• Toru Watanabe.
• Department of Pediatrics, Niigata City General Hospital, 463-7 Shumoku, Chuo-ku, Niigata City 950-1197, Japan. twata@hosp.niigata.niigata.jp
• Eur. J. Pediatr. 2013 Jan 1; 172 (1): 15-22.

AbstractRenal complications of influenza A virus infections are uncommon but can contribute to a deterioration in the patient's condition, which include acute kidney injury (AKI) in critically ill patients, rhabdomyolysis, hemolytic uremic syndrome (HUS), acute glomerulonephritis (AGN), disseminated intravascular coagulation (DIC), Goodpasture's syndrome, and acute tubulointerstitial nephritis (TIN). The clinical characteristics of AKI in critically ill patients with pandemic influenza A(H1N1) 2009 virus (A(H1N1)pdm09) infection are similar to uninfected patients. Underlying conditions associated with AKI include older age, diabetes mellitus, obesity, pregnancy, history of asthma, and chronic kidney disease. Histologic examination of the kidneys from patients with A(H1N1)pdm09 infection who died include acute tubular necrosis (ATN), myoglobin pigment, and DIC. A(H1N1)pdm09 is present in the kidneys of some patients. The clinical characteristics of patients with rhabdomyolysis associated with influenza A include younger age and the frequent occurrence of muscle symptoms. AKI occurs in approximately one third of patients with rhabdomyolysis due to influenza A. HUS is associated with A(H1N1)pdm09 as follows: Streptococcus pneumoniae-associated HUS following A(H1N1)pdm09 infection, HUS triggered by A(H1N1)pdm09 in patients with genetic complement dysregulation, and HUS associated with A(H1N1)pdm09 without known underlying disorder. AGN, Goodpasture's syndrome, and acute TIN are extremely rare complications of influenza A virus infection. Although the pathogenesis underlying renal injuries due to influenza A virus has not been delineated, some hypotheses have been advanced, including ATN due to renal hypoperfusion or rhabdomyolysis, glomerular microthrombosis due to DIC, direct viral injury to the kidney, and an altered immune system with systemic mononuclear cell activation following influenza A virus infections.

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