Acute Kidney Injury and 2009 H1N1 Influenza-Related Critical IllnessBellomo R.a · Pettilä V.a · Webb S.A.R.b · Bailey M.a · Howe B.a · Seppelt I.M.c
aAustralian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Melbourne, Vic.; bDepartment of Intensive Care Medicine, Royal Perth Hospital, Perth, WA, and School of Population Health and School of Medicine and Pharmacology, University of Western Australia, Crawley, WA, and cDepartment of Intensive Care Medicine, Nepean Hospital, and Discipline of Intensive Care Medicine, Sydney Medical School – Nepean, University of Sydney, Sydney, NSW, Australia
The year 2009 was characterized by a pandemic with a new virus, the 2009 H1N1 influenza virus. This pandemic was responsible for thousands of deaths worldwide, many more hospital admissions, and thousands of admissions to intensive care units (ICUs). Among those admitted to ICUs, the pandemic was associated with a mortality of approximately 16%, a high incidence of acute lung injury and, in some cases, acute respiratory distress syndrome severe enough to require support with extracorporeal membrane oxygenation. As part of such a critical illness, a percentage of patients developed acute kidney injury (AKI) which complicated their clinical course and, in some patients, required support by renal replacement therapy. In a case series from Mexico, the incidence of severe AKI was reported in about 30% of the patients. Similarly, at the Austin Hospital, of 13 cases, 8 developed AKI with 3 being classified in the failure category of the RIFLE classification. Among the patients with AKI, hospital mortality was approximately 25%. Of the AKI patients, 3 (37.5%) received renal replacement therapy and, among these, 1 died. In a case of severe AKI and multi-organ failure from whom histological material was obtained, the renal histopathological findings were typical of acute tubular necrosis. One patient who suffered from hypoxic brain injury due to cardiac arrest at home secondary to H1N1 pneumonia became a kidney and liver donor. There was no evidence of viral infiltration on kidney biopsy and the recipient did not develop H1N1 infection.
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