ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: SA-PO079

Kidney Prostaglandin Synthesis Alterations in a Case of NSAID-Induced AKI: A Clinical Pathologic Molecular Correlation

Session Information

  • AKI: Mechanisms - III
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Menez, Steven, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Knight, Richard A., American Association of Kidney Patients, Tampa, Florida, United States
  • Rosenberg, Avi Z., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Parikh, Chirag R., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Rovin, Brad H., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Parikh, Samir V., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Group or Team Name

  • KPMP
Introduction

The Kidney Precision Medicine Project (KPMP) seeks to establish a molecular atlas of the kidney in health and disease, to improve the understanding of molecular drivers of kidney disease. We describe the case of a woman who underwent a kidney biopsy in the setting of acute kidney injury (AKI) as part of the KPMP, with associated tissue proteomics.

Case Description

A 38-year-old woman with no significant medical history (baseline serum creatinine (sCr) 0.7-0.8 mg/dL), presented at 36 weeks gestation with premature rupture of membranes. She underwent successful cesarean section delivery. On post-operative day (POD) 0, she received 3 doses of the non-steroidal anti-inflammatory drug (NSAID) ketorolac (15 mg) intravenously, transitioned to oral ibuprofen 800 mg every 6 hours. She was discharged on POD 4, but presented to the emergency room the next day with new onsent fatigue. Labs were notable for a sCr of 2.3 mg/dL, peaking at 3.7 on POD 7. Clinical adjudication determined the likely etiology of AKI to be associated with NSAID. She underwent percutaneous kidney biopsy on POD 11, with findings consistent with mild acute tubular injury and no significant interstitial fibrosis nor tubular atrophy. Tissue proteomic analysis demonstrated tissue inflammation and extracellular matrix changes in the glomeruli and tubule-interstitium (Table 1). These cellular changes were present without histologic correlates.

Discussion

As NSAIDs were considered to be the primary driver of the participant’s AKI, at the molecular level we suspected that prostaglandin expression may have been altered. However, proteomic interrogation revealed a more dynamic molecular landscape, with changes noted in prostaglandin synthesis in response to NSAIDs as well as signs of intra-renal inflammation and fibrosis not evident by histopathology alone. These findings illustrate that routine histology techniques do not necessarily capture the full complexity of cellular injury.