Abstract
Background
Pregnancy-associated atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) caused by uncontrolled activation of the complement system during pregnancy or the postpartum period. In the intensive care unit, aHUS must be differentiated from sepsis-related multiple organ dysfunction, thrombotic thrombocytopenic purpura (TTP), hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. Early recognition of aHUS is critical for effective treatment and improved prognosis. Although tests such as the ADAMTS13 level, peripheral blood smears, complement testing, and blood cultures are useful for diagnosing aHUS, these tests are time-consuming and may not be widely available. This report describes a case of severe aHUS in a pregnant woman during the coronavirus disease 2019 (COVID-19) pandemic.
Case presentation
A 26-year-old patient with a history of four pregnancies and one delivery (P4G1) presented at 30 weeks and 2 days of gestation with vaginal fluid leakage and fetal growth restriction detected by ultrasound at a different hospital. During labor induction, the patient developed a high fever and coagulopathy, followed by heart failure, acute kidney injury, anemia, and severe thrombocytopenia. The patient remained alert and coherent, with no evidence of neurological dysfunction. She was transferred to our department and was given invasive respiratory support, blood transfusion, continuous renal replacement therapy, capacity management, and other comprehensive treatments. Due to the ongoing COVID-19 pandemic, ADAMTS13 testing and complement inhibitor therapy were unavailable. A diagnosis of pregnancy-associated aHUS was made based on the patient's history, clinical presentation, and standard laboratory results. The patient was prescribed 13 sessions of hemodialysis. Post-treatment evaluation showed normalized complement C3 and C4 levels, stabilized platelet and hemoglobin levels, and gradual normalization of liver function. Renal function improved gradually, and a bone marrow biopsy revealed no fragmented red blood cells. The patient was transferred to the Department of Nephrology on day 40 and back to the local hospital on day 42. The patient was followed up for 3 years, during which her renal function returned to normal, with no recurrence of thrombocytopenia or microangiopathic hemolytic anemia.
Conclusions
This case highlights the challenges and importance of diagnosing and managing pregnancy-associated aHUS and multiple organ failure in a low-resource setting.
Keywords: Atypical hemolytic uremic syndrome, Pregnancy, Differential diagnosis, Multiple organ dysfunction in sepsis, Thrombotic thrombocytopenic purpura (TTP), HELLP syndrome, Survival
Background
Atypical hemolytic uremic syndrome (aHUS) is a life-threatening disease caused by dysregulation of the complement system, leading to systemic thrombotic microangiopathy (TMA). aHUS manifests clinically as microangiopathic hemolytic anemia, thrombocytopenia, and kidney injury [1–3]. Pregnancy-associated aHUS resembles the thrombotic thrombocytopenic purpura (TTP), sepsis-associated multiple organ dysfunction, hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. These clinical similarities complicate the diagnosis and treatment of aHUS in the intensive care unit (ICU) [4, 5]. Pregnancy-associated aHUS can result in end-stage kidney disease and mortality. To date, there is no consensus on the diagnosis and treatment of aHUS in the ICU [4]. This report details the ICU management of a woman who developed fever, heart failure, acute kidney injury, anemia, and thrombocytopenia during pregnancy termination (induction). The patient was diagnosed with pregnancy-related aHUS in a multidisciplinary clinic and was treated in the ICU with integrated organ function management, continuous renal replacement therapy, and plasma exchange.
Case presentation
A 26-year-old P4G1 patient underwent pregnancy termination at 30 weeks and 2 days due to fetal growth restriction and premature rupture of membranes. Following the termination, the patient gradually developed fever, anemia, thrombocytopenia, acute kidney injury, and coagulation dysfunction. The patient was transferred to the ICU of a local hospital due to respiratory failure, acute diffuse intravascular coagulation, and multiple organ dysfunction. She received ventilator support, antimicrobial therapy, fluid resuscitation, cardiac support, vasopressors, anticoagulation, and blood transfusions. Although the patient had a history of chronic hepatitis B, her liver function and hepatitis B virus (HBV) DNA levels had not been monitored. She had no other underlying medical conditions or family history of related diseases. The patient had undergone a cesarean section in 2015, with no complications reported during that pregnancy. She was diagnosed with gestational diabetes during this pregnancy, which was managed through dietary control without the need for insulin. Blood glucose levels remained within the normal range during follow-up prenatal examinations. An ultrasound at 23 weeks showed the fetus was two weeks smaller than expected, while the placenta appeared normal. There were no reports of abdominal pain or diarrhea before admission. The results of some laboratory tests performed at the local hospital are shown in Fig. 1 and Table 1.
Fig. 1.
Hemoglobin, platelet and creatinine levels before being transferred to the ICU at the local hospital. The horizontal axis shows the duration of pregnancy termination by drug injection
Table 1.
Blood tests at the local hospital
Admission | Day 3 (ICU) | Day 4 | Day 5 | D,ay 6 | Day7 | Day 8 | Day 9 | |
---|---|---|---|---|---|---|---|---|
PLT*109/L | 214 | 25 | 26 | 5 | 9 | 8 | 25 | 48 |
INR | 0.85 | 1.65 | 2.32 | 1.41 | 1.32 | 1.44 | 1.36 | 1.31 |
APTTs | 28.7 | 61.3 | 134 | 46.8 | 43 | 63.8 | 150 | 91.2 |
PT s | 10.1 | 19.7 | 27.8 | 16.8 | 17.2 | 15.6 | ||
TTs | 15.7 | 24.6 | 29.5 | 17.5 | 1·9.1 | 1–8.2 | ||
Fib g/L | 3.4 | 1.24 | 0.98 | 2.74 | 4.31 | 3.4 | 2.39 | 2.69 |
DD ug/ml | 1.8 | 22.7 | 12.6 | 19.6 | 2.58 | |||
Cr· umol/L | 38 | 230 | 278 | 136 | 71 | 54.8 | 75.9 | 68.2 |
BUN mmol/L | 2.7 | 4.09 | 7.26 | 6.1 | 4.1 | 3.6 | 5.2 | 4.72 |
TBIL umol/L | 8.4 | 8.9 | 15.6 | 60.5 | 74.6 | 53.8 | 34 | 16.1 |
AST U/L | 27.8 | 119 | 465 | 406 | 419 | 271 | 190 | 169 |
ALT U/L | 18 | 24 | 109 | 143 | 184 | 152 | 95.7 | 123 |
PLT platelet, INR international normalized ratio, APTT activated partial thromboplastin time, PT prothrombin time, TT thrombin time, Fib fibrinogen, DD d dimer, Cr creatinine, BUN blood urea nitrogen, AST aspartate aminotransferase, ALT alanine aminotransferase
The patient was transferred from the local hospital to the ICU of our hospital in critical condition on day 7 post-pregnancy termination. Upon ICU admission, her body temperature was 34.4℃, with a heart rate of 104 beats per minute, and a blood pressure of 111/66 mmHg (norepinephrine 0.4 μg⋅kg−1⋅min−1). She remained on ventilator support under sedation and analgesia, showing severe eyelid and bulboconjunctival edema, reduced bilateral respiratory sounds, and no rales. Apart from ventilator-assisted breathing, the patient received antimicrobial therapy, vasopressors, transfusions, continuous renal replacement therapy, heparin anticoagulatory treatment, and other supportive measures. A multidisciplinary consultation on day 3 considered the diagnoses of septicemia-related multiple organ dysfunction, TTP, HELLP syndrome, and aHUS. Due to the COVID-19 pandemic, measurement of ADAMTS13 activity and genetic testing were unavailable; instead, analysis of peripheral blood smears was performed to assess the presence of fragmented red blood cells.
On day 4, the results of stool and blood cultures, autoantibody tests, the Coombs test, hepatitis B DNA, and cervical secretion culture were all negative. Her peripheral blood smear showed the presence of fragmented red blood cells and decreased levels of complement C3 and C4. The pelvic computed tomography (CT) scan showed no intrauterine infection. aHUS was confirmed as the final diagnosis, and the patient underwent plasmapheresis without anti-complement therapy. Following treatment, her vital signs improved. The antibiotic therapy was discontinued, and the patient underwent three consecutive plasma exchanges based on her clinical needs.
On day 8 after admission, the patient's blood pressure and hemoglobin level decreased, and her abdominal tension increased. Abdominal ultrasound revealed a large hematoma above the bladder. Computed tomography angiography (CTA) and digital subtraction angiography (DSA) confirmed the presence of a pelvic hematoma and multiple ruptures in the left femoral artery. A stent was implanted in the left femoral artery, and the abdominal hematoma was removed. The patient received antimicrobial therapy post-surgery.
The patient subsequently underwent nine sessions of plasma exchange, along with intermittent hemofiltration, blood transfusions, and additional treatments. Her condition improved and a bone marrow biopsy showed no fragmented red blood cells. The C3, C4, and platelet levels returned to normal, the hemoglobin remained stable, and the urine output increased to 1300 mL/day. With clinical and biological improvement, the patient was transferred to the general ward on day 40 and returned to the local hospital on day 42 (Tables 2 and 3).
Table 2.
Laboratory tests during our ICU
Day 1 | Day 2 | Day 3 | Day 4 | Day 5 | Day 6 | Day 7 | Day 8 | Day9 | |
---|---|---|---|---|---|---|---|---|---|
Hb g/L | 75 | 83 | 77 | 90 | 88 | 88 | 81 | 68 | 74 |
PLT*109/L | 33 | 25 | 48 | 45 | 42 | 47 | 97 | 224 | 97 |
WBC *109/L | 23.4 | 16.1 | 21.2 | 22.7 | 19 | 18.2 | 21.7 | 36.7 | 17.3 |
PCT ng/ml | 27.8 | 22.9 | 10.9 | 15.8 | 14.7 | 7.6 | 9.95 | 45.8 | |
IL-6 pg/ml | 43.1 | 104.5 | 195 | 282.6 | 313.8 | 204 | 178 | ||
CRP mg/L | 65.5 | 106.6 | 121.1 | 141.9 | 131.9 | 131 | 100 | ||
Adr ug/kg/min | 0.6 | 0.15 | 0.1 | 0.15 | 0.3 | ||||
NA ug/kg/min | 1.25 | 0.3 | 0.6 | 0.4 | 0.4 | 0.2 | 0.15 | 1.8 | 0.5 |
PO2/FiO2 | 216 | 402 | 369 | 342 | 403 | 407 | 470 | 356 | 370 |
Lac mmol/L | 2.4 | 1.6 | 1.7 | 1.2 | 0.6 | 0.6 | 0.7 | 5.7 | 1.5 |
INR | 1.36 | 1.21 | 1.07 | 1.05 | 0.98 | 0.99 | 0.94 | 1.19 | 1.08 |
APTT s | 238 | 58.4 | 46.7 | 83.8 | 71.1 | 81 | 60.5 | 31.9 | 56.7 |
Fib g/L | 1.93 | 2.87 | 3.33 | 4.09 | 3.59 | 3.5 | 3.29 | 2.46 | 2.67 |
Cr umol/L | 94.9 | 155.4 | 144.2 | 146.5 | 142.8 | 172.4 | 182.1 | 295.7 | 177.9 |
BUN mmol/L | 3.17 | 9.2 | 10.5 | 11.5 | 9.71 | 11.9 | 13.9 | 18.17 | 16.83 |
TBIL umol/L | 29.8 | 29.1 | 34.1 | 37.9 | 31.8 | 51.2 | 28.6 | 27.9 | |
LDH U/L | 1933 | 1753.6 | 847 | 837 | 799 | 984.7 | |||
AST U/L | 382.7 | 580.7 | 540 | 276.7 | 115 | 65.8 | 51.2 | 97.2 | |
ALT U/L | 117.4 | 121.4 | 106.9 | 77.4 | 42 | 0.1 | 28.6 | 30.6 | |
BNP pg/ml | > 5000 | > 5000 | > 5000 | > 5000 | 3330 | 3392 | 2980 | ||
Myo ug/L | > 3000 | > 3000 | > 3000 | 1580 | 712.9 | 571.3 | |||
Hypersensitive | |||||||||
troponin ug/L | 0.215 | 0.406 | 0.386 | 0.399 | 0.313 | ||||
fragmented RBC | 3% | 1.2% | 1.1% | 0.2% | |||||
C3/C4 g/L | 0.43/0.11 |
ICU intensive care unit, Hb hemoglobin, PLT platelet, WBC white blood cell, PCT procalcitonin, CRP c -reactive protein, INR international normalized ratio, APTT activated partial thromboplastin time, PT prothrombin time, TT thrombin time, Fib fibrinogen, DD d dimer, Cr creatinine, BUN blood urea nitrogen, AST aspartate minotransferase, ALT alanine aminotransferase, NA noradrenaline, Adr adrenaline, Myo myoglobin, Lac lactate, BNP brain natriuretic peptide, C3/C4 complement3/complement4, RBC red blood cell, LDH lactate dehydrogenase
Table 3.
Laboratory tests during our ICU
Day 11 | Day 13 | Day 15 | Day 17 | Day 20 | Day 24 | Day 28 | Day 32 | Day35 | Day 40 | |
---|---|---|---|---|---|---|---|---|---|---|
Hb g/L | 88 | 83 | 74 | 74 | 80 | 75 | 57 | 76 | 77 | 86 |
PLT*109/L | 68 | 89 | 94 | 182 | 238 | 211 | 139 | 98 | 117 | 137 |
WBC *109/L | 8.38 | 7.89 | 11.11 | 14.2 | 11.12 | 8.23 | 8.42 | 8.02 | 9.49 | 6.2 |
PCT ng/ml | 36.15 | 17.88 | 5.52 | 14.08 | 6.61 | 3.26 | 2.93 | 1.93 | ||
IL-6 pg/ml | 174.1 | 111.4 | 130.6 | 24.91 | 38.2 | 138.3 | 113.6 | 72.85 | ||
CRP mg/L | 125.3 | 76.17 | 69.42 | 59.23 | 21.99 | 29.67 | 117 | 119 | 73.37 | |
Cr umol/L | 130.6 | 200.1 | 232.5 | 278.4 | 626 | 454.6 | 685 | 300 | 223.3 | 320.3 |
BUN mmol/L | 15.5 | 16 | 17.34 | 17.4 | 35.1 | 21.96 | 20.71 | 10.77 | 10.12 | 11.5 |
Urine ml | 140 | 480 | 540 | 760 | 1080 | 1150 | 1390 | 1300 | ||
AST U/L | 43.6 | 27.9 | 30.1 | |||||||
ALT U/L | 37.8 | 27.3 | 20.4 | |||||||
Myo ug/L | 1787 | 536 | ||||||||
BNP pg/ml | 1932 | 1182 | 1382 | 856 | ||||||
C3/C4 g/L | 0.74/0.22 | 0.8/0.22 |
The patient began to perform off-ventilator training on day13, she got off the ventilator and extubation on day18
Due to economic conditions, the patient was unable to return to the hospital for follow-up laboratory tests. After over three years of follow-up, the patient's renal function returned to normal, with no recurrence of thrombocytopenia or microangiopathic hemolytic anemia.
Discussion
aHUS, a rare variant of TMA, is caused by endothelial cell dysfunction and microvascular thrombosis resulting from dysregulation of the complement system [6]. Approximately 10–20% of aHUS cases occur during pregnancy, termed pregnancy-associated aHUS [7, 8]. Distinguishing p-aHUS from sepsis-related multiple organ dysfunction, TTP, and HELLP syndrome is challenging due to their similar clinical manifestations [4, 5, 8].
In this case, following a medically induced pregnancy termination, the patient gradually developed fever, anemia, thrombocytopenia, coagulopathy, and acute kidney injury. Given the premature rupture of membranes and the risk of infection, sepsis-related multiple-organ dysfunction could not be ruled out. However, despite active antimicrobial treatment and repeated negative bacterial and blood cultures, the patient's condition did not improve. Therefore, the multiple organ dysfunction was attributed to alternative underlying disease(s). The patient had no history of hypertension, diabetes, or chronic kidney disease. Although she had been diagnosed with gestational diabetes during the current pregnancy, she did not present with abdominal pain or diarrhea upon admission. HELLP syndrome, aHUS, and TTP were the primary differential diagnoses. The presentation of sudden anemia, thrombocytopenia, elevated liver enzymes, and renal insufficiency suggested a possible diagnosis of HELLP syndrome. Typically, kidney function recovers gradually after delivery [9, 10]; however, this patient's renal function showed no improvement. Thus, HELLP syndrome was considered less likely, and TMA was strongly suspected.
Pregnancy-related aHUS is an acute, life-threatening condition primarily affecting the kidneys and can result in morbidity and mortality if untreated [7, 11]. TMA can be categorized into TTP, hemolytic uremic syndrome (HUS), and aHUS. TTP typically presents with fever, mild renal insufficiency, severe thrombocytopenia, and neurological involvement. HUS is more common in children, and most cases are associated with Shiga toxin infection, usually within 1–2 weeks post-infection. Progressive kidney deterioration without neurological involvement strongly suggests aHUS [9, 12]. It is possible to differentiate between TTP and aHUS by measuring ADAMTS13 activity and complement assessments [4, 5]. In this case, tests for ADAMTS13 activity were unavailable due to the COVID-19 pandemic; however, the patient exhibited no abdominal pain or diarrhea before disease onset. Furthermore, there was progressive renal deterioration with no neurological abnormalities after disease onset. Based on these findings, the team diagnosed the patient with pregnancy-related aHUS.
The current international consensus on aHUS states that its clinical presentation and management are consistent, regardless of whether it is inherited, acquired, or of unknown etiology. Complement inhibitors, such as eculizumab, have been approved by the FDA for effective aHUS treatment [7, 13]. A systematic review of English-language articles by Megha Gupta et al. on aHUS during pregnancy or postpartum found that patients with first-episode pregnancy-related aHUS who were treated with eculizumab had a significantly higher remission rate (88%) compared to those who did not receive eculizumab (57%, P = 0.02) [7]. Unfortunately, eculizumab is costly and not easily accessible, and reimbursement for its use may not be available in the current healthcare system [7, 13–15]. Thus, the current consensus recommends immediate plasma exchange upon aHUS diagnosis in centers where complement inhibitors are unavailable [4–6, 14, 15].
Although plasma exchange has reduced the mortality rate of aHUS from 50 to 25%, approximately 67% of adult patients still die or progress to end-stage renal failure within a 3-year follow-up period [11, 16–18]. After effective organ function support and plasma exchange, the patient was transferred from the ICU to the general ward. After three years of follow-up, her renal function had returned to normal, with no recurrence of thrombocytopenia or microangiopathic hemolytic anemia.
Clinical data and treatment experiences related to pregnancy-associated aHUS remain limited. This case report highlights the importance of prompt identification and management of aHUS, including respiratory and circulatory support, organ function maintenance, nutritional support, and multidisciplinary care.
Conclusion
The diagnosis of pregnancy-associated aHUS is challenging [18, 19]. Biological tests, such as ADAMTS13 activity, C3b, factor H, and genetic analyses, can aid in diagnosis; however, a lack of resources can often restrict the availability of these tests, delaying patient management [5, 20]. Current studies have shown that serum creatinine, platelet count, and anti-nuclear antibody values can assist in the diagnosis of aHUS with high specificity (98.1%) but low sensitivity (46.9%) [21–23]. Therefore, patient history and clinical manifestations should be carefully evaluated in the diagnosis of aHUS, although additional data are needed to improve diagnostic accuracy.
Authors’ contributions
Y. Y. and X.L. conceived the case report, wrote, translated and revised the manuscript. H.Y. and J.X. contributed to the drafting and data analysis of the manuscript. P.L. and Z.W. assisted with drafting, translation and revision of the manuscript. All authors have read and approved the final manuscript.
Funding
This work was supported by the Chongqing Medical Key Discipline Development Project (No.zdxk202102).
Data availability
Data is provided within the manuscript.
Declarations
Ethics approval and consent to participate
The study has been approved by the Committee of Research Ethics of Army Medical Center of PLA, and informed consent was obtained from the relative of the patient.
Consent for publication
Written informed consent for publication of the clinical details were obtained from the relative of the patient.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Yan Yang and Xiao-jin Li are co-first author.
Contributor Information
Peng-Fei Li, Email: dplipengfei@tmmu.edu.cn.
Zhen Wang, Email: dpicuwz@tmmu.edu.cn.
References
- 1.Pishko AM, Levine LD, Cines DB. Thrombocytopenia in pregnancy: Diagnosis and approach to management. Blood Rev. 2020;40:100638. [DOI] [PubMed] [Google Scholar]
- 2.Catarci S, et al. A case report of an atypical haemolytic uremic syndrome in pregnancy: something wicked this way comes. BMC Anesthesiol. 2023;23(1):94. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Yoshida Y, et al. Pathogenesis of atypical hemolytic uremic syndrome. J Atheroscler Thromb. 2019;26(2):99–110. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Azoulay E, et al. Expert statements on the standard of care in critically ill adult patients with atypical hemolytic uremic syndrome. Chest. 2017;152(2):424–34. [DOI] [PubMed] [Google Scholar]
- 5.Gaggl M, et al. Thrombotic microangiopathy: relevant new aspects for intensive care physicians. Med Klin Intensivmed Notfmed. 2016;111:434–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Fakhouri F, Schwotzer N, Frémeaux-Bacchi V. How I diagnose and treat atypical hemolytic uremic syndrome. Blood J Am Soc Hematol. 2023;141(9):984–95. [DOI] [PubMed] [Google Scholar]
- 7.Gupta M, Govindappagari S, Burwick RM. Pregnancy-associated atypical hemolytic uremic syndrome: a systematic review. Obstet Gynecol. 2020;135(1):46–58. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Bruel A, et al. Hemolytic uremic syndrome in pregnancy and postpartum. Clin J Am Soc Nephrol. 2017;12(8):1237–47. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Gupta M, Feinberg BB, Burwick RM. Thrombotic microangiopathies of pregnancy: Differential diagnosis. Pregnancy Hypertens. 2018;12:29–34. [DOI] [PubMed] [Google Scholar]
- 10.Fang CJ, et al. Advances in understanding of pathogenesis of aHUS and HELLP. Br J Haematol. 2008;143(3):336–48. [DOI] [PubMed] [Google Scholar]
- 11.Huerta A, et al. A retrospective study of pregnancy-associated atypical hemolytic uremic syndrome. Kidney Int. 2018;93(2):450–9. [DOI] [PubMed] [Google Scholar]
- 12.Choi HS, et al. Atypical hemolytic uremic syndrome after childbirth: a case report. Ann Transl Med. 2021;9(1):79. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Noris M, Mescia F, Remuzzi G. STEC-HUS, atypical HUS and TTP are all diseases of complement activation[J]. Nat Rev Nephrol. 2012;8(11):622–33. 10.1038/nrneph.2012.195. [DOI] [PubMed] [Google Scholar]
- 14.Basnayake BMDB, et al. Atypical hemolytic uremic syndrome: a case report. J Med Case Reports. 2020;14:1–5. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Jokiranta TS. HUS and atypical HUS. Blood J Am Soc Hematol. 2017;129(21):2847–2856. [DOI] [PMC free article] [PubMed]
- 16.Noris M, et al. Relative role of genetic complement abnormalities in sporadic and familial aHUS and their impact on clinical phenotype. Clin J Am Soc Nephrol. 2010;5(10):1844–59. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Michael M, et al. Interventions for hemolytic uremic syndrome and thrombotic thrombocytopenic purpura: a systematic review of randomized controlled trials. Am J Kidney Dis. 2009;53(2):259–72. [DOI] [PubMed] [Google Scholar]
- 18.Scully M, Goodship T. How I treat thrombotic thrombocytopenic purpura and atypical haemolytic uraemic syndrome. Br J Haematol. 2014;164(6):759–66. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Tshilanda M, et al. Diagnostic dilemma in postpartum associated hemolytic uremic syndrome in a 38th week pregnant 31-year-old Congolese: a case report. BMC Pregnancy Childbirth. 2020;20:1–6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Ouzeddoun N, et al. Le syndrome hémolytique et urémique à propos de 50 cas. Médecine de Magrheb. 1997;63:21–6. [Google Scholar]
- 21.Dierickx D, et al. Thrombotic Microangiopathy Following Intestinal Transplantation: A Single Center Experience. Transplant Proc. 2010;42(1):79-81. [DOI] [PubMed]
- 22.Asif A, Vachharajani T, Salman L, et al. A simplified approach to the diagnosis of atypical HUS: clinical considerations and practical implications. Open Urol Nephrol J. 2014;7(1):91–4.
- 23.Raina R, et al. Atypical hemolytic-uremic syndrome: an update on pathophysiology, diagnosis, and treatment. Ther Apher Dial. 2019;23(1):4–21. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data is provided within the manuscript.