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

2017 ◽  
Vol 49 (11-12) ◽  
pp. 840-846 ◽  
Author(s):  
Tuula K. Outinen ◽  
Paula Mantula ◽  
Outi K. Laine ◽  
Ilkka Pörsti ◽  
Antti Vaheri ◽  
...  
2014 ◽  
Vol 79 (2) ◽  
pp. 166-170 ◽  
Author(s):  
Miklós Oldal ◽  
Viktória Németh ◽  
Mónika Madai ◽  
Gábor Kemenesi ◽  
Bianka Dallos ◽  
...  

2020 ◽  
Author(s):  
Fengqi Qiu ◽  
Congcong Li ◽  
Jianya Zhou

Abstract Background Hemorrhagic fever with renal syndrome (HFRS) is caused by hantaviruses presenting with high fever, hemorrhage, acute kidney injury. Microvascular injury and hemorrhage in mucus was often observed in patients with hantavirus infection. Infection with bacterial and virus related aortic aneurysm or dissection occurs sporadically. We present a previously unreported case of hemorrhagic fever with concurrent Stanford B aortic dissection. Case presentation: A 56-year-old man complained of high fever, generalized body ache, with decreased platelet counts of 10 × 10^9/L and acute kidney injury. The ELISA test for Hantaan virus of IgM and IgG antibodies were both positive. During the convalescent period, he complained sudden onset acute chest pain radiating to the back and the CTA revealed an aortic dissection of the descending aorta extending to iliac artery. He was diagnosed with Hemorrhagic fever with renal syndrome and Stanford B aortic dissection. The patient recovered completely after surgery with other support treatments. Conclusion We present a case of HFRS complicated with aortic dissection,and no study has reported the association of HFRS with aortic disease. However, we suppose that hantavirus infection not only cause microvascular damage but may be risk factor for acute macrovascular detriment. A causal relationship has yet to be confirmed.


Pathogens ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 615
Author(s):  
Paula Mantula ◽  
Johanna Tietäväinen ◽  
Jan Clement ◽  
Onni Niemelä ◽  
Ilkka Pörsti ◽  
...  

Transient proteinuria and acute kidney injury (AKI) are characteristics of Puumala virus (PUUV) infection. Albuminuria peaks around the fifth day and associates with AKI severity. To evaluate albuminuria disappearance rate, we quantified albumin excretion at different time points after the fever onset. The study included 141 consecutive patients hospitalized due to acute PUUV infection in Tampere University Hospital, Finland. Timed overnight albumin excretion (cU-Alb) was measured during the acute phase in 133 patients, once or twice during the convalescent phase within three months in 94 patients, and at six months in 36 patients. During hospitalization, 30% of the patients had moderately increased albuminuria (cU-Alb 20–200 μg/min), while 57% presented with severely increased albuminuria (cU-Alb >200 μg/min). Median cU-Alb was 311 μg/min (range 2.2–6460) ≤7 days after fever onset, 235 μg/min (range 6.8–5479) at 8–13 days and 2.8 μg/min (range 0.5–18.2) at 14–20 days. After that, only one of the measurements showed albuminuria (35.4 μg/min at day 44). At six months, the median cU-Alb was 2.0 μg/min (range 0.6–14.5). Albuminuria makes a flash-like appearance in PUUV infection and returns rapidly to normal levels within 2–3 weeks after fever onset. In the case of AKI, this is a unique phenomenon.


Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1553
Author(s):  
Sirpa Koskela ◽  
Satu Mäkelä ◽  
Tomas Strandin ◽  
Antti Vaheri ◽  
Tuula Outinen ◽  
...  

Puumala hantavirus (PUUV) causes a hemorrhagic fever with renal syndrome (HFRS), also called nephropathia epidemica (NE), which is mainly endemic in Europe and Russia. The clinical features include a low platelet count, altered coagulation, endothelial activation, and acute kidney injury (AKI). Multiple connections between coagulation pathways and inflammatory mediators, as well as complement and kallikrein–kinin systems, have been reported. The bleeding symptoms are usually mild. PUUV-infected patients also have an increased risk for disseminated intravascular coagulation (DIC) and thrombosis.


PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208017 ◽  
Author(s):  
Paula S. Mantula ◽  
Tuula K. Outinen ◽  
Pia Jaatinen ◽  
Mari Hämäläinen ◽  
Heini Huhtala ◽  
...  

2021 ◽  
Vol 34 (2) ◽  
pp. 141-143
Author(s):  
Sinan Çetin ◽  
Ahmet Melih Şahin

Hantaviruses are viruses belonging to the Bunyaviridae family, and they cause two forms of acute illness in humans: hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS). HFRS form seen in our country progresses with fever, acute kidney injury, thrombocytopenia and bleeding. Therefore, hantavirus infections should be kept in mind in the differential diagnosis of patients presenting with these symptoms and signs. This report presents a case followed up with the differential diagnosis of coronavirus disease-19 (COVID-19) during the pandemic and diagnosed with HFRS due to hantavirus.


Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 45
Author(s):  
Tuula K. Outinen ◽  
Satu Mäkelä ◽  
Ilkka Pörsti ◽  
Antti Vaheri ◽  
Jukka Mustonen

Annually, over 10,000 cases of hemorrhagic fever with renal syndrome (HFRS) are diagnosed in Europe. Puumala hantavirus (PUUV) causes most of the European HFRS cases. PUUV causes usually a relatively mild disease, which is rarely fatal. However, the severity of the infection varies greatly, and factors affecting the severity are mostly unrevealed. Host genes are known to have an effect. The typical clinical features in PUUV infection include acute kidney injury, thrombocytopenia, and increased vascular permeability. The primary target of hantavirus is the endothelium of the vessels of different organs. Although PUUV does not cause direct cytopathology of the endothelial cells, remarkable changes in both the barrier function of the endothelium and the function of the infected endothelial cells occur. Host immune or inflammatory mechanisms are probably important in the development of the capillary leakage. Several immunoinflammatory biomarkers have been studied in the context of assessing the severity of HFRS caused by PUUV. Most of them are not used in clinical practice, but the increasing knowledge about the biomarkers has elucidated the pathogenesis of PUUV infection.


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