Pettila et al. [8] and Nin et al. [9] reported the epidemiology of AKI associated with severe H1N1 infections in different parts of the world. They found incidence rates of AKI of between 34 and 51%, demonstrating the high frequency of this complication in patients suffering from H1N1 infection. The occurrence of AKI was associated with a significantly increased risk of hospital mortality. Nin et al. specifically addressed the question of early AKI versus late AKI (after ICU day 2), and found a worse outcome for the latter, indicating that a large proportion of early AKI occurring in the context of H1N1 infection is presumably due to pre-renal factors like dehydration or hypotension, which can be easily corrected, resulting in rapid renal recovery. However, as demonstrated in accompanying correspondence by Nin et al. [10] , viral particles could also be found within renal tissue obtained from a few biopsies, which possibly contributed to AKI. These studies provide further insight into the pathophysiology of AKI in the setting of severe viral infections; it is most probably a mixture of pre-renal causes combined with endothelial damage and severe disturbance of the coagulation system caused by exaggerated inflammatory response and finally complicated by secondary bacterial infections. Direct renal effects of viral infiltration of the kidney, however, appear to be a very rare mechanism for AKI [11] .