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BMC Nephrol. 2016 Sep 6;17(1):125. doi: 10.1186/s12882-016-0330-7.

Collapsing glomerulopathy in a young woman with APOL1 risk alleles following acute parvovirus B19 infection: a case report investigation.

Author information

  • 1Section of Nephrology, Yale University, 330 Cedar Street, BB 121, New Haven, CT 06520-8029, USA.
  • 2Government Medical College & Hospital Chandigarh Sector, Chandigarh, India.
  • 3Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • 4Section of Nephrology, Yale University, 330 Cedar Street, BB 121, New Haven, CT 06520-8029, USA. ursula.brewster@yale.edu.

Abstract

BACKGROUND:

Collapsing Glomerulopathy (CG), also known as the collapsing variant of Focal Segmental Glomerulosclerosis (FSGS), is distinct in both its clinical severity and its pathophysiologic characteristics from other forms of FSGS. This lesion occurs disproportionally in patients carrying two APOL1 risk alleles, and is the classic histologic lesion resulting from Human Immunodeficiency Virus (HIV) infection of podocytes. Other viral infections, including parvovirus B19, and drugs such as interferon that perturb the immune system, have also been associated with CG. Despite significant advances, explaining such genetic and immune/infectious associations with causative mechanisms and supporting evidence has proven challenging.

CASE PRESENTATION:

We report the case of a healthy (HIV-negative) pregnant 36 year-old Caribbean-American woman who presented with nephrotic syndrome and fetal demise in the setting of acute parvovirus B19 infection. A series of three renal biopsies and rapid clinical course showed progression from significant podocyte injury with mild light microscopy findings to classic viral-associated CG to ESRD in less than 3 months. Genetic analysis revealed two APOL1 G1 risk alleles.

CONCLUSIONS:

This is the first published case report of CG in the setting of acute parvovirus infection in a patient with two APOL1 risk allelles, and parvoviral proteins identified in renal epithelium on kidney biopsy. These findings support the causative role of parvovirus B19 infection in the development of CG on the background of APOL1 genetic risk.

KEYWORDS:

APOL1; Collapsing Glomerulopathy; FSGS; Immunohistochemistry; Interferon; Nephropathy; Parvovirus

PMID:
27600725
PMCID:
PMC5013576
DOI:
10.1186/s12882-016-0330-7
[PubMed - in process]
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