Kidney disease in Puumala hantavirus infection

Abstract

Acute kidney injury (AKI) remains a predominant clinical expression of nephropathia epidemica (NE). Its pathogenesis is not yet fully understood. Here, we describe the tissue injury comprehensively and present new data aimed to characterize the injury and explain its pathophysiology. When compared to tubulointerstitial nephritis of a wide variety of other aetiologies, a high degree of proteinuria is a distinguished trait of NE, a finding that is also helpful in the clinical suspicion of the disease. Recently, novel biomarkers for the prediction of severe AKI, including neutrophil gelatinase-associated lipocalin (NGAL), have been identified and ultrastructural tissue changes have been more accurately described. A role for soluble urokinase-type plasminogen activator (suPAR) in the pathogenesis of NE has been suggested, and data on gene polymorphisms, in relation to the severity of AKI have been presented. Smoking is a risk factor for NE and smoking is also associated with aggravated AKI in NE. Although no specific treatment is in sight, recent case reports concerning therapy directed against vascular permeability and vasodilation are of interest. In fact, future work trying to explain the pathophysiology of AKI might need concentrated efforts towards the mechanisms of increased vascular permeability and vasodilatation, which irrespective of organ manifestation, are two major determinants of NE.

Keywords:

• Acute kidney injury
• hantavirus infection
• haematuria
• proteinuria
• Puumala virus

Acknowledgements

The research of the authors has been supported by Sigrid Juselius Foundation, The Competitive State Research Funding of the Expert Responsibility Area of Tampere University Hospital, Tampere Tuberculosis Foundation and Finnish Kidney Foundation. The skillful technical assistance of Ms. Katriina Ylinikkilä, Ms. Reeta Kulmala and Ms. Eini Eskola is greatly appreciated.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Additional information

Funding

The research of the authors has been supported by Sigrid Juselius Foundation, The Competitive State Research Funding of the Expert Responsibility Area of Tampere University Hospital, Tampere Tuberculosis Foundation and Finnish Kidney Foundation.