Septic acute kidney injury and tubular apoptosis: never a Lone Ranger

Excerpt

Until recently, acute kidney injury (AKI) in intensive care was, on the whole, considered to be a condition of haemodynamic origin and, consequently, nearly all efforts were concentrated on increasing renal flow by increasing cardiac flow and perfusion pressure [1]. In this context, AKI was thought to be a result of low renal blood flow, induced by either cardiogenic shock or distributive (septic) shock, or both. Early in this decade, Bellomo’s group presented data shedding new light on the animal model of septic AKI. These researchers found that renal blood flow, both medullar and cortical, is maintained and even increases during severe septic shock [2], thereby undermining earlier concepts and definitively demonstrating that septic AKI is a totally different physiological phenomenon to non-septic AKI. In an even earlier study, Hotchkiss et al. demonstrated that apoptosis—and not necrosis alone—plays an important role in sepsis and septic shock [3]. Despite these findings and although animal models provided substantial advances in the elucidation of the aetiology of lesions such as tubular apoptosis [4], debate remained ongoing whether apoptosis really played a key role in mechanisms of organ dysfunction in humans [5]. This debate is clearly reflected by the authors of the study on the histopathological features of AKI, which has recently been published in this journal [6]. In their introduction, the authors state that there is a paucity of histopathological data in humans and that most of the data currently available were published in studies carried out before the 1980s [6]. In their study, these authors compared kidney biopsies taken early post-mortem in 19 consecutive patients dying from septic shock with biopsies taken from eight dead trauma patients and nine dead patients without sepsis with only mild renal dysfunction [6]. …