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Acute Kidney Injury (AKI) biomarker
1Department of Clinical Pathology, Faculty of Medicine, University of Indonesia-Cipto Mangunkusumo Hospital, Jakarta, Indonesia.
Abstract:
The kidney has a remarkable capacity to withstand insults for an extended period of time. The sensitivities of individual renal cells to injury vary depending on their type, position in the nephron, local vascularization, and the nature of injury. The resulting kidney injury is a product of the interplay between cell dysfunction, cell death, proliferation, inflammation, and recovery. The Acute Kidney Injury Network (AKIN) defined Acute Kidney Injury (AKI) as "functional and structural disorder or signs of renal damage including any defect from blood and urine test, or tissue imaging that is less than 3 months". RIFLE (Risk, Injury, Failure, Loss, End-Stage Kidney Disease) criteria is the most frequently used system. Ideal biomarker for AKI should be affordable, quick and measurable, precise and accurate, with prognostic ability to define severity of renal dysfunction, specific for renal, increase in the early stage dysfunction, with high sensitivity and specificity. Efforts to detect AKI in the earlier stage has resulted in some promising biomarkers such as KIM-1, NGAL, IL-18, Clusterin, etc. Cystatin C is a biomarker for glomerular filtration function, while 2-microglobulin, 1-microglobulin, NAG, RBP, IL-18, NGAL, Netrin-1, KIM-1, Clusterin, Sodium Hydrogen Exchanger Isoform and Fetuin A are biomarkers for tubular reabsorption function.
Insights
Acute Kidney Injury (AKI) involves complex kidney damage. Early detection through novel biomarkers like KIM-1 and NGAL is crucial for timely intervention and improved patient outcomes.
Area of Science:
- Nephrology
- Biomarker Discovery
- Renal Pathophysiology
Background:
- Kidneys possess significant resilience to injury, but cell type, location, and injury type influence sensitivity.
- Kidney injury results from a complex interplay of cellular dysfunction, death, proliferation, inflammation, and recovery processes.
- Acute Kidney Injury (AKI) is defined by the Acute Kidney Injury Network (AKIN) as renal damage or dysfunction lasting less than 3 months, often assessed using RIFLE criteria.
Purpose of the Study:
- To explore the characteristics and sensitivities of renal cells to injury.
- To understand the multifactorial nature of kidney injury.
- To identify and evaluate ideal biomarkers for early and accurate detection of Acute Kidney Injury (AKI).
Main Methods:
- Review of existing literature on renal cell injury mechanisms.
- Analysis of the definition and diagnostic criteria for AKI (AKIN and RIFLE).
- Evaluation of the desired characteristics for ideal AKI biomarkers.
Main Results:
- Renal cell injury is influenced by various factors including cell type and injury nature.
- Several promising biomarkers, including KIM-1, NGAL, IL-18, and Clusterin, are being investigated for early AKI detection.
- Specific biomarkers are associated with either glomerular filtration (e.g., Cystatin C) or tubular reabsorption function (e.g., KIM-1, NGAL).
Conclusions:
- Early detection of AKI is critical and relies on identifying sensitive and specific biomarkers.
- Ongoing research focuses on biomarkers that can accurately assess renal function and predict AKI severity.
- A range of biomarkers show potential for diagnosing glomerular and tubular dysfunction in AKI.
Related Concept Videos
01:22Acute Kidney Injury I: Introduction
01:30Acute Kidney Injury IV: Diagnostic Studies and Prevention
01:29Acute Kidney Injury II: Pathophysiology
01:29Acute Kidney Injury III: Clinical Manifestations
01:20Acute Kidney Injury V: Interprofessional Care
01:22Acute Kidney Injury VI: Nursing Management