Abstract: TH-PO0539
Infection-Related Glomerular Injury: Malaria Unmasking IgAN
Session Information
- Glomerular Diseases: IgAN, IgA Vasculitis, and More
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Hassan, Seerat, Baylor University Medical Center, Dallas, Texas, United States
- Akinfolarin, Akinwande A., Baylor University Medical Center, Dallas, Texas, United States
Introduction
Malaria is a parasitic infection occurring in the tropics with associated acute kidney injury (AKI). AKI is typically due to acute tubular necrosis (ATN) and/or interstitial nephritis. Rarely malaria has been associated with immunoglobulin A (IgA) nephropathy characterized by IgA deposition, mesangial proliferation, and matrix expansion. We present a case of Plasmodium falciparum infection associated with IgA nephropathy, highlighting an important association rarely reported.
Case Description
52-year-old male with no history of renal disease presented with fevers, myalgias, nausea, vomiting, and diarrhea, ten days after returning from a trip to Africa. Initial workup showed Hgb of 9.8 g/dL, platelet count 46 K/uL, and creatinine of 6.4 g/dL. Urinalysis: 3+ Protein, 2+ blood, urine protein-to-creatinine ratio was 1.1 g/g. Serological workup was negative for antinuclear antibody (ANA) titers, Antineutrophil cytoplasmic antibodies (ANCA), anti-double stranded DNA (dsDNA), and antistreptolysin O (ASO). Complements C3 and C4 and immunofixation electrophoresis were normal. Haptoglobin <10 mg/dL, LDH 733 U/L, ADAMTS13 activity 27%. Ultrasound showed increased renal cortical echogenicity without hydronephrosis. Blood smear was positive for Plasmodium falciparum and therapy was initiated with IV artesunate. Kidney biopsy revealed diffuse acute tubular injury with focal tubulointerstitial nephritis, IgA deposition with (M0 E0 S1 T0 C0) with no evidence of thrombotic microangiopathy or collapsing glomerulopathy. Immunofluorescence staining revealed: IgG (trace), IgA (2-3+), IgM (trace to 1+), C3 (trace), kappa (2-3+), and lambda (2-3+). Tubular casts-stained 3+ for IgA, kappa, and lambda, 2-3+ arteriolar staining for C3. C1q and fibrinogen were negative. He required kidney replacement therapy but not plasmapheresis or steroids and recovered kidney function.
Discussion
IgA nephropathy is a rarely reported renal complication of Plasmodium falciparum malaria. Latent IgA nephropathy is difficult to prove without a prior biopsy, but infections such as Haemophilus parainfluenzae, Staphylococcus species, Mycoplasma pneumoniae have been associated with secondary IgA nephropathy. Co-existence of IgA disease as a by-stander in malarial parasitemia must be entertained to prevent unwarranted therapies.