Biomarkers in pursuit of precision medicine for acute kidney injury: hard to get rid of customs (krcp-ksn.org)
Proposed strategies for managing AKI.
The definition of AKI encompasses an escalation in serum creatinine levels, a decrease in urine output, and the presence of kidney damage and stress biomarkers. Various biomarkers, some of which are accessible at the point of care, may assist in the early detection of AKI. These biomarkers can facilitate the timely identification of patients who exhibit potential endotypes, amenable traits for targeted interventions, or suitability for specific preventive measures. AKI subphenotypes, which are delineated by their clinical attributes, have already been integrated into routine clinical practice, including considerations such as etiology, AKI staging, severity, and duration. However, the integration of biomarkers into these subphenotypes may offer a more comprehensive and informative framework, culminating in predictive and prognostic insights. This refined definition of subphenotypes aims to distinguish patient subgroups with comparable outcomes (prognostic enrichment) or similar responses to therapeutic interventions (predictive enrichment). The evolution of treatment strategies requires further development and fine-tuning. Moreover, the nuanced categorization of AKI subphenotypes will advance with the discovery of novel biomarkers and more precise clinical and biomarker-derived subphenotypes.
AI, artificial intelligence; AKD, acute kidney disease; AKI, acute kidney injury; APACHE II, Acute Physiology and Chronic Health Evaluation II; CKD, chronic kidney disease; FST, furosemide stress test; IGFBP7, insulin-like growth factor-binding protein 7; KDIGO, Kidney Disease Improving Global Outcomes; KIM-1, kidney injury molecule-1; LIION, low perfusion, inflammation/immune, obstruction, nephrotoxin/envenomation; NGAL, neutrophil gelatinase-associated lipocalin; sCr, serum creatinine; TIMP-2, metalloproteinase 2; UO, urine output.
Proposed strategies for managing AKI.
The definition of AKI encompasses an escalation in serum creatinine levels, a decrease in urine output, and the presence of kidney damage and stress biomarkers. Various biomarkers, some of which are accessible at the point of care, may assist in the early detection of AKI. These biomarkers can facilitate the timely identification of patients who exhibit potential endotypes, amenable traits for targeted interventions, or suitability for specific preventive measures. AKI subphenotypes, which are delineated by their clinical attributes, have already been integrated into routine clinical practice, including considerations such as etiology, AKI staging, severity, and duration. However, the integration of biomarkers into these subphenotypes may offer a more comprehensive and informative framework, culminating in predictive and prognostic insights. This refined definition of subphenotypes aims to distinguish patient subgroups with comparable outcomes (prognostic enrichment) or similar responses to therapeutic interventions (predictive enrichment). The evolution of treatment strategies requires further development and fine-tuning. Moreover, the nuanced categorization of AKI subphenotypes will advance with the discovery of novel biomarkers and more precise clinical and biomarker-derived subphenotypes.
AI, artificial intelligence; AKD, acute kidney disease; AKI, acute kidney injury; APACHE II, Acute Physiology and Chronic Health Evaluation II; CKD, chronic kidney disease; FST, furosemide stress test; IGFBP7, insulin-like growth factor-binding protein 7; KDIGO, Kidney Disease Improving Global Outcomes; KIM-1, kidney injury molecule-1; LIION, low perfusion, inflammation/immune, obstruction, nephrotoxin/envenomation; NGAL, neutrophil gelatinase-associated lipocalin; sCr, serum creatinine; TIMP-2, metalloproteinase 2; UO, urine output.