March31, 2023

Abstract Volume: 4 Issue: 1 ISSN:

A Rare Case: Acute Kidney Injury in Pregnancy with Pre-Existing Aortic Stenosis
Dr Deepa Pai Nadkarni1*, Dr Sujatha Kumari2, Dr Srividhya Budithi3 #

1. Junior Clinical fellow –Wrexham Maelor Hospital.

2,3. Consultant- Wrexham Maelor Hospital.

Corresponding Author: Dr Deepa Pai Nadkarni, Junior Clinical fellow –Wrexham Maelor Hospital

Copy Right: © 2022 Dr Deepa Pai Nadkarni, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received Date: October 17, 2022

Published Date: November 01, 2022

DOI: 10.1027/margy.2022.0180




AKI- Acute Kidney Injury

HELLP- Hemolysis Elevated liver enzymes and Low platelets

AFLP- Acute fatty liver of pregnancy

P-TMA- Pregnancy associated thrombotic microangiopathies.

A Rare Case: Acute Kidney Injury in Pregnancy with Pre-Existing Aortic Stenosis


Acute kidney injury (AKI) that occurs during pregnancy or in the post-partum period is a serious obstetric complication with an increased risk of maternal and fetal morbidity and mortality. First trimester causes of AKI in pregnancy include hyperemesis gravidarum and septic abortion. In the third trimester causes such as preeclampsia, acute fatty liver of pregnancy, HELLP syndrome, and the thrombotic microangiopathies (thrombotic thrombocytopenic purpura, atypical hemolytic uremic syndrome) exhibit overlapping features and often present as a diagnostic dilemma.[1,2] Clinical judgment and experience along with laboratory investigations become paramount in making an accurate diagnosis.[3,4]

Case Presentation

A 26-year-old primigravida with a known case of aortic stenosis with bicuspid aortic valve, who presented at 39+4 weeks of gestation with headache and generalised oedema. Examination findings and laboratory investigations(on admission) were otherwise normal except for raised blood pressure, 2+ proteins in urine and raised PCR(PCR=150). She was started on anti-hypertensive medication on admission. Her past surgical history was significant as she underwent 2 aortic balloon valvoplasty and then Ross procedure for aortic stenosis. She was offered induction of labour for premonitory symptoms and raised blood pressure after detailed counselling.

Intrapartum, she developed oliguria, and she was catheterised to monitor urine output. Her observations (vitals) were otherwise fine and no sign of dehydration and CTG was suggestive of fetal tachycardia. Initially she was encouraged to have oral fluids, later was given IV fluids as fluid challenge, inspite of this she had less than 25cc urine in 4 hours. The fetal tachycardia settled later on. After senior review all blood investigations repeated again, which revealed rising creatinine and decreasing eGFR. After 30 minutes from last review, she developed hematuria. Her total urine output was less than 50cc in 7hours. Diagnosis of Acute Kidney Injury was made and she was urgently assessed by the medical team and the anaesthetist. After multidisciplinary team review, decision was taken for Category 2 caesarean section. The caesarean section was uneventful, and baby cried immediately after birth, and blood loss at caesarean was 500ml. Post-delivery her urine output and laboratory investigations improved. She was kept on close monitoring and baby and mother were discharged 5 days later with a plan for follow-up.



We observed that preeclampsia/eclampsia is the most common cause of AKI in late third trimester and postpartum periods followed by puerperal sepsis and postpartum hemorrhage [5]. Preeclampsia is a multi- organ disorder characterized by systemic hypertension and renal, hepatic, and cerebral vascular pathology.

These clinical manifestations are consistent with widespread endothelial dysfunction, vasoconstriction, and end-organ ischemia. Abnormal placental angiogenesis during pregnancy resulting from high levels of the anti-angiogenic factors, soluble fms-like tyrosine kinase and soluble endoglin, has been implicated in preeclampsia.[7] Redman et al. have suggested that preeclampsia is an extreme end of a continuous spectrum of inflammatory responses that are a feature of pregnancy itself [8]. This hypothesis is also supported by studies that demonstrate that when a single dose of endotoxin or interleukins is given to pregnant animals, they manifest clinical features of preeclampsia, but not the controls[9.10]. The treatment of AKI in pregnancy is generally supportive, often coupled with expedient delivery, especially when diagnosis is severe preeclampsia, AFLP or HELLP[6]. Given the recent trends of increasing maternal age at the time of pregnancy, as well the availability of modern reproductive methods both of which may be associated with significant co-morbidities, the issues surrounding AKI in pregnancy may become more relevant in the coming years.



  1. Prakash J, Kumar H, Sinha DK, Kedalaya PG, Pandey LK, Srivastava PK, et al. Acute renal failure in pregnancy in a developing country: Twenty years of experience. Ren Fail. 2006;28:309–13. [PubMed] [Google Scholar]
  2. Jayakumar M, Prabahar MR, Fernando EM, Manorajan R, Venkatraman R, Balaraman V. Epidemiologic trend changes in acute renal failure – A tertiary center experience from South India. Ren Fail. 2006;28:405–10. [PubMed] [Google Scholar]
  3. Selcuk NY, Tonbul HZ, San A, Odabas AR. Changes in frequency and etiology of acute renal failure in pregnancy (1980-1997) Ren Fail. 1998;20:513–7. [PubMed] [Google Scholar]
  4. Kumar KS, Krishna CR, Kumar VS. Pregnancy related acute renal failure. J Obstet Gynaecol India. 2006;56:308–10. [Google Scholar]
  5. Huang, C., Chen, S. Acute kidney injury during pregnancy and puerperium: a retrospective study in a single center. BMC Nephrol 18, 146 (2017). 0551-4
  6. Guntupalli SR, Steingrub J. Hepatic disease and pregnancy: An overview of diagnosis and management. Crit Care Med. 2005;33(10 Suppl):S332–[PubMed] [Google Scholar]
  7. Bdolah Y, Skhatme VP, Karumanchi SA. Angiogenic imbalance in the pathophysiology of preeclampsia: Newer insights. Semin Nephrol. 2004;24(6):548– 556.
  8. Redman CW, Sacks GP, Sargent IL. Preeclampsia: An excessive maternal inflammatory response to pregnancy. Am J Obstet Gynecol. 1999;180:499–506.
  9. Faas MM, Schuling GA, Baller JF, Visscher CA, Bakker WW. A new animal model for human preeclampsia: Ultra low dose endotoxin infusion in pregnant rats. Am J Obstet Gynecol. 1994;171:158–164.
  10. Hayakawa S, Fujikawa T, Fukuoka H, et al. Murine fetal resorption and experimental preeclampsia are induced by both excessive Th1 and Th2 activation. J Reprod Immunol. 2000;41:121–138.


Figure 1

Figure 2