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ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

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Kidney Week

Abstract: PO0182

Postpartum Thrombotic Microangiopathy of Unknown Etiology: Is It Too Late to Save the Kidneys?

Session Information

  • AKI Mechanisms - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 103 AKI: Mechanisms


  • Guirguis, John Kimy Demian, Indiana University School of Medicine, Indianapolis, Indiana, United States
  • Sher, S. Jawad, Indiana University School of Medicine, Indianapolis, Indiana, United States
  • Doshi, Simit, Indiana University School of Medicine, Indianapolis, Indiana, United States

Thrombotic microangiopathy (TMA) is a rare (0.004%) but life threatening complication in pregnancy. Differentials include uncontrolled hypertension, Hemolysis elevated liver enzymes low platelet count (HELLP) syndrome, atypical Hemolytic Uremic Syndrome (HUS), Thrombotic Thrombocytopenic Purpura (TTP) among others. Lack of randomized trials and absence of gold standard laboratory tests can make diagnosis and treatment challenging. We present a patient with post-partum TMA confirmed on renal biopsy with no conclusive etiology identified.

Case Description

A 36 years old African American patient, G7P5 with history of Hypertension (HTN) and preeclampsia was noted to have blood pressure elevated to 180/103 mmHg during an antenatal care visit at 36 weeks of gestation. Serum Creatinine (sCr) was 0.5mg/dl with urine protein/Cr ratio (UPCR) of 0.75 g/g. She had an induced labor with persistent HTN postpartum. She left against medical advice and was readmitted 10 days later with acute kidney injury (AKI) with sCr of 6 mg/dl and UPCR was 4g/g, urinalysis showed positive protein but no RBCs. BP was elevated to 143/97 mmHg/ Laboratory data showed AST 33 U/L, ALT 24 U/L, Hb 9.5 g/dL, platelet counts 211 X109/L, C3 of 74 mg/dL, C4<2 mg/dL, negative ANA, ADAMTS 13 >94, Cryo results was inconclusive although RF was elevated at 160 IU/mL. Blood smear showed no schistocytes. She was started on pulse steroids for clinical suspicion of eclampsia related TMA. While awaiting biopsy therapeutic plasma exchange (TPE) was initiated, it was stopped after 3 sessions. Kidney biopsy on day 12 of delivery showed TMA, with negative immune-florescence (IF), minimal interstitial fibrosis/tubular atrophy, focal 2/15 glomerular crescents and minimal arterial intimal thickening. Patient became progressively oliguric, requiring hemodialysis. At the time of writing this report, there has been no recovery at 4 weeks as patient remains oliguric on thrice weekly dialysis.


Peri-partum care is crucial in early detection and prompt management of TMA in patients with pre-eclampsia/Eclampsia. Benefit of TPE in post-partum period is not well established. A kidneybiopsy was obtained but the diagnosis remained elusive with negative IF in setting of reduced complement levels. Further studies should evaluate treatment strategies in the late-presenting patient to avoid irreversible kidney injury.