| Biomarker | ELOVL7 / SOCS3 / ACSL4 / CLU / PRKAR1A / ABCG1; cg26345888 / DAB1; Flavonifractor plautii; Phytosphingosine; ApoA2 / ACE-2 / IL-33 / FoxP3 | Full name | / | Molecular Type | Gene expression / mRNA; DNA methylation / Epigenetic; Gut microbiome; Metabolite; Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Constitution identification, early warning, metabolic-risk assessment, vascular endothelial function assessment |
| Disease(or Constitution) | Phlegm-dampness constitution (PDC) | Disease Subtypes | Obesity; metabolic disorder susceptibility | ||
| Organ | Intestine; vascular system; gut–liver axis | Test Sample / Technology Platform | PBMCs (gene-expression microarray, qRT-PCR, pyrosequencing); feces (metagenomic sequencing, qPCR); serum (proteomics, metabolomics, LC-MS/MS); EndoPAT | ||
| Pathobiological Mechanisms | PDC is associated with abnormalities in metabolic and inflammatory regulation. Differential gene expression and DNA methylation are linked to metabolic susceptibility; reduced F. plautii and phytosphingosine are associated with higher PDC scores and metabolic abnormalities; altered ApoA2, ACE-2, IL-33 and FoxP3 are associated with impaired vascular endothelial function. | ||||
| Clinical Availability Status | Research-stage | ||||
| Notes and Dynamics | Representative biomarkers span transcriptomic, epigenetic, microbiome, metabolomic and proteomic levels. Some changes, particularly reduced F. plautii and phytosphingosine, were observed even in PDC individuals with normal metabolic indices, suggesting potential value for early risk assessment. | ||||
| Biomarker | UNa / FEK | Full name | Urinary sodium/ fractional excretion of potassium | Molecular Type | Electrolyte / function index |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early warning, microcirculation stress assessment |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（Electrolyte detection, biochemical calculation） | ||
| Pathobiological Mechanisms | The decrease of UNa reflects renal microcirculation stress, and the increase of FEK indicates early renal tubular injury. | ||||
| Clinical Availability Status | Clinical routine use ( functional evaluation ) | ||||
| Notes and Dynamics | UNa decreased 1-2 days before AKI.FEK was not affected by diuretics and was more sensitive than fractional excretion of sodium ( FENa ). | ||||
| Biomarker | mtDNA / nDNA)/ nucleosome | Full name | Mitochondrial DNA / nuclear DNA )/ nucleosome | Molecular Type | Nucleic Acid/ Nucleic Acid Protein Complex |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early diagnosis、Tissue injury assessment |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Plasma（PCR、ELISA） | ||
| Pathobiological Mechanisms | The damage-associated molecular pattern ( DAMP ) released during cell necrosis reflects systemic and renal cell injury. | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | The high level of admission predicts post-traumatic AKI, and nDNA can be used as an early intervention target. | ||||
| Biomarker | TIMP-2×IGFBP7 | Full name | Tissue inhibitor of metalloproteinases-2 × Insulin-like growth factor-binding protein 7 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early warning, cell cycle arrest monitoring |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（NephroCheck™/Kits/Bedside testing） | ||
| Pathobiological Mechanisms | The release of renal tubular epithelial cells after stress reflects cell cycle arrest, suggesting the risk of AKI. | ||||
| Clinical Availability Status | FDA approval / Cinical application | ||||
| Notes and Dynamics | The only FDA-approved AKI risk assessment marker that predicts moderate to severe AKI within 12-24 hours has been validated in trauma ICU populations. | ||||
| Biomarker | DKK3 | Full name | Dickkopf-3 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Microorganism、Risk of fibrosis |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine / Serum（ELISA） | ||
| Pathobiological Mechanisms | It is secreted during renal tubular stress, participates in the Wnt / β-catenin pathway, and promotes renal fibrosis | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | Predict the risk of postoperative AKI and long-term renal injury, CI-AKI independent predictors | ||||
| Biomarker | CCL14 | Full name | C-C motif chemokine ligand 14 | Molecular Type | Chemotactic factor |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Microorganism、Persistent injury prediction |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（ELISA） | ||
| Pathobiological Mechanisms | It is released when continuous renal tubular injury mediates inflammatory signals, suggesting prolonged injury. | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | Strongly predict persistent stage 2-3 AKI and guide the timing of targeted intervention. | ||||
| Biomarker | L-FABP | Full name | Liver-type fatty acid-binding protein | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early diagnosis、Hypoxia monitoring |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（Immunoassay, bedside semi-quantitative detection） | ||
| Pathobiological Mechanisms | Oxidative stress-induced expression during renal tubular hypoxia reflects renal tubular ischemia-reperfusion injury | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | The elevation of 2-4 hours can dynamically monitor the optimization effect of renal perfusion, and bedside detection can quickly determine the ischemic state. | ||||
| Biomarker | IL-18 | Full name | Interleukin-18 | Molecular Type | Cytokines |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early diagnosis、Inflammation association |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（ELISA） | ||
| Pathobiological Mechanisms | Renal tubular epithelial cells are released after injury and participate in the inflammatory cascade reaction. | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | The diagnostic value of in sepsis-related AKI is outstanding, and the increase in TBI patients is related to AKI. | ||||
| Biomarker | KIM-1 | Full name | Kidney injury molecule-1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early diagnosis、Localization of renal tubular injury |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（Immunoassay、ELISA） | ||
| Pathobiological Mechanisms | Proximal renal tubular epithelial cells were highly expressed and detached after injury, which specifically reflected renal tubular injury. | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | AKI is highly sensitive to ischemic and toxic AKI, and elevated baseline in CKD patients will reduce specificity. | ||||
| Biomarker | NGAL | Full name | Neutrophil gelatinase-associated lipocalin | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early diagnosis |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Plasma / Urine（SIMOA、ELISA） | ||
| Pathobiological Mechanisms | Released after renal tubular epithelial cell injury or neutrophil activation, ischemia / nephrotoxic injury increases early. | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | It can be elevated in 2-3 hours to predict the severity of AKI and the need for renal replacement therapy, which is affected by systemic inflammation. | ||||
| Biomarker | Cys-C | Full name | Cystatin C | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis (early) |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum（immunoassay、ELISA） | ||
| Pathobiological Mechanisms | Glomerular free filtration, unaffected by muscle mass, reflects changes in GFR earlier. | ||||
| Clinical Availability Status | Study test | ||||
| Notes and Dynamics | It is more sensitive than creatinine, and can be combined with creatinine to optimize diagnostic accuracy. There is a lack of ICU population-specific formula. | ||||
| Biomarker | SCRE | Full name | Serum creatinine | Molecular Type | Metabolites |
| Molecular Formula | C₄H₇N₃O | Molecular Weight | 113.12 g/mol | Core Functional Dimensions | Diagnosis (delay) |
| Disease(or Constitution) | Acute Kidney Injury (AKI) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum（Routine biochemical tests） | ||
| Pathobiological Mechanisms | Diagnosis ( early glomerular filtration function decreased and then accumulated, only increased when renal function loss ≥ 50 % ) | ||||
| Clinical Availability Status | Clinically routine use | ||||
| Notes and Dynamics | Delay index, affected by muscle mass and body fluid status, can not distinguish between functional and structural damage. | ||||
| Biomarker | Urine IL-6、TGF-β1 | Full name | Urinary interleukin-6、Urinary transforming growth factor-beta 1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease progression prediction |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine | ||
| Pathobiological Mechanisms | Elevated levels of urinary IL-6 and TGF-β1 are associated with an increased risk of IgAN progression, and urinary IL-6 is an independent risk factor for IgAN progression. | ||||
| Clinical Availability Status | Research verification stage：The predictive value is clear and needs to be verified by clinical application. | ||||
| Notes and Dynamics | It provides an important basis for the prognostic stratification of IgAN and can guide the timing of clinical intervention. | ||||
| Biomarker | u-sCD163 | Full name | Urinary soluble CD163 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease severity assessment and remission status prediction |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（ELISA） | ||
| Pathobiological Mechanisms | he shedding of monocytes and macrophages is related to the excessive activation of macrophages. The level of u-sCD163 is related to the histopathological activity, clinical manifestations and remission status of IgAN. | ||||
| Clinical Availability Status | Research verification stage：Non-invasive assessment of disease status requires large sample verification. | ||||
| Notes and Dynamics | It can be used as an important non-invasive index for disease monitoring and efficacy evaluation of IgAN patients, and is highly correlated with disease activity. | ||||
| Biomarker | Urinary miR-106a | Full name | Urinary MicroRNA-106a | Molecular Type | RNA（miRNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine（Liquid biopsy） | ||
| Pathobiological Mechanisms | The level of miR-106 a in urine has excellent sensitivity for the identification of IgAN and avoids the interference of markers related to renal scar formation. | ||||
| Clinical Availability Status | Research verification stage: High sensitivity, need to verify the role of screening | ||||
| Notes and Dynamics | Based on liquid biopsy technology, it is a potential marker for non-invasive diagnosis of IgAN, and its specificity needs to be further confirmed. | ||||
| Biomarker | Serum and urine metabolic fingerprints ( based on NPELDI-MS ) | Full name | Serum and urine metabolic fingerprints ( based on NPELDI-MS ) | Molecular Type | Metabolome |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Early diagnosis、Prognostic evaluation |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum、Urine（NPELDI-MS、Machine learning） | ||
| Pathobiological Mechanisms | The metabolic fingerprints were obtained by nanoparticle-enhanced laser desorption / ionization mass spectrometry. The model had high diagnostic efficiency for IgAN ( AUC = 0.81-0.95 ), and the dynamic changes of key metabolites reflected the prognosis. | ||||
| Clinical Availability Status | Research verification stage：The diagnostic efficiency is high, which needs to be verified by clinical transformation. | ||||
| Notes and Dynamics | The combination of mass spectrometry and machine learning to achieve non-invasive, accurate diagnosis and prognosis evaluation of IgAN is a typical case of metabolomics application. | ||||