Small elevations in serum creatinine may reflect significant kidney damage and be associated with poor patient outcomes, thus rendering creatinine to be a late marker of acute kidney injury (AKI). AKI researchers refer to the AKI biomarker quest as the "search for the renal troponin I," implying that such putative earlier AKI biomarker use could allow for earlier intervention. We consider the analogy to troponin I and its acceptance to prompt evaluation and therapeutic intervention to treat myocardial ischemia and prevent myocardial infarction an informative and potentially applicable model to the AKI field. Because AKI does not hurt, there is no validated equivalent of chest pain or anginal equivalent to increase suspicion for AKI presence on the part of the clinician. So, although biomarkers may ultimately be validated to detect AKI early, unless nephrologists and intensivists can define "renal angina" to initiate "renal troponin I" assessments, AKI biomarkers may never realize their full potential to improve patient care and outcomes. The purpose of this article is to review both adult and pediatric AKI literature to devise a definition for a renal anginal syndrome equivalent.