Final Diagnosis -- Parvovirus B19-related Glomerulonephritis




Renal manifestations in immunocompetent adults with parvovirus B19 infection include glomerulonephritis, nephrotic syndrome, frank hematuria, or a combination of the above. Histologically, the most common light microscopic findings include mesangial or endocapillary proliferation, although one study evaluating PCR-diagnosed parvovirus B19 in kidney biopsies with focal segmental glomerulosclerosis showed a statistically significant higher number with collapsing features [1]. The most common clinical and laboratory presentation of parvovirus infection in adults includes arthralgia, fever, occasional rash, cytopenias, and positive ANA; therefore, it can mimic or exacerbate systemic lupus erythematosus (SLE), and provide a challenge to distinguish between the two entities [2].

This patient presented with fatigue and anemia, and initial laboratory findings triggered further workup, which included both infectious and autoimmune laboratory evaluation. Autoimmune studies were non-contributory; parvovirus B19 antibodies (IgG and IgM) were positive and suggestive of a recent infection. The histologic and EM findings, such as mesangial and endocapillary proliferation and electron dense deposits support involvement in the kidney by parvovirus. Immunofluorescence was notable for a 'full house' pattern, which has been infrequently reported in the literature. This pattern is classically associated with SLE, and therefore must be ruled out, even in a patient such as this one without a suggestive history. The infection may provide a trigger for development of the full disease, or may exacerbate (as yet) unrecognized symptoms; this has been seen in other case reports [2]. However, this patient has no personal or family history, and therefore the antibodies present are likely secondary to the parvovirus infection. Of note, a polymerase chain reaction for parvovirus B19 performed on the formalin-fixed, paraffin-embedded renal biopsy tissue was positive for parvovirus B19. The positive PCR test cannot distinguish between viral infection of renal cells, viral antigen in immune deposits, and circulating, infected white blood cells. A parvovirus immunoperoxidase stain was negative for parvoviral protein.

The patient was started on prednisone, and his renal function has gradually improved (the most recent serum creatinine value was 1.2 mg/dL), and his anemia is resolving. However, some patients have resolution of their signs and symptoms rapidly enough that medications are not needed [3, 4]. Other patients may require supportive therapy, such as blood transfusions during marked anemia. Although no specific antiviral therapy is currently available, commercial immunoglobulin (IVIG) is a significant source of anti-parvovirus B19 antibodies, and may be used in immunocompromised patients who cannot mount an adequate immune response to eradicate the virus [4]. In general, patients can be monitored by evaluation of reticulocyte count, in addition to hemoglobin and hematocrit. However, some patients may continue to have low levels of virus, thus permitting relapse of disease in a setting of immune compromise.


  1. Tanawattanacharoen S, Falk RJ, Jennette JC, Kopp JB. Parvovirus B19 DNA in kidney tissue of patients with focal segmental glomerulosclerosis. Am J Kidney Dis. 2000;35:1166-1174.
  2. Nesher G, Osborn TG, Moore TL. Parvovirus infection mimicking systemic lupus erythematosus. Semin Arthritis Rheum. 1995;24:297-303.
  3. Taylor G, Drachenberg C, Faris-Young S. Renal involvement of human parvovirus B19 in an immunocompetent host. CID. 2001;32:167-169.
  4. Waldman M, Kopp JB. Parvovirus B19 and the Kidney. Clin J Am Soc Nephrol. 2007;2:S47-S56.

Contributed by Alicia F Liang, MD and Sheldon Bastacky, MD

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