Abstract: FR-PO0419
Renal Hemosiderosis as a Distinct Clinicopathologic Entity: An International Multicenter Study of Etiology, Histologic Patterns, and Kidney Outcomes
Session Information
- AKI: Biomarkers, Diagnostics, and Risk Prediction
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
- Jaturapisanukul, Solos, Navamindradhiraj University, Bangkok, Thailand
- Arriola Montenegro, Jose J., Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Galeano, Belinda, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Grande, Joseph P., Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Gonzalez Suarez, Maria Lourdes, Mayo Clinic Minnesota, Rochester, Minnesota, United States
Background
Renal hemosiderosis is an under-recognized consequence of chronic intravascular hemolysis, with limited data on its clinicopathologic spectrum and prognostic determinants. We sought to characterize its etiologies, histopathologic features, and clinical outcomes across diverse populations.
Methods
We performed a retrospective multicenter study of adults with biopsy-proven renal hemosiderosis from nephropathology archives at Mayo Clinic (USA) and Vajira Hospital (Thailand). Diagnosis was confirmed by Prussian blue staining. Clinical characteristics, laboratory data, histologic findings, and outcomes were compared by geographic region and underlying etiology. Associations between pathologic features and kidney outcomes were evaluated.
Results
Ten patients were identified (USA n=6; Thailand n=4), median age 57 years; 50% were male. Acute kidney injury occurred in 80%, and nephrotic-range proteinuria in 44%. Etiologies differed significantly by region, with mechanical valve–related hemolysis and thrombotic microangiopathy predominating in the USA, and hemoglobinopathies with iron overload in Thailand (p=0.033). All cases demonstrated acute tubular injury with universal proximal tubular iron deposition; additional involvement included distal tubules (67%), interstitium (67%), and Bowman’s space (33%). Coexisting glomerular disease was present in 50%, most commonly IgA nephropathy. Patients with non–valve-related etiologies had lower hemoglobin and higher RDW, consistent with more severe hemolysis. Over a median follow-up of 28.5 months, 50% progressed to kidney failure and 40% died. Greater interstitial fibrosis and tubular atrophy (IFTA) was associated with adverse kidney outcomes.
Conclusion
In this multicenter cohort, renal hemosiderosis emerges as a heterogeneous but clinically significant entity with distinct etiologic and regional patterns. Despite a predominantly tubular process, outcomes are poor, with high rates of kidney failure and mortality.
Hemosiderosis light and electron microscopy findings.