Parvovirus B19-related membranoproliferative glomerulonephritis presenting with positive glomerular staining for nephritis-associated plasmin receptor: a case report and review of the literature

Haruka Takahashi; Yukihiro Wada; Takuya Yamazaki; Kazuhiro Takeuchi; Tetsuya Abe; Shokichi Naito; Togo Aoyama; Takashi Sano; Rika Moriya; Takashi Oda; Yasuo Takeuchi

doi:10.1007/s13730-024-00956-1

Parvovirus B19-related membranoproliferative glomerulonephritis presenting with positive glomerular staining for nephritis-associated plasmin receptor: a case report and review of the literature

CEN Case Rep. 2024 Dec 15. doi: 10.1007/s13730-024-00956-1. Online ahead of print.

Authors

Affiliations

¹ Department of Nephrology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa, 252-0375, Japan. Haruka.bi0531@gmail.com.
² Department of Nephrology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa, 252-0375, Japan.
³ Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji, Japan.

PMID: 39674998
DOI: 10.1007/s13730-024-00956-1

Abstract

Several cases of glomerulonephritis occurring after infection with human parvovirus B19 (PVB19) have been reported. However, the pathogenesis and clinicopathological features of PVB19-related glomerulonephritis remain elusive. We describe the case of a 34 year-old woman who showed nephrotic syndrome and microscopic hematuria 10 days after PVB19 infection. Blood pressure and renal function were within normal ranges. Laboratory tests showed positive results for anti-PVB19 immunoglobulin (Ig)M antibody and complement 3 (C3) hypocomplementemia. Antibody to streptolysin O (ASO) was slightly elevated, but bacterial cultures yielded no colonies. Light microscopy of renal biopsy was compatible with membranoproliferative glomerulonephritis (MPGN). Immunofluorescence microscopy showed intense staining for C3 and faint staining for IgG on the glomerular capillary wall and paramesangial area. Electron micrography showed subendothelial electron-dense deposits (EDDs), but hump-shaped subepithelial EDDs were not evident. PBV19-DNA was absent from renal tissue. Moreover, glomeruli showed positive staining for nephritis-associated plasmin receptor (NAPlr) and plasmin activity with similar distribution. Around 6 months after PVB19 infection, levels of anti-PVB19 IgM antibody spontaneously tuned negative with an apparent reduction of proteinuria and improvement of hypocomplementemia, although ASO level remained unchanged. This appears to represent the first description of positive glomerular staining for NAPlr in MPGN after PVB19 infection. Based on a review of 27 cases, including our own case, the MPGN lesions could be attributable to PVB19 infection. Clinicopathological features of this case were incompatible with post-streptococcal acute glomerulonephritis. We presume that a PBV19-derived glomerular pathogen that cross-reacts with anti-NAPlr antibody might be involved in the development of PVB19-related MPGN.

Keywords: IRGN; MPGN; NAPlr; PVB19 infection; Plasmin activity.