignatko ◽  
D.N. Protsenko ◽  
...  

2007 ◽  
Vol 21 (2) ◽  
pp. 241-245 ◽  
Author(s):  
Érika B. Rangel ◽  
Adriano M. Gonzalez ◽  
Marcelo M. Linhares ◽  
Sérgio R.R. Araújo ◽  
Marcello F. Franco ◽  
...  

Author(s):  
Polina I. Kukina ◽  
Anastasiya V. Moskatlinova ◽  
Irina M. Bogomazova ◽  
Elena V. Timokhina

Thrombotic microangiopathy (TMA) is a clinical and morphological syndrome, which is based on damage of the endothelium. Clinically, TMA is characterized by a triad of symptoms: thrombocytopenia, microangiopathic hemolytic anemia, and target organ damage. In obstetric practice, TMA most often occurs with preeclampsia or HELLP syndrome, atypical HUS, TTP. The review presents the basic differential criteria for the diagnosis of TMA during pregnancy and after childbirth, as well as the management of patients.


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