The kidney in acute renal failure: innocent bystander, victim or still a suspect?

Excerpt

Despite great progress in critical care, acute renal failure (ARF) is a frequent and fatal complication contributing significantly to morbidity and mortality among critically ill patients [1]. The incidence of ARF in intensive care units ranges from 3 to 25% depending on the criteria applied, underlining the problem of more than 30 definitions. Today the two widely accepted classification systems are the RIFLE criteria and the staging system for acute kidney injury (AKI) as established by the Acute Dialysis Quality Initiative (ADQI) and the Acute Kidney Injury Network (AKIN), respectively [2, 3]. Regardless of modern renal replacement therapies and promising preclinical and clinical treatment trials, ARF-related hospital mortality ranges between 25 and 80% [2‐4]. This unacceptably high mortality as well as increasing costs of critical care treatment exerts pressure to develop a better understanding of the underlying pathology of this disease and to generate new therapeutic strategies with the potential to attenuate ARF. Although the pathophysiology of ARF is not fully understood, there is general agreement that in several clinical situations renal hypoperfusion and a concomitant lowering of the glomerular filtration rate (GFR), induced by a decrease in systemic and/or renal perfusion pressure, are hallmarks of the genesis of ARF [5‐10]. …