Evidence of a Link between Hepatitis E Virus Exposure and Glomerulonephritis Development

Mohamed A El-Mokhtar; Ayat M Kamel; Ehsan M W El-Sabaa; Sahar A Mandour; Ahmed Shawkat Abdelmohsen; Abdelmajeed M Moussa; Eman H Salama; Sahar Aboulfotuh; Lobna Abdel-Wahid; Essam M Abdel Aziz; Nashwa Mostafa A Azoz; Ibrahim M Sayed; Amal A Elkhawaga

doi:10.3390/v15061379

Evidence of a Link between Hepatitis E Virus Exposure and Glomerulonephritis Development

Viruses. 2023 Jun 15;15(6):1379. doi: 10.3390/v15061379.

Affiliations

¹ Department of Medical Microbiology and Immunology, Faculty of Medicine, Assiut University, Assiut 71515, Egypt.
² Microbiology and Immunology Department, Faculty of Pharmacy, Assiut University, Assiut 71515, Egypt.
³ Department of Microbiology and Immunology, Faculty of Pharmacy, Deraya University, Minia 11566, Egypt.
⁴ Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Assiut University, Assiut 71515, Egypt.
⁵ Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Aswan University, Aswan 81528, Egypt.
⁶ Department of Clinical Pathology, Faculty of Medicine, Sohag University, Sohag 82524, Egypt.
⁷ Gastroenterology and Hepatology Unit, Internal Medicine Department, Assiut University, Assiut 71515, Egypt.
⁸ Department of Internal Medicine, Nephrology Division, Faculty of Medicine, Assiut University, Assiut 71515, Egypt.

Abstract

Viruses can trigger glomerulonephritis (GN) development. Hepatitis viruses, especially Hepatitis C virus and Hepatitis B viruses, are examples of the viruses that trigger GN initiation or progression. However, the proof of a correlation between GN and Hepatitis E virus infection is not clear. Some studies confirmed the development of GN during acute or chronic HEV infections, mainly caused by genotype 3. While others reported that there is no relation between HEV exposure and GN development. A recent study showed that a reduced glomerular filtration rate was developed in 16% of acute HEV genotype 1 (HEV-1) infections that returned to normal during recovery. HEV-1 is endemic in Egypt with a high seroprevalence among villagers and pregnant women. There is no available data about a link between HEV and GN in Egypt.

Methods: GN patients (n = 43) and matched healthy subjects (n = 36) enrolled in Assiut University hospitals were included in this study. Blood samples were screened for hepatotropic pathogens. Tests for HEV markers such as HEV RNA and anti-HEV antibodies (IgM and IgG) were performed. Laboratory parameters were compared in HEV-seropositive and HEV-seronegative GN patients.

Results: Anti-HEV IgG was detected in 26 (60.5%) out of 43 GN patients. HEV seroprevalence was significantly higher in GN than in healthy controls, suggesting that HEV exposure is a risk factor for GN development. None of the GN patients nor the healthy subjects were positive for anti-HEV IgM or HEV RNA. There was no significant difference between seropositive and seronegative GN patients in terms of age, gender, albumin, kidney function profiles, or liver transaminases. However, anti-HEV IgG positive GN patients had higher bilirubin levels than anti-HEV IgG negative GN patients. HEV-seropositive GN patients had a significantly elevated AST level compared to HEV-seropositive healthy subjects.

Conclusion: exposure to HEV infection could be complicated by the development of GN.

Keywords: HEV; anti-HEV IgG; extrahepatic disorder; glomerulonephritis; seroprevalence.

MeSH terms

Female
Glomerulonephritis* / epidemiology
Hepatitis Antibodies
Hepatitis E virus* / genetics
Hepatitis E* / complications
Hepatitis E* / epidemiology
Humans
Immunoglobulin G
Immunoglobulin M
Pregnancy
RNA, Viral
Seroepidemiologic Studies

Substances

Hepatitis Antibodies
RNA, Viral
Immunoglobulin M
Immunoglobulin G

Grants and funding

This research received no external funding.