Cystatin C and α-1-Microglobulin Predict Severe Acute Kidney Injury in Patients with Hemorrhagic Fever with Renal SyndromeVisa övriga samt affilieringar
2020 (Engelska)Ingår i: Pathogens, E-ISSN 2076-0817, Vol. 9, nr 8, artikel-id 666Artikel i tidskrift (Refereegranskat) Published
Abstract [en]
Puumala orthohantavirus causes hemorrhagic fever with renal syndrome (HFRS) characterized by acute kidney injury (AKI), an abrupt decrease in renal function. Creatinine is routinely used to detect and quantify AKI; however, early AKI may not be reflected in increased creatinine levels. Therefore, kidney injury markers that can predict AKI are needed. The potential of the kidney injury markers urea, cystatin C, α1-microglobulin (A1M) and neutrophil gelatinase-associated lipocalin (NGAL) to detect early AKI during HFRS was studied by quantifying the levels of these markers in consecutively obtained plasma (P) and urine samples (U) for 44 HFRS patients. P-cystatin C and U-A1M levels were significantly increased during early HFRS compared to follow-up. In a receiver operating characteristic (ROC) curve analysis, P-cystatin C, U-A1M and P-urea predicted severe AKI with area under the curve 0.72, 0.73 and 0.71, respectively, whereas the traditional kidney injury biomarkers creatinine and U-albumin did not predict AKI. Nearly half of the HFRS patients (41%) fulfilled the criteria for shrunken pore syndrome, which was associated with the level of inflammation as measured by P-CRP. P-cystatin C and U-A1M are more sensitive and earlier markers compared to creatinine in predicting kidney injury during HFRS.
Ort, förlag, år, upplaga, sidor
MDPI, 2020. Vol. 9, nr 8, artikel-id 666
Nyckelord [en]
acute kidney injury, hemorrhagic fever with renal syndrome, orthohantavirus, puumala virus, viral hemorrhagic fever, cystatin C, alpha-1-microglobulin, neutrophil gelatinase-associated lipocalin, creatinine
Nationell ämneskategori
Klinisk medicin
Identifikatorer
URN: urn:nbn:se:umu:diva-175094DOI: 10.3390/pathogens9080666ISI: 000565645700001PubMedID: 32824680Scopus ID: 2-s2.0-85089656216OAI: oai:DiVA.org:umu-175094DiVA, id: diva2:1469560
Forskningsfinansiär
Åke Wibergs Stiftelse, M18-00312020-09-222020-09-222025-02-18Bibliografiskt granskad