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CEN Case Rep. 2019 Nov;8(4):285-291. doi: 10.1007/s13730-019-00409-0. Epub 2019 Jun 19.

Acute kidney injury in an adult patient with IgA nephropathy and chronic replicative Epstein-Barr virus infection.

Author information

1
Department of Internal Medicine, Nagaoka Red Cross Hospital, 2-297-1 Sensyu, Nagaoka, Niigata, 940-2085, Japan. yuyasato337@gmail.com.
2
Department of Internal Medicine, Nagaoka Red Cross Hospital, 2-297-1 Sensyu, Nagaoka, Niigata, 940-2085, Japan.
3
Department of Dermatology, Nagaoka Red Cross Hospital, 2-297-1 Sensyu, Nagaoka, Niigata, 940-2085, Japan.
4
Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, Niigata, Niigata, 951-8510, Japan.

Abstract

Most of the adult population are infected with Epstein-Barr virus (EBV), but as EBV replication is usually under immune system control, the majority of individuals remain asymptomatic. On the other hand, some individuals continuously retain a high EBV antibody titer and a high EBV DNA load in their blood, suggesting a defect of EBV replication control. To date, only a limited number of reports have addressed the relationship between this chronic form of EBV infection and renal involvement. Here, we describe an 80-year-old woman who developed acute kidney injury shortly after an episode of mosquito bites, accompanied by a severe skin rash, which raised a suspicion of chronic EBV infection. She was subsequently diagnosed as having chronic replicative EBV infection. Renal biopsy revealed a diagnosis of IgA nephropathy with crescent formation. Although the relationship between IgA nephropathy and EBV infection has been discussed, no substantial understanding has yet emerged. The patient's characteristic clinical course suggested that the renal failure may have been partly attributable to chronic EBV infection. This case suggests that physicians may need to consider the possibility that chronic EBV infection may affect the clinical course of IgA nephropathy, or exacerbate the disease.

KEYWORDS:

Epstein–Barr virus; Glomerulonephritis; IgA nephropathy; Renal failure

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