Biomarkers of Acute Renal Failure
Progression From Pre-renal to Acute Tubular Necrosis

August 2009
Typically patients with acute kidney injury progress from a period of prerenal decline in kidney function, where they are at risk for structural kidney damage, as shown on this slide. These patients are in a prerenal state due to some initial insult that decreases blood pressure and renal perfusion. At some point the situation is compounded by a second insult, for example, infection or administration of a nephrotoxic agent, or perhaps the patient has prolonged and severe hypotension such that irreversible ischemic damage occurs to the kidney. This is indicated by the second insult on the slide. At this point, the patient is destined to develop true acute tubular necrosis. Nevertheless, serum creatinine is not likely to begin to rise for another 24 to 48 hours. During this time, progressive kidney damage is continuing to occur. It would be ideal to identify patients very early after injury so that appropriate interventions can take place. This is indicated by the “window of opportunity” on the slide, which spans the prerenal stage of acute kidney injury through early acute tubular necrosis. This would, in many ways, parallel the situation in acute myocardial infarction. There are patients identified very early with elevated enzymes such as troponin. Such patients can be effectively treated with thrombolytics and other interventions in order to save additional myocardium that is at risk. In a similar manner, if we can identify patients with acute kidney injury very early, then we could possibly save them from additional kidney damage and impact on their overall course. Examples of potential interventions would include specific medications or growth factors that might hasten kidney recovery or limit damage. In fact, previous studies using potentially promising growth factors may have failed to demonstrate benefit because patients were already at the stage where their creatinine had gone up and a large amount of irreversible kidney damage had already occurred.
Pre-renal to Acute Tubular Necrosis |
Jump to section:
- Introduction
- Acute Kidney Injury
- Common Causes of Acute
- Progression From Pre-renal to Acute Tubular Necrosis
- Towards a Kidney Troponin
- Origin of Formed Elements in Urinalysis
- Urinanalysis: A Traditional Biomarker of AKI
- Hyaline Casts
- Renal Epithelial Cell Cast
- Leukocyte Cast
- RBC Cast
- Pigmented Cast
- Granular Cast
- Other Helpful Indices
- Potential Sources of Urinary Biomarkers
- NGAL as a Biomarker
- Studies Support NGAL as a Biomarker of AKI in the Following Situations
- Mayo Renal Laboratory Urinary NGAL Normals
- Normal Urinary NGAL Levels are Not Dependent on Age, but are Higher in Women than Men
- Ongoing Mayo Clinic Clinical Validation Study
- Ongoing Mayo Clinic Clinical Validation Study: Preliminary Results
- Study
- Other Potential Markers on the Horizon
- Mayo Clinic Goals
- Conclusions
- References
- Questions?


