Abstract: FR-PO0482
AKI in a Patient with Cancer: Can Steroids Save the Kidneys?
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
- Al Any, Haya, Mayo Clinic Arizona, Scottsdale, Arizona, United States
- Yang, Shaun, Mayo Clinic Arizona, Scottsdale, Arizona, United States
Introduction
Rapidly progressive glomerulonephritis (RPGN) is defined as rapid decline in kidney function causing acute kidney injury and end-stage renal disease within days to weeks. It is caused by immune mechanisms leading to capillary wall destruction, inflammatory cell recruitment, and crescentic fibrosis of epithelial cells then nephron loss. One mechanism is deposition of aberrant IgA immune complexes, as in IgA nephropathy or IgA vasculitis nephropathy (IgAVN). IgA vasculitis (IgAV) has been linked to malignancy, often diagnosed within one month of malignancy diagnosis. Here, we present a patient with malignancy and RPGN with a subtle exam clue to IgAV and likely IgAVN.
Case Description
A 74-year-old male with newly diagnosed metastatic cholangiocarcinoma presented with hypotension (87/59 mmHg), AKI III (creatinine 2.33 mg/dL, baseline 0.95 six weeks prior), and leukocytosis. Urinalysis showed proteinuria, microscopic hematuria, hyaline casts, and urine sodium 25 mEq. CT ascites and no hydronephrosis. Management included fluids, albumin, paracentesis, and empiric antibiotics; infectious workup was negative and kidney function only mildly improved. On day 2, faint palpable purpura was noted on the feet. Skin biopsy showed leukocytoclastic vasculitis with granular IgA deposition in dermal vessel walls, confirming IgAV. IgAVN was suspected and prednisone was started; creatinine improved from 2.39 to 2.03. He was discharged on a steroid taper with continued improvement (creatinine 1.35). One day after completing the taper, he presented with recurrent hypotension (68/46) and AKI (creatinine 1.70). Infectious workup was negative. Hydrocortisone and paracentesis led to improvement. Retrospective review revealed a 65.9% eGFR decline in under three weeks (85 to 29), meeting KDIGO criteria for RPGN. Kidney biopsy, the gold standard for diagnosing RPGN, was not performed due to poor prognosis and hospice enrollment.
Discussion
IgAV has been reported in association with malignancy and can cause RPGN from secondary IgAVN. KDIGO guidelines recommend that all adults with IgAV and IgAVN be screened for malignancy as treatment centers on cancer-directed therapy in this case rather than the ANCA Associated Vasculitis protocol with induction and maintenance therapy. However, our case represents an example where systemic glucocorticoids may still help preserve kidney function as a bridge to disease-directed cancer therapy.
Acknowledgment
My esteemed mentor and supervisor Dr. Shaun Yang, M.D. for his guidance during our time taking care of the patient and with writing this abstract