An analysis of the mechanisms of acute kidney injury and novel biomarkers
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Citation
Abstract
Acute Kidney Injury (AKI) is a prevalent systemic disorder that has an extremely high rate of mortality even after detection. Historically, the diagnosis and treatment of AKI was marred by the lack of universally accepted criteria defining AKI. Therefore, reports of incidence and mortality varied widely depending on location and the criteria used at the time, but all reports indicated a poor prognosis for the patient. Until recently, the only modes of detecting AKI were primarily through measurements of three clinical findings: serum creatinine concentration, blood urea nitrogen concentration, and urine output. While these measurements are still widely used as standard practice, they have limitations in their utility because their values can fluctuate depending on a person's age, gender, race, diet, and other comorbid conditions. Nevertheless, as these were the only universally accepted units of measurement for kidney function, the Acute Dialysis Quality Initiative (ADQI) used them to create the Risk, Injury, Failure, Loss, and End stage kidney disease (RIFLE) criteria to classify the severity of kidney injury across clinical settings. Eventually, modifications were made by the Acute Kidney Injury Network (AKIN) to increase the sensitivity of AKI diagnosis. It was not until the last decade that new biomarkers of kidney injury began to be researched that provided earlier detection of physical kidney injury before functional manifestations would present themselves. Some of these new biomarkers include cystatin C, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase associated lipocalin (NGAL). This study will investigate how the properties of these new biomarkers are superior when compared to those of serum creatinine in early detection of AKI and specification as to the local site of injury within the nephron. The conclusion is that cystatin C has the potential to indicate damage to glomerular filtration while KIM-1 and NGAL have the ability to indicate damage to the proximal tubule. Along with the ability to provide information as to the specific site of renal injury, the levels of cystatin C, KIM-1, and NGAL increase much more rapidly and to a much higher value than serum creatinine once physical renal damage has occurred. These characteristics along with future research will allow for earlier detection of AKI, more personalized treatment plans, and an overall better prognosis for the patient.