The Metamorphosis of Acute Renal Failure to Acute Kidney Injury

Abstract

Successive generations of scientists and nephrologists have failed to prevent or cure Acute Kidney Injury (AKI) and thousands every year die because of this. Recent innovations in proteomics and genomics have brought hope and renewed interest in preventing this blight. Motivated by high incidence and lack of effective treatments, researchers have focussed on how to detect AKI early in the disease process so as to provide the maximum opportunity for early intervention and positive outcomes. AKI Incidence is greatest in the intensive care, at about 11-52% in larger studies (n>500) (Ahlstrom et al. (2006); Bagshaw et al. (2008); Cruz et al. (2007)). Cardiac surgery and procedures involving radiocontrast pose smaller, but significant, risk of AKI with an incidence of 3-15% depending on cohort (Harjai et al. (2008); Lassnigg et al. (2008)). From 13 studies the mortality with AKI was 31.2% and was associated with an increase in relative risk of death from 2.40 to 6.15 depending on AKI severity (Ricci et al. (2008)). Stimulating much recent research has been the discovery of new kidney injury biomarkers, some of which appear to have sufficient sensitivity and specificity to be clinically useful. This chapter will outline the history of the development of the concepts of clearance, acute renal failure, and acute kidney injury. This history provides the context for the current clearance based AKI diagnostic paradigm. The discovery of novel kidney injury biomarkers is challenging that paradigm. We will discuss the nature of that challenge and the opportunity it provides for development of early intervention treatments. All epidemiology, biomarker studies and clinical trials rely on tools to quantify AKI and assess efficacy of diagnostic or treatment efficacy. In section 3 we will discuss those tools before moving on to considering how they may best be applied in practice (section 4).