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

TitleCollapsing glomerulopathy in a young woman with APOL1 risk alleles following acute parvovirus B19 infection: a case report investigation.
Publication TypeJournal Article
Year of Publication2016
AuthorsBesse, W, Mansour, S, Jatwani, K, Nast, CC, Brewster, UC
JournalBMC Nephrol
Volume17
Issue1
Pagination125
Date Published2016 Sep 06
ISSN1471-2369
KeywordsAcute Disease, Adult, Alleles, Apolipoprotein L1, Female, Glomerulosclerosis, Focal Segmental, Humans, Kidney Failure, Chronic, Parvoviridae Infections, Parvovirus B19, Human, Pregnancy, Pregnancy Complications, Infectious
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.

DOI10.1186/s12882-016-0330-7
Alternate JournalBMC Nephrol
PubMed ID27600725
PubMed Central IDPMC5013576
Grant ListT32 DK007276 / DK / NIDDK NIH HHS / United States
U54 HG006504 / HG / NHGRI NIH HHS / United States
UL1 TR001863 / TR / NCATS NIH HHS / United States