Abstract: SA-PO0059
Acute Tubular Necrosis in a Patient with Triple-Positive Antiphospholipid Antibodies: Coincidence or Association?
Session Information
- AKI: Novel Patient Populations and Case Reports
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Laghrib, Sanae, CHU Brugmann, Brussels, Belgium
- Jacobs, Lucas, CHU Brugmann, Brussels, Belgium
- Kaysi, Saleh, CHU Brugmann, Brussels, Belgium
- Nortier, Joelle L., CHU Brugmann, Brussels, Belgium
- Taghavi, Maxime, CHU Brugmann, Brussels, Belgium
Introduction
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by thrombotic manifestations and vasculopathy. The kidneys are a major target organ in APS, primarily marked by thrombosis that can affect any vascular site within the kidneys. APS-associated nephropathy, which includes microvascular renal involvement, has recently been included in the classification criteria for APS. However, acute tubular necrosis has not been described.
Case Description
We report the case of a 58-year-old woman who was admitted to the nephrology ward due to severe acute kidney injury (AKI) (plasma creatinine (PCr) 10,9 mg/dL) necessitating the initiation of hemodialysis. She had a history of well-controlled hypertension without renal artery stenosis, managed with lisinopril, and untreated triple-positive antiphospholipid antibody positivity without clinical manifestation. On the admission, she was normotensive. The history and physical examination were unremarkable. A CT scan and Doppler ultrasound excluded obstructive AKI and renal artery/vein thrombosis. Urine analysis indicated low-grade proteinuria (UPCR 0.72 g/g creatinine and UACR 242 mg/g creatinine) without hematuria. Anticoagulation and steroids were initiated empirically, and a kidney biopsy was conducted, revealing severe acute tubular necrosis (ATN) without acute vascular renal or glomerular lesions suggestive of APS nephropathy. Nevertheless, mild fibrous intimal hyperplasia was observed. Steroids were discontinued, and the patient was maintained on a low-dose aspirin regimen. She partially recovered, with a PCr of 1.2 mg/dL.
Discussion
In the context of APS, AKI primarily results from thrombotic microangiopathy lesions, with or without fibrin thrombi in arterioles or glomeruli. Additionally, AKI has been linked to renal artery and vein thrombosis, as well as catastrophic antiphospholipid syndrome. This case describes a severe ATN in the absence of prerenal azotemia or an apparent cause of ischemic or toxic events or sepsis. APS-associated ATN has not been previously documented in the literature. However, since an acute ischemic event can precipitate acute tubular necrosis, we hypothesize that aPL positivity can be a risk factor for ATN. It would be interesting to evaluate this association further.