Acute kidney injury ? Authors' reply

Rinaldo Bellomo, John A Kellum, Claudio Ronco

Research output: Contribution to journalLetterOther

1 Citation (Scopus)


We appreciate the concerns expressed by Athanasios Chalkias and Theodoros Xanthos about the role of increased intra-abdominal pressure in the pathogenesis of acute kidney injury (AKI), and indeed mention this possibility in our Seminar.1 However, as shown in a prospective investigation,2 although increased intra-abdominal pressure is common in patients in intensive care, its clinical meaning and renal consequences remain unclear in the absence of a full abdominal compartment syndrome. Therefore, we argue that routine measurement of intra-abdominal pressure is not justified unless intra-abdominal compartment syndrome seems clinically likely and renal function is being rapidly lost. Moreover, until randomised trials indicate that patients whose intra-abdominal pressure is routinely monitored achieve or maintain better renal function than do patients assigned standard care, we regard selective measurement of intra-abdominal pressure as a more rational approach. We fully share Alain Rudiger and Mervyn Singer s view that changes in intrarenal blood flow are most likely to be responsible for AKI, especially in sepsis.3 Thus, at least in the early phases, AKI seems to be a disease of the microcirculation. If this is correct, as many observations now suggest, the therapeutic implications are substantial. In particular, the administration of large amounts of fluids in a futile attempt to resuscitate the kidney might well aggravate rather than attenuate AKI.4 Such fluid-based therapy remains the unproven and pathophysiologically unjustified cornerstone of AKI treatment in critically ill patients. Accordingly, in our Seminar, we specifically sought to begin the process of formally challenging yet another unproven dogma in medicine. We fear that, until physicians are better informed about these developing insights into the pathogenesis of septic AKI, many patients will suffer from iatrogenic disease induced by flawed pathophysiological paradigms. RB and CR have received consultancy and speaking fees from Alere, Abbott Diagnostics, Gambro, Fresenius, B Braun, and Edwards Lifesciences. JAK has received consultancy and speaking fees from Alere, Abbott Diagnostics, Gambro, Baxter, and Fresenius.
Original languageEnglish
Pages (from-to)1905 - 1905
Number of pages1
JournalThe Lancet
Issue number9857
Publication statusPublished - 2012

Cite this