We present an uncommon case of allograft adenovirus tubulointerstitial nephritis in a 63-year-old male 6 weeks following cadaveric renal transplantation for end-stage renal failure secondary to hypertensive nephrosclerosis. The patient presented with acute onset of fevers, dysuria, haematuria and diarrhoea with acute graft dysfunction.

A renal biopsy demonstrated necrotizing tubulointerstitial nephritis with viral cytopathic changes and no evidence of rejection. Adenovirus was identified as the pathogen. Treatment involved the reduction in the patient's usual immunosuppression, intravenous immunoglobulin, piperacillin–tazobactam and ganciclovir. We present the clinical and pathological findings of necrotizing adenoviral nephropathy, highlighting the importance of considering this diagnosis in renal transplant recipients presenting with interstitial nephritis in the setting of a systemic illness.

With the rising number of solid organ transplantations worldwide, and the subsequent growing population of immunosuppressed patients, we treat an increasing number of opportunistic infections. Viral pathogens are a common cause in renal transplant recipients, complicating the course and possibly compromising allograft survival.

Adenoviruses are a family of double-stranded DNA viruses that readily infect human epithelial cells exhibiting a characteristic cytopathic effect. While most infections associated with adenoviruses are self-limiting, those occurring in immunocompromised hosts can be more severe, or even fatal. The most common urologic manifestation of adenovirus infection in adults is haemorrhagic cystitis. In the immunocompromised patient, adenovirus, specifically subgroup B types 11, 34 and 35, has been shown to cause both haemorrhagic cystitis and tubulointerstitial nephritis. Although more commonly caused by human polyoma viruses, there have been multiple case reports of adenovirus-related renal allograft tubulointerstitial nephritis over the past 30 years.

In this report we present the clinical and pathological findings of necrotizing adenoviral nephropathy and highlight the importance of considering this diagnosis in renal transplant recipients presenting with interstitial nephritis in the setting of a systemic infective illness.

The importance of considering adenovirus as a potential pathogen in any renal transplant patient presenting with interstitial nephritis in the setting of a systemic infective illness. In addition, it supports the role of early allograft biopsy for histological diagnosis in order to implement appropriate treatment and reduction in immunosuppression. This case also identifies the need for further evaluation of appropriate antiviral therapy, particularly investigation of the possible role of ganciclovir and the emerging role of cidofovir.

Conclusion

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