Post-Partum Acute Kidney Injury: A case report

Jaisha

Nursing Supervisor, Kauvery Hospital, Hosur, Tamil Nadu

Introduction

Pregnancy Associated Acute Kidney Injury (PRAKI) is a serious complication following childbirth that involves a sudden loss of kidney function. It is caused by conditions like severe HELLP, postpartum hemorrhage, atypical HUS, acute pyelonephritis, SLE and sepsis. PRAKI is associated with significant risks for both mother and baby, including chronic kidney disease and cardiovascular issues. Diagnosis is based on elevated serum creatinine levels, decreased urine output and other symptoms, with early detection and management being crucial for improving outcomes.

We had two young patients who had postpartum AKI, we successfully transplanted one patient who did well and the other patient stopped the dialysis.

Case Presentation

Case 1

A 19 years old female patient whose obstetrical score was P1L1, no history of pre-eclampsia, had LSCS on 25/2/25 for fetal indication (low birth weight). On 3rd day of post LSCS, patient developed jaundice, oliguria and hypertension, excessive vaginal bleeding for which she had blood transfusion. She was received to rule out Acute Kidney Injury.  On evaluation creatinine: 6.5mg/dl; urine routine:  protein 1+, RBC 8-10/HPF   USG abdomen:  Bilateral normal sized kidneys, normal liver.

The differential diagnosis at this stage were: HELLP, AFLP, atypical HUS/TTP, sepsis induced ATN, obstructive uropathy.

She underwent hemodialysis for elevated creatinine and subsequently renal biopsy on 12/3/25. Renal biopsy report revealed 10 glomeruli, no global sclerosis, patchy cortical necrosis 10% to 20% and 5 glomeruli in necrotic areas. In addition, fibrin thrombi in afferent arterioles and focal lymphocytic infiltration in interstitium was seen. Impression was thrombotic microangiopathy with cortical necrosis.

She was an orphan and was being taken care by her maternal aunt, hence had financial constraints for treatment.

The differential diagnosis for this biopsy finding:

  • Complement mediated TMA,
  • ADAMTS 13 associated TMA,
  • HELLP,
  • Accelerated hypertension induced TMA, and
  • Drug induced TMA, APS

Based on biopsy findings she was initiated on plasma exchange; she had 4 sessions of plasma pheresis from 14/3/25. Genetic testing for complement mutations has been sent. Patient did not have improvement in renal function and haemodialysis was continued. She skipped dialysis for 3 weeks in 7/4/25. She had seizures with accelerated hypertension, therefore shifted to St’Johns hospital and treated with antiepileptics, at the same time dialysis was also initiated through IJV and PRBC transfusion done. USG on 7/4/25 revealed bilateral small rigid kidneys. She was declared dialysis dependent and was asked to continue haemodialysis and construct an AV Fistula.The patient presented to kauvery hospital Hosur on 8/5/25 for continuation of maintenance haemodialysis with zero hope of renal recovery. She was depressed about herself and the baby. USG showed bilateral small kidneys. However, we did not give up here. The genetic mutation was ready but did not reveal any evidence of complement mediated mutations. Hence further complement work up was sent which included anti CFH, CFH levels, ADAMTS 13 level and Anti ADAMTS 13, for which anti CFH was found to be positive. Hence diagnosed as complement mediated TMA- Anti CFH associated.

Treatment for anti CFH associated TMA:

As patient had already received plasmapheresis. Due to affordability issues Inj.Rituximab was not given and started on pulse doses of steroids with MMF. Following the treatment her creatinine stabilised at 3.2mg/dL and was off haemodialysis. She was  followed up here with good outcome. Now she is looking after her baby and can continue her daily activities without any morbidities. With the availability of recent advances with proper work up and treatment, it was possible to get her out of dialysis and provide effective life.

Case 2

A 24 years old female primi gravida, who never had any antenatal follow-up during her entire pregnancy period, was admitted in Shimoga GH on 15/4/24 with leaking PV. She had a vaginally delivered IUD. Patient had history of fever, foul smelling lochia and increased blood pressures post-delivery. She had anaemia and anuria, when she was found to have elevated creatinine level 5.5mg/dl, procalcitonin-125, urine routine: +protein for which 1 session of saline dialysis was done.

In this case, the most likely differential diagnosis would be

  • Septicemia from puerperal sepsis (foul lochia + fever)
  • Hypertensive disorder- related AKI (postpartum pre-eclampsia/HELP)
  • Postpartum hemorrhage leading to ischemic ATN/cortical necrosis)
  • Thrombotic microangiopathy (Postpartum HUS)

Therefore, she was treated with antibiotics, 4 units of FFP and 1 unit of PRBC. She was initiated on haemodialysis and renal biopsy was done which revealed acute cortical necrosis (17/5/2024). She was abandoned by her husband, as she became dialysis dependent.

Differential diagnosis

She came to our hospital for further management. She was found to have bilateral small kidneys with creatinine 8mg/dL. She was worked up for atypical HUS including anti CFH, CFH levels and ADAMTS13 levels and anti ADAMTS 13. ADAMTS 13 level was found to be mildly deficient which was attributed to sepsis. Subsequently patient was planned for live related renal transplant and started work up for ABO compatible transplantation with her mother as prospective donor. She was admitted on 19/7/25 and transplanted on 21/7/25 successfully. During hospitalization, her creatinine level gradually came down from 7.8 to 0.6. In addition, her TAC level was maintained within the limit and good urine output.

During discharge, she was advised to follow doctors order. Post-transplant she had healthy weight gain with good appetite and remarkable improvement in her quality of life. She is going to pursue her dream job of becoming a health inspector this October. This transplant has given her a second life, a ray of hope and smile on the faces of her family members.

Discussion

Pregnancy Associated Acute Kidney Injury is a different entity with pregnancy associated TMA a heterogenous disorder with unique diagnostic challenges. We have two patients who have been successfully treated one with complement mediated TMA and the other with acute cortical necrosis. Identifying the specific form of p-TMA is critical for appropriate and timely management. There is no established best treatment for FH auto antibodies. A combination of many different therapies has been used and reported over the years in nonpregnant patients. These include PLEX, eculizumab, prednisone, rituximab, and cyclophosphamide. In our experience, none of these therapies by themselves have been effective in removing FH autoantibodies. A combination of PLEX and steroids has sometimes helped with decreasing auto Ab titers. Also, in a subset of kidney transplant patients, the auto antibody titers declined after being on maintenance immunosuppression for 6 to 24 months. For pregnancy and postpartum, however, the options are very limited.

Pregnancy is considered as physiological phenomenon, but the incidence of several types of pregnancy associated TMAs makes us raise a question of it’s physiology. The onset of renal failure and then dialysis was devastating for a female who has already undergone the stress of bearing a child and underwent delivery process. The lack of understanding and support by the family members during her suffering needs a change in this society. As we all know female are less likely to receive a kidney when affected with end stage renal disease, but female contribute 80% of renal donors in our society. The story of our patients is a call to address the invisible barriers faced by countless women.

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