Application of urine soluble CD11b in clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy

Abstract

The invention belongs to the technical field of biomedicine, and particularly discloses application of urine soluble CD11b in clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy. According to the invention, the u-sCD11b level of a base line during renal puncture of a patient is detected, and statistical analysis is carried out on the base line and various indexes of the base line in six months of subsequent follow-up visit, so that a biomarker u-sCD11b which can be used for reflecting the disease severity of the IgAN patient and predicting the prognosis of the patient is provided, and meanwhile, the risk stratification of clinical workers on the IgAN patient in clinical practice is provided, and the risk stratification of the IgAN patient in clinical practice is provided. A certain reference value is provided for judging which patients need positive follow-up visit and treatment, the curative effect of the IgAN can be effectively improved, and the patients are fully benefited.

Description

Technical Field

[0001] The present invention relates to the field of biomedical technologies, and particularly to the application of urinary soluble CD11b in the clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy. Background Art

[0002] IgA (IgA nephropathy, IgAN) nephropathy is the most common primary glomerulonephritis worldwide. A multi-center study showed that in the Asian population, IgAN accounts for 39.5% of glomerular diseases. IgAN is one of the important reasons for patients to progress to end stage renal disease (ESRD). Approximately 15%-20% of patients progress to ESRD during 10-year follow-up, and the progression rate can reach 30%-40% during 20-year follow-up. Therefore, early identification of IgA nephropathy patients with poor prognosis and corresponding clinical intervention have extremely high value.

[0003] Due to the great differences in clinical manifestations and disease processes among IgAN patients, it is difficult to screen out patients at risk of rapid progression using only clinical indicators. Compared with constructing a prognosis model using only clinical data during renal biopsy (including estimated glomerular filtration rate, proteinuria, mean arterial pressure), further combining Oxford pathological classification indicators (including mesangial cell proliferation, endocapillary proliferation, glomerular segmental sclerosis, tubular atrophy / interstitial fibrosis) can significantly improve the predictive ability of the model. Compared with the prognosis model constructed using only clinical indicators obtained during 2-year follow-up, the model constructed by combining clinical indicators during renal biopsy and Oxford pathological classification has the same ability in predicting prognosis, and can predict risks early, avoiding problems such as patient loss to follow-up. However, renal biopsy is an invasive operation, and its implementation is limited by equipment reasons, operator qualifications, patient willingness, etc., and the pathological evaluation by pathologists is subjective, all of which affect the accuracy of pathological index prediction. Therefore, a large number of studies have tried to find effective and reliable biomarkers to improve the predictive ability of the model. Summary of the Invention

[0004] One object of the present invention is to provide a biomarker that can be used to prompt or evaluate the treatment and prognosis of IgA nephropathy patients, and further used to guide clinical diagnosis and treatment. This biomarker is urinary soluble CD11b (u-sCD11b).

[0005] During the pathogenesis of IgAN, immune factors play an important role, and macrophages are the main immune cells infiltrating the kidney tissues of IgAN patients. Macrophages are highly heterogeneous and plastic, and are classified into classically activated M1 macrophages and alternatively activated M2 macrophages. Generally, circulating monocytes are recruited to the inflammatory site after recognizing signals such as injury and inflammation, and mainly polarize towards the M1 direction in the early stage of inflammation, playing a role in phagocytosis, promoting inflammatory responses, and participating in tissue damage. In the later stage or chronic stage of inflammation, macrophages mainly polarize towards the M2 direction, participating in injury repair and tissue reconstruction. Macrophages can polarize in different directions according to the differences in the stimulating signals they receive and are always in a dynamic balance in the body. Therefore, the related signaling pathways regulating macrophage polarization have always been a research hotspot.

[0006] CD11b is a member of the integrin family and is highly expressed on the surfaces of immune cells such as macrophages, monocytes, and neutrophils. CD11b is generally considered a pro-inflammatory molecule that mediates leukocyte activation, adhesion, migration, and tissue recruitment, and participates in the regulation of phagocytosis, but it can also negatively regulate the inflammatory responses induced by Toll-like receptor (TLR)-related pathways. CD11b can regulate the polarization direction of macrophages. Activation of CD11b promotes the polarization of macrophages towards a pro-inflammatory phenotype, while inhibition of CD11b can promote the polarization of macrophages towards an immunosuppressive phenotype. After being stimulated by inflammatory signals, activated leukocytes release CD11b. Soluble CD11b (sCD11b) can be detected in the urine of patients with lupus nephritis (LN) and antineutrophil cytoplasmic autoantibody-associated glomerulonephritis (ANCA-GN), and urinary sCD11b can reflect the infiltration of renal leukocytes.

[0007] GWAS studies suggest that ITGAM encoding CD11b is a susceptibility gene in IgAN patients, especially in the Asian population, and integrin αM (CD11b) is encoded by ITGAM and ITGAX. The inventors' research found that the concentration of u-sCD11b was positively correlated with the number of CD11b-positive cells in renal tissues (r = 0.482, P = 0.009). Further analyzing the relationship between the concentration of u-sCD11b and the infiltration of CD11b-positive cells in the glomerular and tubulointerstitial regions respectively, the concentration of u-sCD11b was positively correlated with the number of CD11b-positive cells in the tubulointerstitial region (r = 0.441, P = 0.019), while there was no significant correlation with the degree of glomerular infiltration (P>0.05).

[0008] sCD11b in urine can indicate the disease severity and predict the prognosis, and the level of sCD11b in the urine of IgAN patients is positively correlated with the CD11b-positive cells in the renal tissue. This provides certain reference value for us to stratify the risks of IgAN patients in clinical practice and determine which patients need active follow-up and treatment, which can effectively improve the treatment effect for IgAN and enable patients to fully benefit.

[0009] The second object of the present invention is to provide the use of u-sCD11b as a biomarker in the preparation of a kit for clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy.

[0010] The third object of the present invention is to provide the use of a reagent for detecting the concentration of u-sCD11b in the preparation of a kit for clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy.

[0011] Furthermore, the kit includes a reagent for detecting the concentration of u-sCD11b, and the reagent for detecting the concentration of u-sCD11b is an enzyme-linked immunosorbent reagent, specifically, it can be the ELISA kit (product number MBS702254) of MyBioSource.

[0012] Furthermore, the kit also includes a urine creatinine detection reagent, specifically, it can be the creatinine test kit (product number DICT-500) of BioAssay Systems. The concentration of u-sCD11b detected by enzyme-linked immunosorbent assay needs to be corrected by dividing by the creatinine concentration.

[0013] Furthermore, the application method is as follows: Use the enzyme-linked immunosorbent reagent and the urine creatinine detection reagent to test the concentrations of soluble u-sCD11b and urine creatinine in the urine of patients respectively, and use the soluble u-sCD11b concentration / urine creatinine concentration as the corrected u-sCD11b concentration value. If this value belongs to the high-concentration group of u-sCD11b (in a specific embodiment, the high-concentration group is the corrected u-sCD11b concentration > 4.44 ng / mg), it indicates a high risk of progression of IgAN nephropathy and poor prognosis, and more active follow-up and treatment are required; otherwise, it indicates a better prognosis.

[0014] The present invention has the following beneficial effects:

[0015] The present invention has established a relatively large database of IgAN patients and found a relatively reliable and non-invasive biomarker to study the clinical value of urine samples of Chinese populations in evaluating the disease severity of IgAN patients reflected by urinary soluble CD11b and the ability of u-sCD11b concentration during renal biopsy to predict the prognosis of patients.

[0016] This study provides a potentially useful biomarker for IgAN and offers certain reference value for risk stratification of IgAN patients in clinical practice, determining which patients need active follow-up and treatment, which can effectively improve the efficacy of IgAN and enable patients to fully benefit. When actually applied, urine is collected for measuring the urine sCD11b level during the preparation for renal biopsy, and the renal biopsy pathological results can be used together with the prediction model to evaluate the prognosis of patients. If the prognosis is poor, treatment can be strengthened or close follow-up can be carried out, thus hopefully improving the prognosis of patients. Brief Description of the Drawings

[0017] Figure 1 : Flow chart of the inclusion of IgA nephropathy patients in Example 1 in the study.

[0018] Figure 2 : Correlation analysis of u-sCD11b concentration with Oxford pathological score (A), proportion of global sclerosis (B), proportion of segmental sclerosis (C), tubulointerstitial score (D), and proportion of crescents (E) in Example 1.

[0019] Figure 3 : Comparison of kidney survival rates in different u-sCD11b concentration groups in Example 2. Detailed Embodiments

[0020] The present invention will be further described below in conjunction with the drawings and specific embodiments.

[0021] Case selection in the following embodiments:

[0022] Inclusion criteria: Patients who entered the IgA nephropathy follow-up cohort of Zhongshan Hospital, Fudan University from 2018 to 2021. All cases were confirmed as primary IgAN by renal biopsy, with baseline proteinuria > 1 g / d, and the renal tissue included more than 8 glomeruli. There were proteinuria data at 6 months of follow-up.

[0023] Objective: To collect the baseline urine specimens taken before renal biopsy from patients (from the renal biopsy specimen bank of the Department of Nephrology, Zhongshan Hospital, Fudan University, and this biological specimen bank has obtained ethical approval from the Ethics Committee of Zhongshan Hospital, Fudan University), detect the level of urinary soluble CD11b (u-sCD11b), and compare the severity of the disease and prognosis of patients with different u-sCD11b levels during renal biopsy.

[0024] Example 1: Correlation between u-sCD11b level and baseline disease condition

[0025] 1.1 Determination of u-sCD11b concentration

[0026] Obtaining and processing of urine specimens: Patients collected morning urine before renal biopsy. The urine biological samples were centrifuged at 2500 rpm for 20 minutes at 4°C, and the supernatant was aliquoted and stored at -80°C or below until use.

[0027] Method for detecting urinary CD11b: Detect the level of urinary CD11b by enzyme-linked immunosorbent assay (MyBioSource; catalog number MBS702254), and determine urinary creatinine by the modified Jaffe method (using BioAssay Systems; catalog number DICT-500 kit, and operate according to the instructions of this kit). All urinary CD11b levels are corrected by urinary creatinine (to eliminate the result deviation caused by different urine concentration or dilution), expressed as u-sCD11b, with the unit of ng / mg.

[0028] The specific process of detecting urinary CD11b is as follows: Determine the concentration of u-sCD11b by enzyme-linked immunosorbent assay (ELISA), and each sample is in duplicate.

[0029] 1) Sample addition: Add 100 μL of sample or standard to each sample well. Seal the plate and incubate at 37 °C for 2 hours.

[0030] 2) Biotin addition: Discard the liquid in the wells completely. Add 100 μL of Biotin to each well. Seal the plate and incubate at 37 °C for 1 hour.

[0031] 3) Plate washing: Discard the liquid in the wells completely, pat dry on the absorbent paper, add 200 μL of washing solution to each well, and let it stand at room temperature of 18 °C - 25 °C for 2 minutes. Discard the liquid in the wells completely and pat dry. Repeat the plate washing 3 times.

[0032] 4) Enzyme-labeled reagent addition: Add 100 μL of enzyme-labeled reagent to each well. Seal the plate and incubate at 37 °C for 1 hour.

[0033] 5) Plate washing: Repeat the plate washing operation in 3) 3 times.

[0034] 6) Substrate chromogenic solution addition: Add 90 μL of substrate chromogenic solution to each well. Seal the plate and protect from light, and incubate at 37 °C for 15 minutes.

[0035] 7) Terminate the reaction and measure the result: Add 50 μL of termination solution to each well and mix evenly. Set the photometric measuring instrument to measure the absorbance at wavelengths of 450 nm and 540 nm (correction wavelength) respectively, subtract the reading at 540 nm from the reading at 450 nm, draw a standard curve, and calculate the sample concentration.

[0036] The process of correcting the u-sCD11b concentration is as follows:

[0037] The urine creatinine concentration in the patient's urine sample was detected using a kit purchased from BioAssay Systems with the catalog number DICT-500. The corrected u-sCD11b concentration was obtained by dividing the concentration measured in step 7) by the urine creatinine concentration of the corresponding sample for subsequent research.

[0038] After applying the inclusion and exclusion criteria, a total of 349 IgA nephropathy patients were included in this study (the flow chart of the study population included in the cohort is as Figure 1 shown).

[0039] 1.2 Correlation between u-sCD11b concentration and baseline renal function indicators

[0040] In this study, laboratory indicators were measured from the blood / urine samples collected from the patients in Zhongshan Hospital, Fudan University.

[0041] In this study, IBM SPSS Statistics 26 software was used for statistical analysis, and GraphPad Prism 10.4 software was used for statistical analysis and plotting. When continuous variables follow a normal distribution, the data are described by mean ± standard deviation. Pearson correlation analysis is used for the correlation analysis between continuous variables, and Spearman correlation analysis is used for the correlation analysis between continuous variables and categorical variables. Logistic regression analysis was used to identify relevant risk factors. P < 0.05 was considered statistically significant.

[0042] The results are shown in Table 1. In terms of baseline renal function indicators, the u-sCD11b concentration was positively correlated with BUN, Scr, CysC, β2MG, 24-hour urinary protein quantification, and urinary ACR (r = 0.130, 0.141, 0.142, 0.173, 0.279, 0.319, all P < 0.05), negatively correlated with eGFR (r = -0.176, P = 0.001), and not significantly correlated with serum uric acid (P > 0.05). Our study found that the u-sCD11b concentration was significantly correlated with indicators such as eGFR, 24-hour urinary protein quantification, and serum albumin, indicating that the u-sCD11b concentration at the time of renal biopsy can well reflect the clinical characteristics of patients.

[0043] Table 1 Correlation analysis between the u-sCD11b concentration of patients and baseline laboratory indicators

[0044]

[0045]

[0046]

[0047] 1.3 Correlation between u-sCD11b concentration and MEST-C pathological score, etc.

[0048] In this study, the MEST-C pathological scores and data related to glomerular lesions were obtained from the detection of specimens in the renal biopsy sample bank of Zhongshan Hospital, Fudan University. The baseline 24-hour urinary protein was measured from the urine samples of the patients. Among them, the MEST-C Oxford pathological classification is as follows:

[0049]

[0050] In this study, IBM SPSS Statistics 26 software was used for statistical analysis, and GraphPad Prism 10.4 software was used for statistical analysis and drawing. When continuous variables followed a normal distribution, the data were described by mean ± standard deviation. Pearson correlation analysis was used for the correlation analysis between continuous variables, and Spearman correlation analysis was used for the correlation analysis between continuous variables and categorical variables. Logistic regression analysis was used to determine the relevant risk factors. P < 0.05 was considered statistically significant.

[0051] The results are as Figure 2 shown. The u-sCD11b concentration was positively correlated with the MEST-C pathological score (ρ = 0.259, P < 0.001, Figure 2 A). In terms of glomerular lesions, the u-sCD11b concentration was weakly positively correlated with the proportion of global sclerosis (r = 0.142, P = 0.010, Figure 2 B), and the proportion of segmental sclerosis (r = 0.168, P = 0.002, Figure 2 C). In terms of tubulointerstitial lesions, the u-sCD11b concentration was positively correlated with the interstitial score (ρ = 0.219, P < 0.001, Figure 2 D). The u-sCD11b concentration was weakly positively correlated with the proportion of crescents (r = 0.170, P = 0.002, Figure 2 E).

[0052] Further subgroup analysis revealed that after stratification according to baseline proteinuria, in the group with low proteinuria (<1 g / 24 h), the concentration of u-sCD11b was positively correlated with the proportion of cellular crescents (r = 0.395, P < 0.001), and not significantly correlated with the proportions of cellular fibrotic crescents and fibrotic crescents (both P > 0.05). In the group with moderate proteinuria (1 - 3.5 g / 24 h), the concentration of u-sCD11b was not significantly correlated with the proportions of cellular crescents, cellular fibrotic crescents, and fibrotic crescents (all P > 0.05). In the group with high proteinuria (>3.5 g / 24 h), the concentration of u-sCD11b in patients was significantly correlated with the proportion of cellular fibrotic crescents (r = 0.581, P = 0.002) and the proportion of fibrotic crescents (r = 0.718, P < 0.001), and not correlated with the proportion of cellular crescents (P > 0.05) (Table 2).

[0053] Table 2 Correlation analysis of u-sCD11b concentration and the proportion of each type of crescent after stratification according to 24-hour urinary protein quantification at baseline

[0054]

[0055] U-PRO: 24-hour urinary protein quantification.

[0056] Further Logistic regression analysis found that u-sCD11b was an independent related factor with higher scores of E, T, and C lesions. Therefore, the concentration of u-sCD11b may have the value of indicating poor prognosis in patients (Table 3).

[0057] Table 3 Logistic regression analysis of u-sCD11b concentration and M, E, S, T, C scores

[0058]

[0059] Adjusted factors: gender, age, MAP, BMI.

[0060] In summary, as a non-invasive, easily obtainable, and convenient-to-detect biomarker, the concentration of u-sCD11b has a good correlation with proteinuria and eGFR levels in IgAN patients, is related to the Oxford pathological score, and can well reflect the severity of the clinical manifestations and pathological changes of patients. For mild patients with low proteinuria, an increase in the concentration of u-sCD11b can indicate pathological changes such as E, T, and C, and indicate the formation of cellular crescents. Therefore, the concentration of u-sCD11b during renal biopsy can reflect the severity of IgAN disease, and a high concentration of u-sCD11b may indicate poor prognosis and require active clinical intervention. The concentration of u-sCD11b has the value for further prognostic research.

[0061] Example 2: Study on the relationship between u-sCD11b level and the prognosis of patients with primary IgA nephropathy

[0062] Inclusion and exclusion criteria: On the basis of the inclusion and exclusion criteria in Example 1, 72 patients with a follow-up time < 6 months and no renal endpoint events during this period were excluded, and 277 patients were included in the study of u-sCD11b and renal prognosis.

[0063] According to the u-sCD11b concentration, patients were divided into tertiles T1, T2, and T3. The low-concentration u-sCD11b group (u-sCD11b / uCr ≤ 4.44 ng / mg, u-sCD11b / uCr T1 group and T2 group) had a higher follow-up endpoint eGFR than the high-concentration u-sCD11b group (u-sCD11b / uCr > 4.44 ng / mg, u-sCD11b / uCr T3 group), while the annual decline rate of eGFR and the 24-hour urinary protein quantification at the endpoint were lower (both P < 0.05). By the follow-up endpoint, 19 cases (6.9%) progressed to ESRD, including 7 cases (3.9%) in the low-concentration u-sCD11b group and 12 cases (12.2%) in the high-concentration u-sCD11b group, and the difference between groups was statistically significant (P = 0.018). A total of 77 cases (27.8%) had renal composite endpoint events by the follow-up endpoint, including 35 cases (19.6%) in the low-concentration u-sCD11b group and 42 cases (42.9%) in the high-concentration u-sCD11b group, and the difference between groups was significant (P < 0.001) (Table 4). Kaplan-Meier survival analysis showed that the cumulative renal survival rate in the high-concentration u-sCD11b group was significantly lower than that in the low-concentration u-sCD11b group (Log-rank X2 = 18.42, P < 0.001)( Figure 3 ), suggesting a poor prognosis in the high-concentration u-sCD11b group (u-sCD11b / uCr > 4.44 ng / mg).

[0064] Table 4 Comparison of follow-up indicators and medications in different u-sCD11b concentration groups among the followed-up patients

[0065]

[0066]

[0067] eGFR: Estimated glomerular filtration rate; ESRD: End-stage renal disease; RASS: Renin-angiotensin-aldosterone system a: Student's t test; b: Chi-square test; c: Fisher's exact probability method; d: Non-parametric test

[0068] Univariate Cox regression analysis showed that the risk of renal endpoint events in the high-concentration u-sCD11b group was significantly higher than that in the low-concentration u-sCD11b group (HR = 2.56, 95% CI 1.64 - 4.02, P < 0.001). After adjustment for demographic indicators (gender, age, MAP, BMI), baseline laboratory indicators (eGFR, 24-hour urinary protein quantification, HGB), renal biopsy MEST-C score, treatment regimens (use of RASS inhibitors, hormones or other immunosuppressants), etc., high-concentration u-sCD11b remained an independent risk factor for predicting renal endpoint events (HR = 1.95, 95% CI 1.16 - 3.28, P = 0.012) (Table 5).

[0069] Table 5 Cox regression analysis of different urinary biomarkers and patient prognosis

[0070]

[0071] Model 1 adjustment factors: gender, age, MAP, BMI; Model 2 adjustment factors: Model 1 adjustment factors + eGFR, 24-hour urinary protein quantification, HGB; Model 3 adjustment factors: Model 2 adjustment factors + MEST-C score; Model 4 adjustment factors: Model 3 adjustment factors + use or non-use of RASS inhibitors + use or non-use of glucocorticoids or other immunosuppressants.

[0072] Example 3: Comparison of multiple renal prognosis prediction models constructed with urinary soluble CD11b

[0073] The predictive ability of u-sCD11b concentration at the time of renal biopsy for renal prognosis at 6 months of patient follow-up was analyzed using the ROC curve. The AUC of u-sCD11b was 0.750 (95% CI 0.684 - 0.815). In the prediction model (Model 1) constructed with baseline clinical data (MAP, eGFR, 24-hour urinary protein quantification) combined with the renal biopsy MEST-C score, the AUC value was 0.772 (95% CI 0.717 - 0.821). On the basis of Model 1, further combined with u-sCD11b concentration (Model 2), the AUC increased significantly (AUC = 0.804, 95% CI, 0.752 - 0.850) (Table 6). Stratification was performed according to baseline eGFR and 24-hour urinary protein quantification, and it was found that in the group with basically normal renal function (eGFR ≥ 60 ml / min / 1.73m 2 ) The predictive ability of Model 2 was significantly improved compared with Model 1 (AUC difference = 0.110, P = 0.012). In the group with reduced renal function (eGFR < 60 ml / min / 1.73m 2)The predictive ability of Model 2 was the strongest (AUC = 0.884, 95% CI 0.798 - 0.943), but there was no significant statistical difference in the predictive ability compared with Model 1 (AUC difference = 0.005, P = 0.674). In the group with a small amount of proteinuria (<1 g / 24 h) and the group with a moderate + large amount of proteinuria (≥1 g / 24 h), there was no significant statistical increase in the AUC of Model 2 compared with Model 1 (AUC differences = 0.050, 0.038, P = 0.076, 0.082) (Table 6).

[0074] Table 6 Comparison of the predictive ability of different models for the 6 - month renal progression of patients by ROC curve

[0075]

[0076] Baseline clinical data: including MAP, eGFR, 24 - hour urinary protein quantification

[0077] In summary, after adjusting for factors such as demographic characteristics, baseline laboratory indicators, MEST - C score, and treatment regimens through Cox regression analysis, it was found that only high - concentration u - sCD11b remained an independent risk factor for predicting renal endpoint events. Univariate Cox regression in this study also showed good correlations between MAP, eGFR, 24 - hour urinary protein quantification and renal endpoint events. When using this model to predict the renal prognosis of patients at 6 - month follow - up, it was found that further combining u - sCD11b could significantly increase the predictive ability of the model (AUC = 0.804, 95% CI 0.752 - 0.850). Baseline eGFR and 24 - hour urinary protein quantification were important stratification factors. In the subgroup analysis, only in patients with eGFR ≥ 60 ml / min / 1.73m 2 could u - sCD11b significantly improve the predictive ability (P = 0.012), indicating that measuring the concentration of u - sCD11b during renal biopsy has higher clinical value in patients with relatively normal renal function.

[0078] This specific implementation manner is only an interpretation of the present invention and not a limitation thereof. Any changes made by those skilled in the art after reading the specification of the present invention will be protected by the patent law as long as they are within the scope of the claims of the present invention.

Claims

1. Application of u-sCD11b as a biomarker in the preparation of a kit for clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy.

2. Application of reagents for detecting the concentration of u-sCD11b in the preparation of a kit for clinical auxiliary diagnosis and prognosis prediction of IgA nephropathy.

3. The use according to claim 1 or 2, characterized in that: The kit comprises a reagent for detecting the concentration of u-sCD11b, and the reagent for detecting the concentration of u-sCD11b is an enzyme-linked immunosorbent assay reagent.

4. The use according to claim 3, characterized in that: The kit also includes a calibration reagent, which is a urine creatinine detection reagent.

5. The use according to claim 4, characterized in that: The application method is: use enzyme-linked immunosorbent reagent and urine creatinine detection reagent to test the soluble u-sCD11b and urine creatinine concentrations in the patient's urine respectively, and use the soluble u-sCD11b concentration / urine creatinine concentration as the corrected u-sCD11b concentration value. If the value belongs to the u-sCD11b high concentration group, it indicates a high risk of progression of IgAN nephropathy and a poor prognosis, and more active follow-up and treatment are required.

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