Haematuria is a marker for the severity of acute kidney injury but does not associate with thrombocytopenia in acute Puumala hantavirus infection

Abstract

Background: Puumala hantavirus (PUUV) causes haemorrhagic fever with renal syndrome characterized by thrombocytopenia, capillary leakage and acute kidney injury (AKI) with proteinuria and haematuria. Although the typical histologic lesion is acute tubulointerstitial nephritis, the amount of glomerular proteinuria predicts the severity of upcoming AKI. Here, we studied the associations of haematuria and proteinuria with the severity of emerging AKI, thrombocytopenia and markers of coagulation and fibrinolysis in PUUV infection.

Methods: We examined 205 consecutive patients treated for serologically confirmed acute PUUV infection at Tampere University Hospital during 1997–2014. The patients were divided into three groups according to the combined positive result in urine haemoglobin and albumin dipstick tests: 0–2 + (n = 58), 3–4 + (n = 100) and 5–6 + (n = 47).

Results: The medians of maximum creatinine concentrations in the three groups were: 0–2 + 100 μmol/L (range 52–1499), 3–4 + 204 μmol/L (range 65–1071) and 5-6 + 361 μmol/l (range 51–1285) (p < .001). The number of blood platelets (p = .069), and the levels of fibrinogen, prothrombin fragments F1 + 2 and d-dimer (p = .602, p = .113, p = .289, respectively) were not significantly different between the groups. When the amount of haematuria in the dipstick test was examined separately, no association with thrombocytopenia was detected (p = .307 between groups 0, 1+ and 2–3+).

Conclusions: Combined positive result of haematuria and proteinuria in the dipstick test at hospital admission predicted the severity of upcoming AKI in acute PUUV infection. As haematuria was not associated with the severity of thrombocytopenia, it did not indicate increased bleeding tendency, but was rather a marker of acute kidney injury.

Keywords:

• Acute kidney injury
• Hantavirus
• haematuria
• Puumala virus
• thrombocytopenia

Acknowledgements

The skilful 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.

Additional information

Funding

This study was financially supported by the Competitive State Research Financing of the Expert Responsibility Area of Tampere University Hospital (9P062), Tampere Tuberculosis Foundation, Sigrid Jusélius Foundation, Magnus Ehrnrooth Foundation, and the Finnish Kidney Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.