https://orcid.org/0000-0001-8109-3429
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ABSTRACT
Introduction
Acute kidney injury (AKI) defined by a substantial decrease in kidney function within hours to days and is often irreversible with higher risk to chronic kidney disease (CKD) transition.
Areas covered
The authors discuss the diagnostic and predictive utilities of serum and urinary biomarkers on AKI and on the risk of AKI-to-CKD progression. The authors focus on the relevant literature covering evidence of circulating and urinary biomarkers’ capability to predict the transition of AKI to CKD.
Expert opinion
Based on the different modalities of serum and urinary biomarkers, multiple biomarker panel seems to be potentially useful to distinguish between various types of AKI, to detect the severity and the risk of AKI progression, to predict the clinical outcome and evaluate response to the therapy. Serum/urinary neutrophil gelatinase-associated lipocalin (NGAL), serum/urinary uromodulin, serum extracellular high mobility group box-1 (HMGB-1), serum cystatin C and urinary liver-type fatty acid-binding protein (L-FABP) were the most effective in the prediction of AKI-to-CKD transition regardless of etiology and the presence of critical state in patients. The current clinical evidence on the risk assessments of AKI progression is mainly based on the utility of combination of functional, injury and stress biomarkers, mainly NGAL, L-FABP, HMGB-1 and cystatin C.
Article highlights
Evaluation of serum levels of creatinine, estimated glomerular filtration rate and detection of proteinuria/albuminuria demonstrate a delay in the detection of acute kidney injury at the early stage.
Stress biomarkers, such as TIMP-2 and IGFBP7, after acute kidney injury can predict clinical outcomes and improve risk stratification in critically ill patients at early stage of the disease.
Functional biomarkers mainly cystatin C demonstrate positive associated with the staging of acute kidney injury.
Assessment of the risk of acute kidney injury progression and mortality is mainly based on the combination of serum/urinary biomarkers of functional abnormality and damage.
Serum/urinary NGAL, L-FABP, HMGB-1 and cystatin C exhibit the best diagnostic and predictive potency for acute kidney injury progression.
Abbreviations
| ACC | = | American College of Cardiology |
| AGEs | = | Advanced glycation end products |
| AHA | = | American Heart Association |
| AKI | = | Acute kidney injury |
| CKD | = | Chronic kidney disease |
| CMPs | = | Cardiomyopathies |
| CV | = | Cardiovascular |
| CVD | = | Cardiovascular disease |
| DM | = | Diabetes mellitus |
| Erk1/2 | = | Extracellular signal-regulated kinase 2 |
| ESC | = | European Society of Cardiology |
| FGF-23 | = | Fibroblast growth factor-23 |
| GFR | = | Glomerular filtration rate |
| HF | = | Heart failure |
| HMGB-1, | = | Extracellular high mobility group box-1 |
| ICU | = | Intensive care unit |
| IL | = | Interleukin |
| JNK | = | C-Junus N terminal kinase |
| KIM-1 | = | Kidney injury molecule-1 |
| NGAL | = | Neutrophil gelatinase-associated lipocalin |
| NSAID | = | Non-steroid anti-inflammatory drugs |
| PAD | = | Peripheral artery disease |
| PCT | = | Polychemotherapy |
| PENK | = | Proenkephalin |
| PI3K | = | Insulin-dependent phosphatidylinositol 3-kinase |
| PPRA | = | Peroxisome proliferator-activated receptor |
| RAAS | = | Renin–angiotensin–aldosterone system |
| TGF-β1 | = | Transforming growth factor beta 1 |
| TNF-α | = | Tumor necrosis factor-alpha |
| UMOD | = | Uromodulin |
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.