A case of anti-GBM nephritis following centipede bites and COVID-19 vaccination

被引:11
|
作者
Nagai, Kei [1 ,2 ]
Iwase, Mamiko [1 ]
Ueda, Atsushi [1 ]
机构
[1] Hitachi Gen Hosp, Dept Nephrol, 2-1-1 Jonan Cho, Hitachi, Ibaraki 3170077, Japan
[2] Univ Tsukuba, Fac Med, Dept Nephrol, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan
基金
日本学术振兴会;
关键词
Rapidly progressive glomerulonephritis; COVID-19; Vaccination; Delayed type hypersensitivity; GROSS HEMATURIA;
D O I
10.1007/s13730-021-00646-2
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
A case of newly developed anti-glomerular basement membrane (GBM) glomerulonephritis (GN) following centipede bites and COVID-19 vaccination is presented. A 70-year-old woman presented for investigation of mild fever, generalized fatigue, and macroscopic hematuria with no past history of renal disease. One year earlier, she had been bitten by a centipede. Based on the governmental policy, she was given the first COVID-19 vaccination, and the second injection was planned 3 weeks later. Accidentally, she was again bitten by a centipede, and the injured site had swollen severely. Based on a physician's judgment, the interval between vaccinations was extended to 8 weeks. One week after the second vaccination, macroscopic hematuria occurred suddenly, coincident with mild fever. Her serum anti-GBM titer was above the upper limit. There was no pulmonary involvement. Renal pathology showed anti-GBM GN, and she was treated with corticosteroid pulse therapy followed by sequential plasmapheresis. She had advanced renal dysfunction, but was independent of dialysis therapy during the one month of the remission induction therapy phase, and she is being treated with immunosuppressant therapy. Both vaccination and animal bites skew towards Th1 immunity, a key mechanism involved in the development of necrotizing GN evoked by anti-GBM antibody. Though there is no direct evidence for causality linking centipede bites, vaccination, and anti-GBM GN, the risk of anti-GBM GN appears to be increased by excessively induced Th1 immunity.
引用
收藏
页码:166 / 170
页数:5
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