Immune Profile and Epstein-Barr Virus Infection in Acute Interstitial Nephritis: An Immunohistochemical Study in 78 Patients

Abstract

Background: Acute interstitial nephritis (AIN) is a common cause of acute kidney injury and is characterised by a dense interstitial cellular infiltrate, which has not been well defined. Previous studies have demonstrated a correlation between Epstein-Barr virus (EBV) infection and AIN. The purpose of our study was to define the nature of the interstitial immune infiltrate and to investigate the possibility of renal infection with EBV. Methods: Seventy-eight patients with AIN were identified from renal biopsy reports in a single centre over an 18-year period. Immunohistochemical staining was performed to define the cellular infiltrate. In situ hybridization and immunohistology were used to detect EBV. Results: A positive correlation between CD68 macrophage infiltration and serum creatinine concentration at presentation was identified. IL-4, eotaxin, CCR3, CCR5 and VCAM-1 were all expressed in biopsies of AIN. Using in situ hybridization and immunohistochemistry, EBV was not detected in any of the AIN sections analysed. Conclusion: This study has assessed the nature of the interstitial infiltrate in AIN. EBV was not detected in the renal biopsies, suggesting that EBV is not a pathogenetic factor in AIN.

Epstein–Barr virus-related hemophagocytic lymphohistiocytosis complicated with coronary artery dilation and acute renal injury in a boy with a novel X-linked inhibitor of apoptosis protein (XIAP) variant: a case report

“…Mansur A et al [ 26 ] performed immunohistochemical staining of renal tissue from 78 patients with EBV infection and AIN and identified a positive correlation between CD68 macrophage infiltration and serum creatinine concentration, as well as expression of IL-4, eotaxin, CCR3, CCR5 and VCAM-1 in biopsies from patients with AIN. In addition, EBV was not detected by in situ hybridization and immunohistochemistry analyses in any of the AIN sections, indicating that EBV is not a pathogenetic factor in AIN [ 26 ]. In addition to AIN, EBV-related renal lesions include glomerular abnormalities such as immune-complex mediated glomerulonephritis, membranous nephropathy, minimal change nephritic syndrome and IgA nephropathy, which are very rare [ 27 – 29 ].…”

“…Moretti M et al systematically reviewed 38 patients with primary EBV infectious mononucleosis complicated by AKI, including 27 cases of acute interstitial nephritides (AIN), three of hemolytic uremic syndromes, one of jaundice-associated nephropathy and seven of myositides [25]. Mansur A et al [26] performed immunohistochemical staining of renal tissue from 78 patients with EBV infection and AIN and identified a positive correlation between CD68 macrophage infiltration and serum creatinine concentration, as well as expression of IL-4, eotaxin, CCR3, CCR5 and VCAM-1 in biopsies from patients with AIN. In addition, EBV was not detected by in situ hybridization and immunohistochemistry analyses in any of the AIN sections, indicating that EBV is not a pathogenetic factor in AIN [26].…”

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

“…However, only a limited number of reports have addressed the relationship between chronic EBV infection and renal complications. Although tubulointerstitial nephritis as a renal complication of EBV infection has been well described [7][8][9], previous reports of glomerular disease in chronic EBV infection have been limited [10][11][12]. Furthermore, as EBV usually affects children or adolescents, descriptions of adult cases have been sparse.…”

Viruses and collapsing glomerulopathy: a brief critical review: Table 1.

“…Viral DNA was similarly localized in the case of an HIV-infected individual with interstitial nephritis [41], but viral DNA was not found in cases of idiopathic acute interstitial nephritis [42, 43]. Kunimoto et al .…”