Takahashi Haruka, Wada Yukihiro, Yamazaki Takuya, Takeuchi Kazuhiro, Abe Tetsuya, Naito Shokichi, Aoyama Togo, Sano Takashi, Moriya Rika, Oda Takashi, Takeuchi Yasuo
Department of Nephrology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa, 252-0375, Japan.
Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Hachioji, Japan.
CEN Case Rep. 2024 Dec 15. doi: 10.1007/s13730-024-00956-1.
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.
已有多例人类细小病毒B19（PVB19）感染后发生肾小球肾炎的病例报道。然而，PVB19相关性肾小球肾炎的发病机制及临床病理特征仍不明确。我们报告了一例34岁女性病例，该患者在PVB19感染10天后出现肾病综合征和镜下血尿。血压和肾功能均在正常范围内。实验室检查显示抗PVB19免疫球蛋白（Ig）M抗体阳性及补体3（C3）低补体血症。抗链球菌溶血素O（ASO）抗体略有升高，但细菌培养未发现菌落。肾活检光镜检查结果符合膜增生性肾小球肾炎（MPGN）。免疫荧光显微镜检查显示肾小球毛细血管壁和系膜旁区C3染色强阳性，IgG染色弱阳性。电子显微镜检查显示内皮下电子致密沉积物（EDD），但未见驼峰状上皮下EDD。肾组织中未检测到PBV19-DNA。此外，肾小球肾炎相关纤溶酶受体（NAPlr）染色阳性，且纤溶酶活性分布相似。PVB19感染约6个月后，抗PVB19 IgM抗体水平自发转阴，蛋白尿明显减少，低补体血症有所改善，尽管ASO水平保持不变。这似乎是PVB19感染后MPGN中NAPlr肾小球染色阳性的首次描述。基于对包括我们自己病例在内的27例病例的回顾，MPGN病变可能归因于PVB19感染。该病例的临床病理特征与链球菌感染后急性肾小球肾炎不符。我们推测，一种与抗NAPlr抗体发生交叉反应的PVB19衍生的肾小球病原体可能参与了PVB19相关性MPGN的发生发展。
