| Biomarker | U-Gly | Full name | Urinary glycine | Molecular Type | Metabolite |
| Molecular Formula | C₂H₅NO₂ | Molecular Weight | 75.07 g/mol | Core Functional Dimensions | Diagnosis, prognosis ( protective markers ) |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine ( Nuclear Magnetic Resonance Metabolomics ) | ||
| Pathobiological Mechanisms | Through nuclear magnetic resonance metabolomics identification, urinary glycine level is associated with IgAN and is a protective biomarker for IgAN. | ||||
| Clinical Availability Status | Research verification stage: The characteristics of protective markers are clear and need clinical verification. | ||||
| Notes and Dynamics | It provides new metabolic markers for early IgAN diagnosis and Prognostic judgment, and is protective and may become a target for intervention. | ||||
| Biomarker | SNUPE、eSNGFR | Full name | Single Nephron Ultrafiltration Parameters、estimated Single Nephron Glomerular Filtration Rate | Molecular Type | Physiological parameters |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Renal function assessment, disease progression monitoring |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Not clear ( functional assessment ) | ||
| Pathobiological Mechanisms | SNUPE is a sensitive biomarker, and eSNGFR cannot increase compensatoryly with the decrease of functional nephrons, reflecting the compensatory ability of diseased glomeruli. | ||||
| Clinical Availability Status | Research verification stage: It is necessary to standardize clinical detection to reflect glomerular compensatory function. | ||||
| Notes and Dynamics | To evaluate the renal reserve capacity of IgAN from the functional point of view, and to provide a basis for judging the stage of disease progression. | ||||
| Biomarker | NBL1 | Full name | Neuroblastoma oncogenic inhibitory factor 1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Evaluation of renal interstitial fibrosis and prediction of disease progression |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | It was significantly correlated with the severity of renal interstitial fibrosis and the progression of renal disease in IgAN patients, reflecting the degree of renal fibrosis. | ||||
| Clinical Availability Status | Research verification stage：Evaluating the risk of fibrosis requires clinical application verification. | ||||
| Notes and Dynamics | Noninvasive monitoring of the progression of IgAN renal interstitial fibrosis can guide the timing of anti-fibrosis treatment. | ||||
| Biomarker | Urinary complement protein ( involving AP, LP pathway ) | Full name | Urinary complement proteins (alternative pathway, lectin pathway) | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease progression assessment |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine ( Quantitative Proteinomics ) | ||
| Pathobiological Mechanisms | Urine complement protein was enriched in IgAN patients, suggesting that complement alternative pathway ( AP ) and lectin pathway ( LP ) were activated and involved in the progression of IgAN | ||||
| Clinical Availability Status | Research verification stage : It is related to the progression of IgAN and needs to be verified by complement pathway mechanism. | ||||
| Notes and Dynamics | To reveal the role of complement system in IgAN, and provide a basis for targeted complement therapy for IgAN. | ||||
| Biomarker | uNAG | Full name | Urinary N-acetyl-β-D-glucosaminidase | Molecular Type | Enzyme（Protein） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Renal tubulointerstitial injury assessment and remission prediction |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine | ||
| Pathobiological Mechanisms | It is released by the damaged proximal renal tubular epithelial cells, reflecting renal tubular interstitial involvement, and can predict the remission status of IgAN. | ||||
| Clinical Availability Status | Research verification stage : It is related to the remission of IgAN and needs to be verified by clinical promotion. | ||||
| Notes and Dynamics | It is an important non-invasive marker for evaluating renal tubulointerstitial injury and therapeutic effect of IgAN. | ||||
| Biomarker | KMN scheme based on k-means clustering | Full name | Network biomarkers ( KMN scheme based on k-means clustering ) | Molecular Type | Multimolecular integration |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Risk stratification, treatment guidance |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Multi-dimensional data ( network analysis, clustering algorithm ) | ||
| Pathobiological Mechanisms | Combining network biomarkers with unsupervised learning to improve the risk stratification of IgAN and make up for the deficiency of traditional models that only rely on renal indicators. | ||||
| Clinical Availability Status | Research verification stage : KMN protocol is effective and needs to be verified by clinical practice. | ||||
| Notes and Dynamics | It is a new paradigm for the application of biomarkers to achieve refined risk assessment of IgAN and provide decision support for individualized treatment. | ||||
| Biomarker | sIL-2Rα | Full name | Serum soluble interleukin-2 receptor α | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Histological injury assessment and prognosis |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | It is associated with severe inflammatory cell infiltration in IgAN, which can predict the short-term progression of the disease and reflect the degree of histological damage. | ||||
| Clinical Availability Status | Research verification stage : Non-invasive assessment of histological damage requires clinical application verification. | ||||
| Notes and Dynamics | It can avoid partial renal biopsy and provide a non-invasive method for evaluating the degree of inflammation and prognosis of IgAN. | ||||
| Biomarker | UCs | Full name | Urinary cytokines | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognostic prediction |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urine | ||
| Pathobiological Mechanisms | The level of inflammation-related cytokines in urine is related to the prognosis of IgAN patients and can be used as an alternative predictive marker. | ||||
| Clinical Availability Status | Research and exploration stage : Prognostic value, specific cytokines and detection methods need to be clarified | ||||
| Notes and Dynamics | Further screening of key cytokines is needed to improve the specificity and accuracy of prediction. | ||||
| Biomarker | Soluble CD89 | Full name | Soluble Fcα Receptor I | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Pathogenesis-related, biomarkers, therapeutic targets |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | / | ||
| Pathobiological Mechanisms | Participating in the mesangial proliferation of IgAN in children is a key factor in the pathogenesis of IgAN in children. | ||||
| Clinical Availability Status | Research verification stage : The role of IgAN in children is clear, and it is necessary to verify the value of clinical detection. | ||||
| Notes and Dynamics | Aiming at the specific markers of IgAN in children, it provides a specific direction for the diagnosis and treatment of IgAN in children. | ||||
| Biomarker | Escherichia-Shigella | Full name | Escherichia-Shigella | Molecular Type | Microorganism |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis and pathogenesis are related |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Flora samples ( no specific technology ) | ||
| Pathobiological Mechanisms | Intestinal flora imbalance and significant expansion of Escherichia-Shigella in IgAN patients may be involved in the pathogenesis of IgAN. | ||||
| Clinical Availability Status | Research and exploration stage : It is related to IgAN attack and treatment response, which needs mechanism and clinical verification. | ||||
| Notes and Dynamics | It provides a basis for the study of the mechanism of IgAN ' intestine-kidney axis ', and may improve the condition of IgAN by regulating intestinal flora. | ||||
| Biomarker | GMFG | Full name | Glia maturation factor gamma | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Biomarkers, therapeutic targets |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Not clear ( bioinformatics analysis ) | ||
| Pathobiological Mechanisms | Through bioinformatics analysis, it was screened that it was related to IgAN and some tumors, and the specific mechanism needs to be clarified. | ||||
| Clinical Availability Status | Research and exploration stage : Bioinformatics suggests potential, which needs experimental verification. | ||||
| Notes and Dynamics | Cross-disease markers may involve common pathological mechanisms ( such as inflammation, proliferation ), and their pathways need to be further studied. | ||||
| Biomarker | CTSS | Full name | Cathepsin S | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, treatment targets |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Serum, kidney tissue ( specific technology is not clear ) | ||
| Pathobiological Mechanisms | Overexpression in serum and renal tissue of patients with IgAN, elevated levels are associated with an increased risk of IgAN and are involved in renal pathological processes. | ||||
| Clinical Availability Status | Research verification stage：It is related to the pathogenesis of IgAN, which needs to be verified by clinical diagnostic value. | ||||
| Notes and Dynamics | It provides a new candidate marker for the diagnosis of IgAN and may become a potential target for targeted treatment. | ||||
| Biomarker | MASP2 | Full name | Mannan-binding lectin-associated serine protease 2 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Severity assessment and prognosis of renal injury |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Urinary extracellular vesicles | ||
| Pathobiological Mechanisms | Involved in the mannan-binding lectin pathway, the level of MASP2 in UEV is related to IgAN, reflecting the degree of renal injury. | ||||
| Clinical Availability Status | Research verification stage：It is related to the prognosis of IgAN, which needs to be verified by a larger sample size. | ||||
| Notes and Dynamics | It provides a new direction for the study of the mechanism of IgAN renal injury. The characteristics of UEV carrier may improve the specificity of marker detection. | ||||
| Biomarker | TGF-β1、miRNA-21-5p、miR-21 | Full name | Transforming growth factor-beta 1、MicroRNA-21-5p、MicroRNA-21 | Molecular Type | Protein、RNA（miRNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Assessment and prognosis of renal fibrosis |
| Disease(or Constitution) | Glomerulonephritis (GN) | Disease Subtypes | IgAN | ||
| Organ | Kidney | Test Sample / Technology Platform | Blood | ||
| Pathobiological Mechanisms | TGF-β1 is a pro-fibrotic molecule, and miR-21 is associated with renal fibrosis. Both are associated with the degree of renal fibrosis and renal outcome in IgAN. | ||||
| Clinical Availability Status | Research verification stage：For non-invasive evaluation of renal fibrosis, clinical transformation verification is required | ||||
| Notes and Dynamics | Notes and dynamics It can replace some invasive renal biopsy to evaluate the risk of renal fibrosis in patients with IgAN and guide anti-fibrosis treatment. | ||||
| Biomarker | FetA | Full name | Fetuin A | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Renal function assessment、Early warning of complications |
| Disease(or Constitution) | Chronic Kidney Disease (CKD) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Blood, urine (protein detection) | ||
| Pathobiological Mechanisms | Involved in mineral metabolism, abnormal levels are associated with CKD-related bone metabolism disorders. | ||||
| Clinical Availability Status | Research verification stage | ||||
| Notes and Dynamics | Post-translational modified Fetuin A ( uPTM-FetA ) in urine can distinguish diabetic nephropathy from non-diabetic nephropathy, and is a sensitive marker of renal injury. | ||||
| Biomarker | ADMA | Full name | Asymmetric dimethylarginine | Molecular Type | Protein |
| Molecular Formula | C₈H₁₈N₄O₂ | Molecular Weight | 202.25 g/mol | Core Functional Dimensions | Renal function assessment、Early warning of complications |
| Disease(or Constitution) | Chronic Kidney Disease (CKD) | Disease Subtypes | / | ||
| Organ | Kidney | Test Sample / Technology Platform | Blood, urine (protein detection) | ||
| Pathobiological Mechanisms | Inhibition of nitric oxide synthesis, leading to endothelial dysfunction, associated with cardiovascular risk | ||||
| Clinical Availability Status | Research verification stage | ||||
| Notes and Dynamics | It is an independent predictor of cardiovascular disease in CKD patients and is negatively correlated with endothelial dysfunction indicators ( such as brachial artery flow-mediated dilatation ). | ||||