Abstract: FR-PO0443
Noninflammatory Lupus Vasculopathy Presenting as AKI in Systemic Lupus Erythematosus
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Hinojosa, Sebastian, Mass General Brigham Inc, Boston, Massachusetts, United States
- Chadha, Ashima, Mass General Brigham Inc, Boston, Massachusetts, United States
- Gama, Alcino, Mass General Brigham Inc, Boston, Massachusetts, United States
- Avillach, Claire, Mass General Brigham Inc, Boston, Massachusetts, United States
- McMahon, Gearoid M., Mass General Brigham Inc, Boston, Massachusetts, United States
- Mount, David B., Mass General Brigham Inc, Boston, Massachusetts, United States
Introduction
Systemic lupus erythematosus (SLE) is an autoimmune disease with frequent renal involvement. While glomerular lesions of lupus nephritis (LN) are well classified by the ISN/RPS system, vascular involvement is underrecognized. Recognition is critical as standard LN staging may underestimate disease activity and optimal therapy is undefined.
Case Description
A 37-year-old woman with SLE presented with severe diffuse abdominal pain.
Exam showed malar rash and abdominal tenderness. Labs: CRP 57.1 mg/L, C3 76 mg/dL, C4 9 mg/dL, dsDNA 29 IU/mL, creatinine 3.41 mg/dL (baseline 0.6 mg/dL), UPCR 1.35 g/day (baseline 0.1 g/day). Colon biopsies indicated ischemic colitis without vasculopathy.
Kidney biopsy showed moderate acute tubular injury, class II LN, and a prominent non-inflammatory lupus vasculopathy (LV). Arterioles displayed hyaline deposits, luminal narrowing, glomerular hypoperfusion, and vasoconstriction. IF demonstrated vascular wall staining for IgG, IgA, C3, and C1q (Fig. 1).
She received steroid taper and obinutuzumab (1g x2, 2 weeks apart). Colonic symptoms slowly resolved. At 4 months, creatinine improved to 0.7 mg/dL and UPCR to 0.1 g/day.
Discussion
This case highlights LV causing AKI. The accompanying class II LN was felt to be less contributory to the patient’s AKI. High-dose glucocorticoids + obinutuzumab (potent B-cell depletion, superior serologic responses vs MMF per NOBILITY/REGENCY) yielded excellent renal recovery. Her colonic pathology was not felt to be related to LV, in that equivalent vasculopathy was not detected in her full-thickness biopsy. LV remains under-classified and may warrant immunosuppression escalation if ischemic nephropathy is demonstrated, even in the absence of severe LN.
Renal biopsy demonstrating severe arteriolar hyalinosis and downstream glomerular hypoperfusion (PAS, 200X). Immune deposits staining for IgG and C1q along the vascular walls (immunofluorescence 200X).