Application of PRDX2 as a biomarker in the auxiliary diagnosis and prognosis prediction of acute kidney injury

Abstract

The present invention provides the use of PRDX2 as a biomarker in the auxiliary diagnosis and prognosis prediction of acute kidney injury. Specifically, it relates to the use of a reagent for detecting the expression amount of the biomarker PRDX2 in the preparation of an auxiliary diagnosis and prognosis prediction product for acute kidney injury. The present invention is the first to discover that there is differential expression of PRDX2 in samples of patients with acute kidney injury. In this way, PRDX2 can be used as a biomarker for acute kidney injury, for auxiliary diagnosis of acute kidney injury or prognosis prediction, and provides a new approach for the diagnosis and prognosis prediction of acute kidney injury.

Description

Technical Field

[0001] The present invention belongs to the field of biomedicine technology, and specifically relates to the application of PRDX2 as a biomarker in the auxiliary diagnosis and prognosis prediction of acute kidney injury. Background Art

[0002] Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in renal function, manifested by a rapid increase in serum creatinine with or without a sharp decrease in urine volume. The incidence of AKI in hospitalized patients is 10%-15%, and the incidence of AKI in patients in intensive care units can exceed 50%. Currently, there is still a lack of treatment for AKI, and about 2 million patients die each year due to complications of AKI, with a mortality rate of nearly 50%-70%. In addition, the risk of chronic kidney disease (CKD) in AKI survivors increases by about 4 times, resulting in an increase of about 2.4 times in the risk of CKD progression, which has become a heavy burden on society. Therefore, in-depth understanding of the pathogenesis of AKI and the exploration of new targets for early diagnosis and treatment intervention of AKI are of great significance to reducing the risks and burdens brought by AKI.

[0003] Due to their high energy requirements and unique microvascular environment, proximal tubular epithelial cells are extremely susceptible to various stimuli such as ischemia, nephrotoxic drugs, and sepsis. Continuous stimulation leads to irreversible tubular damage. Ferroptosis and apoptosis of proximal tubular epithelial cells have been observed in AKI models induced by ischemia-reperfusion, sepsis, cisplatin, and folic acid, and ferroptosis of proximal tubular epithelial cells is a key event in the initiation of tubular cell damage and inflammation in AKI.

[0004] Peroxiredoxin 2 (PRDX2) belongs to the Peroxiredoxins superfamily and is a typical 2-Cys antioxidant protein of the peroxiredoxin family. The protein is mainly expressed in the cytoplasm and maintains cellular redox homeostasis by reducing peroxide levels. Intracellularly expressed PRDX2 plays an important role in maintaining the normal function of heart, kidney and muscle tissue. When the redox balance of cells is unbalanced, ferroptosis and apoptosis programs will be initiated. PRDX2 does not have a typical signal peptide sequence and can be released to the extracellular space by a vesicle-mediated non-classical secretion pathway. Both inflammation and oxidants can stimulate the extracellular secretion of PRDX2. At present, PRDX2 can be used as a biomarker for screening people with plateau adaptability, depressive disorder-related diseases, hypertension diseases used in pregnancy, high-risk groups for liver cancer and severe chronic obstructive pulmonary disease. Summary of the invention

[0005] The purpose of the present invention is to provide a new biomarker PRDX2 for auxiliary diagnosis and prognosis prediction of acute kidney injury, and to provide a new approach for diagnosis and prognosis prediction of acute kidney injury.

[0006] In order to achieve the above-mentioned object, the present invention provides the use of a reagent for detecting the expression amount of the biomarker PRDX2 in the preparation of a product for auxiliary diagnosis and prognosis prediction of acute kidney injury.

[0007] In a specific embodiment, the acute kidney injury is acute kidney injury caused by ischemia-reperfusion injury or acute kidney injury induced by cisplatin.

[0008] In a specific embodiment, the product comprises a kit or a reagent.

[0009] In a specific embodiment, the test sample of the subject is kidney tissue and / or urine.

[0010] In a specific embodiment, when the expression level of PRDX2 in the renal tissue of the subject is low relative to the expression level of PRDX2 in a normal control or a standard, the subject is diagnosed as being at risk of acute kidney injury.

[0011] In a specific embodiment, when the expression level of PRDX2 in the urine of the subject is high relative to the expression level of PRDX2 in a normal control or a standard, the subject is diagnosed as being at risk of acute kidney injury.

[0012] In a specific embodiment, high expression of PRDX2 in urine is positively correlated with renal tubular damage in conditions associated with acute kidney injury.

[0013] It can be understood here that the concentration value of PRDX2 in urine corresponds to the degree of renal tubular damage, that is, the higher the concentration value of PRDX2 in urine, the more severe the degree of renal tubular damage.

[0014] In the present invention, the biomarker PRDX2 assists in the diagnosis of acute kidney injury in the following steps:

[0015] Step 1) collecting samples from the subjects to be tested and samples from normal controls;

[0016] Step 2) detecting and comparing the expression level of PRDX2 in the samples of the tested subjects and the samples of the normal controls;

[0017] When the expression level of PRDX2 in the renal tissue of the subject is low relative to the expression level of a normal control, the subject is diagnosed as being at risk of suffering from acute kidney injury;

[0018] and / or

[0019] When the expression level of PRDX2 in the urine of the subject is high relative to the expression level of PRDX2 in a sample of a normal control, the subject is diagnosed as being at risk of suffering from acute kidney injury.

[0020] Wherein, the normal control samples are derived from healthy people or healthy tissues of the subjects to be tested.

[0021] The beneficial effects of the present invention include at least:

[0022] 1. The present invention is the first to discover that PRDX2 is differentially expressed in samples of patients with acute kidney injury. Thus, PRDX2 can be used as an AKI biomarker to assist in the diagnosis or prognosis prediction of AKI, providing a new approach for the diagnosis and prognosis prediction of AKI.

[0023] 2. The high expression of PRDX2 in urine is positively correlated with renal tubular damage in acute kidney injury-related diseases. Therefore, the expression level of PRDX2 in urine can be used as a non-invasive indicator to reflect the severity of acute tubular damage, which can effectively reduce the dependence on invasive renal biopsy diagnosis. In addition, urine is easy to obtain and can be used to detect PRDX2 without special processing. The detection is fast and efficient. BRIEF DESCRIPTION OF THE DRAWINGS

[0024] Figure 1 Periodic acid-Schiff staining of renal tissue in the ischemia-reperfusion injury (IR) AKI model. Figure 1 a in the figure is the result of periodic acid-Schiff staining of the Sham group. Figure 1 b in the figure is the identification result of periodic acid-Schiff staining of the IR group;

[0025] Figure 2 The expression of PRDX2 in renal tissue of IR-AKI mouse model. Figure 2 (a) Western blotting results of Sham group and IR group. Figure 2 (a) in (b) is the result of PRDX2 immunofluorescence staining in the sham group. Figure 2 (b) The b in (b) shows the PRDX2 immunofluorescence staining results of the IR group;

[0026] Figure 3 This is the result of periodic acid-Schiff staining of renal tissue in the AKI model induced by cisplatin (CP). Figure 3 a in the figure is the result of periodic acid-Schiff staining of the Ctrl group. Figure 3 b in the figure is the identification result of periodic acid-Schiff staining of the CP group;

[0027] Figure 4 The expression of PRDX2 in renal tissue of CP-AKI mouse model. Figure 4 (a) is the Western blotting test results of the Ctrl group and the CP group. Figure 4 (a) in (b) is the result of PRDX2 immunofluorescence staining in the Ctrl group. Figure 4 (b) The b in (b) shows the immunofluorescence staining results of PRDX2 in the CP group;

[0028] Figure 5 Results of PRDX2 and Merge immunofluorescence staining in renal biopsy tissues of acute tubular necrosis (ATN) and minimal change disease (MCD) without tubular damage. Figure 5 a in the figure is the result of PRDX2 immunofluorescence staining in the MCD group. Figure 5 b is the result of PRDX2 immunofluorescence staining in the ATN group. Figure 5 c in the figure is the Merge immunofluorescence staining result of the MCD group. Figure 5 d in the figure is the Merge immunofluorescence staining result of the ATN group;

[0029] Figure 6 The results are the quantitative analysis of PRDX2 in renal biopsy tissues of acute tubular necrosis (ATN) and minimal change disease (MCD) without tubular damage;

[0030] Figure 7 Based on Figure 6 The results of correlation analysis between the expression of PRDX2 in the blood and the estimated glomerular filtration rate of patients;

[0031] Figure 8 Based on Figure 6 The results of correlation analysis between the expression of PRDX2 in the blood and the serum creatinine of patients;

[0032] Fig. 9 The ELISA was used to detect the expression of NGAL in the urine of patients with radical nephrectomy (RN), patients 48 hours after partial nephrectomy (PN), and patients clinically diagnosed with AKI;

[0033] Fig.10 The expression of PRDX2 in urine of patients with radical nephrectomy (RN), patients 48 hours after partial nephrectomy (PN), and patients clinically diagnosed with AKI was detected by ELISA;

[0034] Fig.11 The expression of KIM 1 in urine of patients with radical nephrectomy (RN) and 48 hours after partial nephrectomy (PN) was detected by ELISA.

[0035] Fig.12 Based on Fig.10 The expression level of PRDX2 in Fig.11The results of correlation analysis of the expression of KIM 1 in

[0036] Fig.13 Based on Fig.10 The expression level of PRDX2 in Fig. 9 The results of correlation analysis of NGAL expression in the rats. DETAILED DESCRIPTION

[0037] The present invention is described in detail below with reference to the accompanying drawings and embodiments, but the present invention can be implemented in many different ways as limited and covered by the claims.

[0038] Materials and reagents used in the following examples, unless otherwise specified, can be obtained from commercial sources. Specifically: polyacrylamide gel (SDS.PAGE) kit was purchased from Yazyme; protease inhibitor cocktail was purchased from Sigma-Aldrich; BCA detection kit and protein ladder were purchased from Invitrogen; anti-PRDX2 (10545-2-AP), anti-BAX (50599-2-Ig), anti-ACTB (66009-1-Ig), anti-alpha Tubulin (11224-1-AP) were purchased from Proteintech; anti-GPX4 (ab125066, 1:1000) was purchased from Abcam; anti-BCL2 (AF6139) was purchased from Affinity; ELISA detection kits human PRDX2ELISA kit (CSB-EL018654HU), human KIM1 ELISA kit (CSB-E08807h), human NGAL ELISA kit (CSB-E09408h) was purchased from Huamei Biotechnology Company.

[0039] The specific operation steps of Western blot, immunofluorescence staining, ELISA and HK2 culture and intervention in the present invention are as follows:

[0040] Western blot

[0041] Total protein or cell protein of kidney tissue was extracted with tissue lysate, and protein concentration was determined by BCA method. 30 mg protein was loaded, 10% or 12% polyacrylamide gel electrophoresis (SDS.PAGE), 120 mA x 1.5 h wet transfer to PVDF membrane, blocked with blocking solution at room temperature for 1 h, eluted with TBST, and incubated overnight at 4 ° C. The membrane was washed 3 times with TBST, each time for 10 min, incubated with corresponding secondary antibody at room temperature for 1 h, and then washed 3 times, each time for 5 min. Antigen-antibody complex was displayed by enhanced chemiluminescence (ECL), exposed and scanned with darkroom X-ray film, and protein quantification was performed by gray value analysis of the target band, and the relative expression of the target protein was expressed by the gray value of the target band / ACTB gray value.

[0042] Immunofluorescence staining

[0043] After paraffin renal tissue sections were dewaxed and hydrated, the sections were placed in a microwave oven for antigen retrieval. After washing with 1xPBS for 3 times, each time for 5 minutes, and blocking with 5% BSA at room temperature for 1 hour, anti-PRDX2 (1:200) was incubated at 4°C overnight; washed with 1xPBS for 3 times, each time for 5 minutes, incubated with the corresponding fluorescent secondary antibody, and incubated at room temperature for 1 hour; washed with 1xPBS for 3 times, the sections were sealed with a sealing agent with DAPI, and the images were taken under a fluorescence microscope. The quantitative analysis of fluorescent positive staining was performed using ImageJ software to quantify the percentage of PRDX2 positive staining area.

[0044] ELISA

[0045] The standard was diluted in a gradient manner, and the urine was also diluted (or not diluted). 100 μl of the diluted standard or sample was added to each well into the 96-well plate containing the corresponding antibody, and incubated at 37°C for 2 hours; the liquid was discarded without washing, and 100 μl of biotin-labeled antibody working solution was added to each well, and incubated at 37°C for 1 hour; the liquid in the well was discarded, washed 3 times and dried, and 100 μl of horseradish peroxidase-labeled avidin working solution was added to each well, and incubated at 37°C for 1 hour, the liquid in the well was discarded, washed 5 times and dried, and 90 μl of substrate solution was added to each well in sequence, and incubated at 37°C in the dark for 20 minutes, and then 50 μl of stop solution was added to each well in sequence to terminate the reaction, and the optical density (OD) of each well was measured at a wavelength of 450 nm using an enzyme reader within 5 minutes. The standard curve was fitted using the measured value of the standard, and the protein expression of each well sample was calculated based on the fitted curve.

[0046] HK2 cell culture and intervention

[0047] HK2 cells were purchased from ATCC and cultured in a complete medium (DMEM / F12 medium containing 10% fetal bovine serum and 1% penicillin / streptomycin) in a cell culture incubator at 5% CO2 and 37°C. If the cells were subjected to hypoxia and reoxygenation treatment, the cells were passaged the day before the treatment; the next day, when the cells grew to about 80%, the medium was replaced with a sugar-free, serum-free medium (purchased from Gibco), and the cells were placed in a hypoxic incubator (1% O2, 5% CO2, 37°C) for 12 hours, the cells were removed from the hypoxic incubator and the medium was replaced with a complete medium, and the cells were cultured under normal conditions for another 12 hours, and then the cells were collected for subsequent analysis.

[0048] Example 1

[0049] Construction of AKI model and detection of PRDX2 expression in renal tissue of AKI model

[0050] 1.1 Construction of IR-AKI mouse model

[0051] The IR-AKI mouse model, namely acute kidney injury caused by renal ischemia reperfusion injury (IR).

[0052] The specific construction method is as follows: 8-12 week old male C57BL / 6 mice were used, and the mice were anesthetized by intraperitoneal injection of pentobarbital (50 mg / kg). A midline incision of about 2 cm was made on the back, and the abdominal wall was cut layer by layer at the location of the kidneys on both sides to find the kidneys and fully expose the renal pedicles. The renal pedicles were clamped with vascular clamps that did not damage the blood vessels. After 30 minutes, the vascular clamps were removed to restore the blood supply to the kidneys. After the kidneys were returned, the back incision was sutured layer by layer. During the operation, the mice were placed on a 37°C constant temperature pad to maintain the body temperature of the mice at 36.5±0.3°C. The control mice underwent sham surgery, that is, except for not clamping the renal pedicles, the rest of the surgical procedures were the same as those of the IR mice. After 24 hours, the kidney tissues of the mice in the IR group and the sham control group were collected and identified by Periodic Acid-Schiff Staining (PAS). The results are detailed in the literature. Figure 1 shown.

[0053] See also Figure 1 , Figure 1 The results of periodic acid-Schiff staining (PAS) of renal tissue in the ischemia-reperfusion injury (IR) AKI model are shown in Figure 1. Figure 1 a in the figure is the result of periodic acid-Schiff staining of the Sham group. Figure 1 b in the figure is the result of periodic acid-Schiff staining of the IR group; Figure 1It can be seen that in the IR-AKI mouse model, the kidney tissue showed typical manifestations of tubular injury, such as loss of tubular brush border, tubular dilatation, and tubular cast formation, indicating that the IR-AKI mouse model was successfully constructed.

[0054] 1.2 Detection of PRDX2 expression in renal tissue of IR-AKI mouse model

[0055] Western blotting and immunofluorescence staining were used to detect the expression of PRDX2 in the renal tissues of mice in the IR group and the sham control group. Figure 2 shown.

[0056] See also Figure 2 , Figure 2 The expression of PRDX2 in the renal tissue of IR-AKI mouse model, Figure 2 (a) Western blotting results of Sham group and IR group. Figure 2 (a) in (b) is the result of PRDX2 immunofluorescence staining in the sham group. Figure 2 (b) shows the immunofluorescence staining result of PRDX2 in the IR group; Figure 2 (a) It can be seen that the expression of PRDX2 in the kidney tissue of the IR-AKI mouse model was significantly decreased. Figure 2 (b) It can be seen that PRDX2 is mainly expressed in renal tubular cells, and its expression level is significantly downregulated in the IR-AKI model.

[0057] 1.3 Construction of CP-AKI mouse model

[0058] CP-AKI mouse model, acute kidney injury induced by cisplatin (CP).

[0059] The specific construction method is as follows: 8-12 week old male C57BL / 6 mice were intraperitoneally injected with cisplatin (30 mg / kg), and the control group (Control, Ctrl) mice were intraperitoneally injected with the corresponding volume of normal saline; 48 hours later, the kidney tissues in the CP group and the Ctrl group were collected for periodic acid-Schiff staining (PAS) identification. The results are detailed in Figure 3 shown.

[0060] See also Figure 3 , Figure 3 The results of periodic acid-Schiff staining (PAS) of renal tissue in the AKI model induced by cisplatin CP are shown in Figure 2. Figure 3a in the figure is the result of periodic acid-Schiff staining of the Ctrl group. Figure 3 b in the figure is the result of periodic acid-Schiff staining of the CP group; Figure 3 It can be seen that in the CP-AKI mouse model, the renal tissue showed typical manifestations of tubular injury, such as loss of tubular brush border, tubular dilatation, and tubular cast formation, indicating that the CP-AKI mouse model was successfully constructed.

[0061] 1.4 Detection of PRDX2 expression in renal tissue of CP-AKI mouse model

[0062] Western blotting and immunofluorescence staining were used to detect the expression of PRDX2 in the renal tissues of mice in the CP group and the Ctrl control group. Figure 4 shown.

[0063] See also Figure 4 , Figure 4 The expression of PRDX2 in the kidney tissue of CP-AKI mouse model, Figure 4 (a) is the Western blotting test results of the Ctrl group and the CP group. Figure 4 (a) in (b) is the result of PRDX2 immunofluorescence staining in the Ctrl group. Figure 4 (b) shows the immunofluorescence staining result of PRDX2 in CP group; Figure 4 (a) It can be seen that the expression of PRDX2 in the renal tissue of the CP-AKI mouse model was significantly decreased. Figure 4 (b) It can be seen that PRDX2 is mainly expressed in renal tubular cells, and its expression level is significantly downregulated in the CP-AKI model.

[0064] Combination Figures 1 to 4 It can be seen that in animal models of acute kidney injury caused by different causes, PRDX2 in renal tissue showed obvious downregulation of expression, with no specificity for the cause of injury.

[0065] Example 2

[0066] Analysis of PRDX2 expression in renal tissue of clinical patients and its correlation with renal function

[0067] Renal tissue specimens (n=6) from patients diagnosed with acute tubular necrosis (ATN) by renal puncture were collected clinically. The control group consisted of renal tissue specimens (n=6) from patients with minimal change disease (MCD) without renal tubular damage and their clinical data. Immunofluorescence staining was used to detect the expression of PRDX2 in the patients' renal tissues, and its correlation with the patients' estimated glomerular filtration rate and serum creatinine was analyzed.

[0068] Table 1 Basic information, estimated glomerular filtration rate, and serum creatinine level of 12 patients undergoing renal biopsy

[0069]

[0070] It should be noted that the abbreviations in Table 1 are as follows: MCD: minimal change disease; ATN: acute tubular necrosis; FSGS: focal segmental glomerulosclerosis.

[0071] See also Figures 5 to 8 ,in, Figure 5 These are the results of PRDX2 and Merge immunofluorescence staining of renal biopsy tissues in patients with acute tubular necrosis (ATN) and minimal change disease (MCD) without tubular damage. Figure 5 a in the figure is the result of PRDX2 immunofluorescence staining in the MCD group. Figure 5 b is the result of PRDX2 immunofluorescence staining in the ATN group. Figure 5 c in the figure is the Merge immunofluorescence staining result of the MCD group. Figure 5 d in the figure is the Merge immunofluorescence staining result of the ATN group; Figure 6 The results of quantitative analysis of PRDX2 in renal biopsy tissues of patients with acute tubular necrosis (ATN) and minimal change disease (MCD) without tubular damage; Figure 7 Based on Figure 6 The results of correlation analysis between the expression of PRDX2 in the blood and the estimated glomerular filtration rate of patients; Figure 8 Based on Figure 6 The results of correlation analysis between the expression level of PRDX2 in the patients and the serum creatinine.

[0072] from Figure 5 and Figure 6 It can be seen that in the renal biopsy tissue of patients with minimal change disease (MCD) without tubular damage, PRDX2 is highly positively expressed, but in the renal biopsy tissue of patients with acute tubular necrosis (ATN), PRDX2 positive expression is significantly reduced, and its expression is mainly located in the tubular cells. This result is similar to the animal experiment results provided in Example 1.

[0073] from Figure 7 and Figure 8 It can be seen that by correlating the expression of PRDX2 in the patient's kidney tissue with renal function-related indicators (estimated glomerular filtration rate and serum creatinine), it was found that the expression of PRDX2 in the kidney tissue was significantly positively correlated with the estimated glomerular filtration rate, with a correlation coefficient of 0.8631. Figure 7 As shown in Figure 2, there is a significant negative correlation with serum creatinine level, with a correlation coefficient of -0.5579. Figure 8 This indicates that the expression of PRDX2 in renal tissue can reflect the severity of renal injury.

[0074] Example 3

[0075] Analysis of PRDX2 expression in urine of clinical patients and its correlation with renal tubular injury

[0076] During partial nephrectomy (PN) surgery, the vascular clamping treatment will be performed on the partially removed kidney, and renal ischemia is one of the important factors leading to renal tubular injury. This example includes two types of patients with renal injury: the first type of patients are patients who undergo partial nephrectomy (PN): preoperative serum creatinine is normal, intraoperative unilateral renal ischemia time is ≥24 minutes, and their urine is collected 48 hours after surgery (sample number n=14); the second type of patients are patients clinically diagnosed with AKI, and the diagnostic criteria for AKI are: ① serum creatinine increases by ≥0.3 mg / dL (≥26.5μmol / L) within 48 hours; or ② compared with the serum creatinine value in the past 7 days, the serum creatinine increases by ≥1.5 times; or ③ after adequate fluid resuscitation, the urine volume decreases to <0.5 mL / kg / hour for at least 6 hours; their urine is collected (sample number n=19).

[0077] The control group included patients who underwent radical nephrectomy (RN) (this surgery completely removed one kidney without renal ischemic injury) and whose serum creatinine was normal before surgery. Their urine was collected 48 hours after surgery (sample number n=8).

[0078] The collected urine was centrifuged at 3000g and 4°C for 10 min, and the urine supernatant was aspirated and the expression of PRDX2 and the expression of renal tubular injury markers (NGAL, KIM 1) were detected by ELISA kit. The correlation analysis was further used to analyze the correlation between PRDX2 expression and renal tubular injury. The expression results and correlation analysis results are detailed in Figure 9~Figure 13 .

[0079] See also Figure 9~Figure 11 ,in, Fig. 9ELISA was used to detect the expression of NGAL in urine of patients who had undergone radical nephrectomy (RN), 48 hours after partial nephrectomy (PN), and patients clinically diagnosed with AKI. Fig.10 The expression of PRDX2 in urine of patients who underwent radical nephrectomy (RN), 48 hours after partial nephrectomy (PN), and patients clinically diagnosed with AKI was detected by ELISA; Fig.11 The expression of KIM 1 in urine of patients with radical nephrectomy (RN) and partial nephrectomy (PN) was detected by ELISA.

[0080] from Fig. 9 It can be seen that compared with radical nephrectomy (RN), the expression of NGAL, a renal tubular injury marker, in the urine of patients who underwent partial nephrectomy (PN) and patients diagnosed with AKI was significantly increased, indicating the occurrence of renal tubular injury. Fig.10 It can be seen that the expression of PRDX2 in the urine of PN patients and AKI patients increased significantly. To further verify the occurrence of renal tubular injury in PN patients, another classic renal tubular injury marker KIM1 was detected in their urine. It was found that the expression of KIM1 in the PN group was significantly increased compared with the control group, as shown in Figure 2. Fig.11 shown. Figures 9 to 11 The combined results showed that the expression of PRDX2 in the urine of patients with renal tubular damage was significantly increased.

[0081] Fig.12 Based on Fig.10 The expression level of PRDX2 in Fig.11 The results of correlation analysis of the expression of KIM 1 in Fig.13 Based on Fig.10 The expression level of PRDX2 in Fig. 9 Correlation analysis results of NGAL expression in Fig.12 and Fig.13 It can be seen that the expression of PRDX2 in the patient's urine is positively correlated with NGAL and KIM1, with correlation coefficients of 0.705 and 0.7819, respectively, indicating that the expression of urinary PRDX2 is closely related to renal tubular damage.

[0082] Combined with the experimental results of Example 1 to Example 3, it can be seen that PRDX2 is differentially expressed in the renal puncture specimens of ATN patients and the renal tissue of the AKI mouse model. Specifically, compared with the control group, PRDX2 is significantly low in ATN and AKI renal tissue, and is closely related to the level of renal function, specifically, its expression is positively correlated with eGFR and negatively correlated with serum creatinine levels; compared with the control group, PRDX2 is significantly highly expressed in the urine of AKI patients and partial nephrectomy patients, and is positively correlated with tubular injury markers KIM-1 and NGAL. It shows that PRDX2 is closely related to tubular injury, can be used as a biomarker for acute kidney injury, and is used to assist in the diagnosis or prognosis prediction of acute kidney injury, providing a new approach for the diagnosis and prognosis prediction of acute kidney injury.

[0083] The above contents are further detailed descriptions of the present invention in combination with specific preferred embodiments, and it cannot be determined that the specific implementation of the present invention is limited to these descriptions. For ordinary technicians in the technical field to which the present invention belongs, several simple deductions and substitutions can be made without departing from the concept of the present invention, which should be regarded as belonging to the protection scope of the present invention.

Claims

1. Application of reagents for detecting the expression of the biomarker PRDX2 in the preparation of products for auxiliary diagnosis and prognosis prediction of acute kidney injury.

2. The use according to claim 1, It is characterized in that The acute kidney injury is acute kidney injury caused by ischemia-reperfusion injury or acute kidney injury induced by cisplatin.

3. The use according to claim 1, It is characterized in that The product includes a kit or a reagent.

4. The use according to any one of claims 1 to 3, It is characterized in that The test samples of the subjects are kidney tissue and / or urine.

5. The use according to claim 4, It is characterized in that When the expression level of PRDX2 in the renal tissue of the subject is low relative to the expression level of PRDX2 in a normal control or a standard, the subject is diagnosed as being at risk of acute kidney injury.

6. The use according to claim 4, It is characterized in that When the expression level of PRDX2 in the urine of the subject is high relative to the expression level of PRDX2 in a normal control or a standard, the subject is diagnosed as being at risk of suffering from acute kidney injury.

7. The use according to claim 6, It is characterized in that High expression of PRDX2 in urine is positively correlated with renal tubular damage in acute kidney injury-related conditions.

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