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Kidney Week

Abstract: PO0104

An Unusual Case of IgA Nephropathy Associated with Parvovirus B19

Session Information

Category: Trainee Case Report

  • 102 AKI: Clinical, Outcomes, and Trials


  • Lakhani, Laila S., Johns Hopkins University, Baltimore, Maryland, United States
  • Abbas, Hashim, Johns Hopkins University, Baltimore, Maryland, United States
  • Atta, Mohamed G., Johns Hopkins University, Baltimore, Maryland, United States

Parvovirus is known to cause upper respiratory infections in children and the immunosuppressed. It’s association with kidney disease has been sporadically reported in literature, mostly causing lupus like glomerulonephritis with endocapillary proliferation. We describe a unique case of IgA Nephropathy (IgAN) in an African American patient associated with Parvovirus B19.

Case Description

A 23 year old African American female with a history of Hemoglobin C disease presented with one week of generalized malaise, abdominal pain and nausea, found to have non-oliguric AKI with Creatinine 2.5 mg/dL (baseline Cr: 0.6 mg/dL). Within one week, her Creatinine peaked at 7.4 mg/dL. Urinalysis showed 3+ protein, 5 white cells and 9 red cells. Urine microscopy was bland. Spot urine protein to creatinine ratio was 3.84g. Serologies were notable for normal Complements, negative ANA, ANCA, Hepatitis B, Hepatitis C and HIV along with unremarkable serum and urine electrophoresis. Renal ultrasound ruled out hydronephrosis. Labs were also notable for worsening hemolytic anemia. A renal biopsy was pursued, that showed diffuse proliferative glomerulonephritis with dominant IgA deposits. Mesangial and endocapillary proliferation was noted without any crescents. The oxford classification was: M1, E1, S0, T0, C0. Given this atypical IgA phenotype, infectious work was pursued, that came back positive for Parvovirus IgM and detectable Parvovirus DNA. She was started on Pulse dose steroids; immunosuppressives were held off given the absence of crescents. Her proteinuria partially responded to steroids along with an improvement in AKI (Cr: 1.1 mg/dL), after which steroids were tapered.


This case provides an example of AKI associated with Parvovirus infection. Since IgAN is predominantly seen in Caucasians, it is not surprising that only 3% African Americans were included in the cohort on which the Oxford Classification was coined. The improvement in acute kidney injury with a short course of steroids is suggestive of Parvovirus related process more than the typical endocapillary proliferation related to IgAN. The extension of Oxford Classification in the African American population can thus be challenging and potentially misleading as seen in this case. A repeat renal biopsy may be warranted to assess the underlying diagnosis of IgA Nephropathy and should be treated based on findings.