Biomarkers of acute kidney injury: Time to learn from implementations

Acute kidney injury (AKI) is a major clinical problem in the community and in hospital, with hospital-acquired AKI reported in about 20% of adult and 30% of paediatric admissions. Laboratory creatinine data from New South Wales support these figures: 16.4% of patients and 12.4% of hospitalisations developed AKI over a 5-year period. This study also highlighted the under-reporting of AKI in Australia based on coding of the International Classification of Diseases, tenth revision, Australian modification (ICD-10-AM) (1.6% incidence) versus laboratory creatinine-based diagnosis (12.4%). In addition, AKI leads to the development of chronic kidney disease (CKD) in many survivors. However, the true incidence of kidney damage following AKI may be even greater, since overt or subclinical AKI may lead to subclinical CKD, which in turn may precede overt CKD. Without measuring renal reserve or performing renal biopsy, subclinical CKD remains undetected, as creatinine remains normal by definition. Along with overt CKD, subclinical CKD remains a risk factor for AKI following repeated kidney exposure to injury. Unfortunately, an inevitable delay in diagnosis is inherent in the functional definition of AKI as recommended by the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. This delay results from creatinine kinetics, with the result that creatinine-based diagnosis has never and will never lead to successful intervention trials in AKI. However, this definition is likely to change because of the recognition that kidney damage biomarkers offer near real-time detection of kidney cellular injury.