Toward Precision Medicine: Exploring the Landscape of Biomarkers in Acute Kidney Injury

Abstract

Acute kidney injury (AKI) remains a complex challenge with diverse underlying pathological mechanisms and etiologies. Current detection methods predominantly rely on serum creatinine, which exhibits substantial limitations in specificity and poses the issue of late-stage detection of kidney injury. In this review, we propose an up-to-date and comprehensive summary of advancements that identified novel biomarker candidates in blood and urine and ideal criteria for AKI biomarkers such as renal injury specificity, mechanistic insight, prognostic capacity, and affordability. Recently identified biomarkers not only indicate injury location but also offer valuable insights into a range of pathological processes, encompassing reduced glomerular filtration rate, tubular function, inflammation, and adaptive response to injury. The clinical applications of AKI biomarkers are becoming extensive and serving as relevant tools in distinguishing acute tubular necrosis from other acute renal conditions. Also, these biomarkers can offer significant insights into the risk of progression to chronic kidney disease CKD and in the context of kidney transplantation. Integration of these biomarkers into clinical practice has the potential to improve early diagnosis of AKI and revolutionize the design of clinical trials, offering valuable endpoints for therapeutic interventions and enhancing patient care and outcomes.

Crosstalk among proximal tubular cells, macrophages, and fibroblasts in acute kidney injury: single-cell profiling from the perspective of ferroptosis

“…It was found that the expression of Havcr1 did progressively increase over time (Supplementary 1 a, c) [ 37 ]. Similarly, Neutrophil Gelatinase-Associated Lipocalin (lipocalin 2, Lcn2), also known as Ngal, a widely recognized biomarker for kidney injury, demonstrated a parallel increasing trend with Havcr1 (Supplementary 1 b, c) [ 38 ]. Building on this foundation, we utilized NMF analysis and defined 4 clusters of proximal tubule cells.…”

Selenoprotein-P1 (SEPP1) Expression in Human Proximal Tubule Cells after Ischemia-Reperfusion Injury: An In Vitro Model

“…Novel biomarkers, anticipating serum creatinine rise, are needed to have a speedy diagnosis of acute kidney injury, and thus, to mitigate and to preserve kidney function with well-timed therapeutic plans. Cystatin C, kidney injury molecule-1, and human neutrophil gelatinase-associated lipocalin have been found to change earlier than creatinine, particularly when measured in combination, so their use in clinical practice can facilitate early diagnosis and treatment of AKI [ 7 ]. The urgency for new markers stems from the critical need to swiftly diagnose AKI and implement timely therapeutic interventions to preserve renal function [ 8 ].…”