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Characteristics of renal pathology and coagulation function in IgA nephropathy and IgA vasculitis associated nephritis

BMC Nephrology volume 25, Article number: 35 (2024) Cite this article

Abstract

Background

The objective of this study is to investigate the clinical and pathological differences between patients with IgA nephropathy (IgAN) and IgA vasculitis associated nephritis (IgAVN).

Methods

A total of 253 patients with IgAN and 71 patients with IgAVN were retrospectively included in the study, and clinical and laboratory data were collected and analysed.

Results

Compared with IgAVN group, months from onset to kidney biopsy were significantly prolonged in IgAN patients because of the lack of obvious symptoms such as rash, abdominal symptoms, and joint pain (13.5 ± 26.6 vs. 10.2 ± 31.6 months, P = 0.007), and the levels of serum creatinine (92.3 ± 94.7 vs. 68.9 ± 69.2 µmol/L, P = 0.015) was higher and eGFR (99.1 ± 35.2 vs. 123.4 ± 41.8 mL/min/1.73m2, P < 0.001) was lower in IgAN group. The pathological results revealed that patients with IgAN have a greater degree of chronic kidney injury compared to patients with IgAVN. In addition, the levels of plasma D-Dimers (1415.92 ± 1774.69 vs. 496.78 ± 711.91 ng/mL, P < 0.001) and fibrinogen degradation products (FDP) (3.92 ± 4.73 vs. 1.63 ± 2.46 µg/mL, P = 0.001) were significantly higher in IgAVN patients than in IgAN patients. The deposition of fibrinogen in the renal tissues was more severe and the cumulative partial remission rate was higher in patients with IgAVN as compared to those with IgAN (P = 0.001).

Conclusions

In comparison, IgAN patients had poorer renal function, whereas IgAVN patients had more severe coagulation abnormalities. These findings provide a basis for the differentiation of the two diseases at an early stage.

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Introduction

IgAN is the most common primary glomerulonephritis worldwide and mainly affects the young population [1]. Approximately 30–40% of patients develop end-stage kidney disease within 20–30 years after their initial clinical presentation [2]. IgAVN is a systemic inflammatory disease that affects small blood vessels and is particularly prevalent among children [3]. However, the relationship between IgAN and IgAVN is controversial. Galactose-deficient IgA1, an important effector molecule in IgAN, has been specifically detected in the glomeruli of IgAVN, but not in the other kidney diseases such as lupus nephritis, HCV-related nephropathy, and membranous nephropathy [4]. In addition, the immune transcriptomes of kidney tissue in IgAN, IgAVN, and IgA-dominant infection-related glomerulonephritis largely overlap [5]. IgAVN shares many pathogenetic features with IgAN, which makes it difficult to distinguish IgAVN from IgAN by pathological characteristic alone. Moreover, renal biopsy, being an invasive examination, is unsuitable for patients with solitary kidney and hydronephrosis, and could lead to complications such as renal bleeding and infection. Therefore, the differences in clinical manifestations and laboratory tests may provide some clues for the diagnosis of the two diseases. Recent studies have indicated that coagulation is involved in the pathogenesis of IgAN and IgAVN [6, 7]. Nevertheless, no studies have compared the discrepancies in the coagulation factors levels between the two groups and explored the potential mechanisms. Therefore, in this study, we retrospectively collected and analyzed the clinical, laboratory, coagulation and pathological data of 253 IgAN patients and 71 IgAVN patients, in order to provide useful basis for the early differentiation of the two diseases.

Methods

Ethical standards

This study was approved by the ethics committee of the Second Affiliated Hospital of Xi’an Jiaotong University and conducted according to the declaration of Helsinki. All study participants were informed of the study’s purpose, and written informed consent was obtained from the patients or their legal representatives.

Inclusion and exclusion criteria

Patients with IgAN and IgAVN who underwent kidney biopsy in the Second Affiliated Hospital of Xi’an Jiaotong University from January 2017 to June 2020 were enrolled in the study. The diagnostic criteria for IgAN: kidney biopsy confirmed that predominant mesangial deposition of IgA, those with secondary causes of mesangial IgA deposits were excluded. The diagnostic criteria for IgAVN meets EULAR/PRINTO/PRES diagnostic criteria [8].

Inclusion criteria were: (1) age 18–70 years; (2) patients with newly diagnosed, biopsy-proven IgAN; (3) patients with renal involvement and the presence of purpura or petechiae predominantly in the lower limbs were diagnosed with IgAVN. Exclusion criteria were: (1) Crohn’s disease, ulcerative colitis, ankylosing spondylitis; (2) Chronic mucosal infections (streptococcus, staphylococcus); (3) HBV, HCV, HIV or Cytomegalovirus infections; (4) autoimmune disorders including ankylosing spondylitis, rheumatoid arthritis, systemic lupus erythematosus, dermatitis herpetiformis, sjögren’s syndrome, psoriasis; (5) malignancies such as IgA myeloma, Non-Hodgkin’s lymphoma, Hodgkin’s lymphoma, cutaneous T-cell lymphoma, lung cancer, renal cell carcinoma; (6) patients receiving anticoagulant or antiplatelets therapy; (7) patients with a history of thromboembolism; (8) thrombocytopenic purpura; (9) ANCA-associated vasculitis; (10) incomplete clinical data; (11) pregnancy or lactation.

Pathology and scoring methods.

The pathological specimens in the study were reviewed independently by two experienced renal pathologists. The histological lesions were scored referring to the study by Jiang L et al. [9], and the glomerular, tubular, interstitial and vascular lesions were scored separately. In addition, pathological data for IgAN and IgAVN were scored using the updated Oxford Classification criteria. The semiquantitative histological scoring of immune complexes in renal tissue was assessed in accordance with the research by Lv Y et al. [10]. The grade of deposition of immune complexes was defined as follows: -, negative; 1 +, weak but definite staining; 2 +, moderate staining; 3 +, strong staining; 4 +, bright staining.

Outcome.

The endpoint was the complete remission rate and partial remission rate. Complete remission was defined as proteinuria ≤ 0.3 g/24 h, serum albumin > 35 g/L, and normal serum creatinine level. Partial remission was defined as proteinuria > 0.3 g/24 h, but > 50% decline from baseline, serum albumin level ≥ 35 g/L, and stable serum creatinine [11].

Statistical analysis.

Statistical analysis was performed using SPSS software (version 26.0, IBM Corporation, Armonk, NY). The data of normal or approximately normal distribution were expressed as the means ± standard deviations (SD), and using the Student’s t-test to compared the differences between two groups. The qualitative data were expressed as percentages and analysed with Chi-squared Test or Fisher’s exact probability test. The remission rates were analyzed by the Kaplan–Meier method and compared by log-rank test. P < 0.05 was considered significant.

Results

Clinical characteristics and laboratory parameters of IgAN and IgAVN

As shown in Table 1, there was no significantly difference in age, gender and hypertension between the two groups. Months from onset to kidney biopsy were significantly prolonged in IgAN patients than in IgAVN patients (13.5 ± 26.6 vs. 10.2 ± 31.6 months, P = 0.007), which may be due to the lack of obvious symptoms such as rash, abdominal symptoms, and joint pain in IgAN patients.

Table 1 Clinical characteristics and laboratory parameters of IgAN and IgAVN patients
Full size table

Laboratory test results in Table 1 showed that the white blood cell count in the IgAVN group was significantly higher than that in the IgAN group (8.1 ± 3.0 vs. 6.5 ± 2.1 *10^9/L, P < 0.001), which may be due to the more severe involvement of small vessels in IgAVN. Although there was no difference in urinary protein excretion and serum albumin levels between the two groups, the levels of urinary kappa and lambda light chains in the IgAVN group was significantly higher than that in the IgAN group. Compared with IgAVN group, the levels of serum creatinine (92.3 ± 94.7 vs. 68.9 ± 69.2 µmol/L, P = 0.015) was higher and eGFR (99.1 ± 35.2 vs. 123.4 ± 41.8 mL/min/1.73m2, P < 0.001) was lower in IgAN group.

The treatment regimens of 207 patients with IgAN and 66 patients with IgAVN were collected (Table 1). The results showed that all patients in the study, except those with contraindications, received angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) to reduce urinary protein excretion and control blood pressure. Additionally, the percentage of patients receiving prednisone was 56% in IgAN group and 78% in IgAVN group, respectively.

Renal pathology of IgAN and IgAVN

As shown in Table 2, renal pathological findings showed that fibrocellular or fibrous crescents, thickness of blood vessel wall, glomerular sclerosis, interstitial inflammatory cell infiltration, interstitial fibrosis and tubular atrophy were more common in IgAN patients (P < 0.05), while cellular crescents were more common in IgAVN patients (P < 0.05). The activity and chronicity indexes of renal lesions were evaluated. Patients with IgAN exhibited higher chronicity index (2.34 ± 1.81 vs. 1.03 ± 1.24, P < 0.001), and total biopsy scores (5.24 ± 2.63 vs. 3.69 ± 2.59, P < 0.001) compared to those with IgAVN. The Oxford Classification of IgAN and IgAVN is shown in Supplementary Table 1. The percentages of IgAN patients were 71.1%, 11.9%, 68.8%, 11.5%, 4.3%, 22.5%, and 1.6% for M1, E1, S1, T1, T2, C1, and C2, respectively. In contrast, the percentages of IgAVN patients were 81.7%, 19.7%, 32.4%, 2.8%, 35.2% and 2.8% for M1, E1, S1, T1, C1, and C2, respectively. Compared to the IgAVN group, the IgAN group had a higher proportion of patients for S1 (P < 0.001) and T1 + T2 (P = 0.002), and a lower proportion for C1 + C2 (P = 0.02).

Table 2 Pathological characteristics of IgAN and IgAVN patients
Full size table

These pathological findings show that patients with IgAN have a greater degree of chronic kidney injury compared to patients with IgAVN, as evidenced by an increased presence of fibrous crescents and more severe interstitial fibrosis and tubular atrophy, which is consistent with the higher serum creatinine and lower eGFR levels observed in the IgAN group.

Coagulation parameters of IgAN and IgAVN

We compared coagulation parameters between IgAVN and IgAN patients. The results showed that the levels of plasma D-Dimers (1415.92 ± 1774.69 vs. 496.78 ± 711.91 ng/mL, P < 0.001) and FDP (3.92 ± 4.73 vs. 1.63 ± 2.46 µg/mL, P = 0.001) were significantly higher in IgAVN patients than in IgAN patients, while the level of APTT (23.82 ± 6.08 vs. 26.93 ± 4.37 s, P = 0.007) was significantly lower in IgAVN patients than in IgAN patients (shown in Table 3). There was no significant difference in the levels of prothrombin time (PT), international normalized ratio (INR), fibrinogen, and thrombin time (TT) between the two groups.

Table 3 Coagulation parameters of IgAN and IgAVN patients
Full size table

Immunopathology data of IgAN and IgAVN

In the analysis of the renal immunopathology data of the patients, we did not observe any difference in the levels of IgA, IgG, IgE and C1q deposition in glomeruli between the IgAN and IgAVN groups (shown in Table 4). The percentage of patients with C3 deposition grade 2 + and 3 + was considerably higher in the IgAN group than in the IgAVN group (70.8% vs. 55%, P = 0.042), whereas the percentage of patients with fibrinogen deposition grade 2 + and 3 + was markedly lower in the IgAN group than in the IgAVN group (19% vs. 46%, P < 0.001).

Table 4 Immunopathological data between IgAN and IgAVN patients
Full size table

The remission rates of IgAVN and IgAN

Kaplan-Meier analysis in Fig. 1 showed that the median time to achieve partial remission was 14 months (95% CI: 10.8–17.1 months) in the IgAN group and 12 months (95% CI: 10.6–13.4 months) in the IgAVN group. The IgAVN group exhibited a higher cumulative partial remission rate compared to the IgAN group (P = 0.001). The median time to complete remission was 21 months (95% CI: 18.5–23.4 months) in the IgAN group and 15 months (95% CI: 10.7–19.3 months) in the IgAVN group. However, the log-rank test revealed no significant difference in the cumulative complete remission rates between the two groups.

Fig. 1
figure 1

Cumulative probability of partial and complete remission rates in IgAN and IgAVN patients. (A) cumulative probability of partial remission rates; (B) cumulative probability of complete remission rates. (IgAN: IgA nephropathy, IgAVN: IgA vasculitis associated nephritis)

Full size image

Discussion

IgAVN shares many pathogenetic features with IgAN, which poses a challenge in distinguishing between the two diseases by pathological characteristics exclusively. Extra-renal symptoms, such as rash, abdominal symptoms, and joint pain are critical in the early diagnosis of IgAVN. In our study, the time from onset to renal biopsy was significantly longer in patients with IgAN than in patients with IgAVN. This difference may be due to the lack of extrarenal manifestations in patients with IgAN. Renal biopsy is a crucial diagnostic method for evaluating renal injury. In our study, the Oxford Classification of IgAN showed that the percentages of patients were 71.1%, 11.9%, 68.8%, 11.5%, 4.3%, 22.5%, and 1.6% for M1, E1, S1, T1, T2, C1, and C2, respectively. These results are consistent with the study by Coppo, R et al. [12], who revealed that M1, S1 and T1–T2 lesions were predictors of poorer kidney survival. Our study revealed that the chronic lesions, including fibrocellular or fibrous crescents, thickness of blood vessel wall, interstitial fibrosis, and tubular atrophy, were more common in IgAN patients, while cellular crescents were more common in IgAVN patients. Furthermore, the IgAN group exhibited a comparatively higher serum creatinine level and lower eGFR levels than the IgAVN group. Our results indicates that IgAN is a more clandestine disease than IgAVN and often leads to poorer renal function at the initial diagnosis. The extent of tubulointerstitial fibrosis and tubular atrophy is strongly correlated with eGFR and the extent of chronic kidney damage, and is associated with the prognosis of the kidney [13].

These outcomes are in line with the investigation carried out by Lv et al. [10], who analysed data obtained from 809 paediatric patients with IgAVN and 236 paediatric patients with IgAN. Their findings revealed that IgAN patients exhibited more severe renal interstitial injury, fibrous crescents, and other chronic injury manifestations than IgAVN patients. Additionally, remission rate is a crucial indicator for evaluating the prognosis of IgAN and IgAVN. The results in our study indicate that the cumulative partial remission rate was lower in the IgAN group compared to the IgAVN group. This difference may be associated with poorer renal function and more severe interstitial fibrosis and tubular atrophy in IgAN patients.

Coagulation dysfunction is an important non-immune factor in the progression of ESKD [14]. Microvascular endothelial cells injury, activation of platelets, and released plasma coagulation factors can lead to diffuse coagulation in the renal microvasculature, then promotes kidney fibrosis [15]. Study has also shown that heparin may reduce the risk of proteinuria in patients with IgAVN [16].

Plasma D-Dimers formation or elevation reflects activation of the coagulation and fibrinolytic systems. Study have shown that plasma D-Dimer was associated with microalbuminuria [17], and high levels of plasma D-Dimer were associated with the progression of IgAN [18]. In addition, the elevated D-Dimers levels were significantly associated with renal involvement in IgAVN [19]. The results in our study showed that the level of D-Dimers was significantly higher in IgAVN patients than in IgAN patients, which suggests that IgAVN is more active than IgAN [20].

As is well-known, fibrinogen plays an essential function in blood clotting, and in vivo study has confirmed its significant involvement in the promotion of kidney fibrosis [21]. Fibrinogen deficiency protects mice with unilateral ureteral obstruction from interstitial damage, tubular disruption, collagen accumulation, and expression of α-smooth muscle actin in the obstructed kidney. In addition, study of Qin et al. [22] has demonstrated that low albumin-to-fibrinogen (< 12.44) is an independent prognostic factor of poor renal prognosis in Chinese IgAN patients, and the glomerular fibrinogen deposition in IgAVN patients exhibit more severe glomerular damage [23]. In our study, glomerular fibrinogen deposition was observed to be more severe in IgAVN despite no significant difference in plasma fibrinogen levels between the IgAN and IgAVN groups. Plasma FDPs, another crucial factor in the fibrinolytic system strongly linked to IgAVN disease activity [24], were found to be significantly greater in IgAVN patients compared to IgAN patients in our study.

Nevertheless, this study has some limitations that must be acknowledged. Firstly, only patients who underwent kidney biopsies were included in this study. Secondly, it’s unclear whether the patients were in the acute or chronic phase at the time of renal biopsy. Additionally, the small sample size may have an impact on the results obtained. Therefore, it is essential to expand the sample size and monitor patients’ prognoses to establish a theoretical foundation for early diagnosis and treatment.

Conclusions

In comparison, IgAN patients had poorer renal function, whereas IgAVN patients had more severe coagulation abnormalities. These findings provide a basis for the differentiation of the two diseases at an early stage.

Data availability

The datasets used and analysed are available from the correasponding author on reasonable request.

Abbreviations

IgAN:

IgA nephropathy

IgAVN:

IgA vasculitis associated nephritis

WBC:

White blood cell

Hb:

hemoglobin

PLT:

Platelet, Kap:kappa light chains

Lam:

Lambda light chains

TP:

Total serum protein

ALB:

Serum albumin

Scr:

Serum creatinine

eGFR:

Estimated glomerular filtration rate

UA:

Serum uric acid

PT:

Prothrombin time

INR:

International normalized ratio

APTT:

Activated partial thromboplastin time

FIB:

Fibrinogen

TT:

Thrombin time

FDP:

Fibrinogen degradation products

ESKD:

End stage kidney disease

ACEI:

Angiotensin-converting enzyme inhibitor

ARB:

Angiotensin receptor blockers

References

  1. Rodrigues JC, Haas M, Reich HN. IgA nephropathy. Clin J Am Soc Nephrol. 2017;12(4):677–86.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Lai KN, Tang SC, Schena FP, Novak J, Tomino Y, Fogo AB, et al. IgA nephropathy. Nat Rev Dis Primers. 2016;2:16001.

    Article  PubMed  Google Scholar 

  3. Pillebout E, Sunderkötter C. IgA vasculitis. Semin Immunopathol. 2021;43(5):729–38.

    Article  CAS  PubMed  Google Scholar 

  4. Suzuki H, Yasutake J, Makita Y, Tanbo Y, Yamasaki K, Sofue T, et al. IgA nephropathy and IgA vasculitis with nephritis have a shared feature involving galactose-deficient IgA1-oriented pathogenesis. Kidney Int. 2018;93(3):700–5.

    Article  CAS  PubMed  Google Scholar 

  5. Kung VL, Avasare R, Friedman MA, Koon SM, Neff TL, Protzek S, et al. Targeted transcriptional analysis of IgA Vasculitis, IgA Nephropathy, and IgA-Dominant infection-related glomerulonephritis reveals both distinct and overlapping Immune signatures. Kidney360. 2023;4(6):e759–e68.

    Article  PubMed  PubMed Central  Google Scholar 

  6. He Z, Zhang Y, Cao M, Ma R, Meng H, Yao Z, et al. Increased phosphatidylserine-exposing microparticles and their originating cells are associated with the coagulation process in patients with IgA nephropathy. Nephrol Dial Transplant. 2016;31(5):747–59.

    Article  CAS  PubMed  Google Scholar 

  7. Demir S, Yet I, Sardan Ekiz M, Sag E, Bilginer Y, Celikbicak O et al. Plasma proteomic analysis reveals the potential role of Lectin and Alternative Complement pathways in IgA Vasculitis Pathogenesis. Diagnostics (Basel). 2023;13(10).

  8. Ozen S, Pistorio A, Iusan SM, Bakkaloglu A, Herlin T, Brik R, et al. EULAR/PRINTO/PRES criteria for Henoch-Schönlein purpura, childhood polyarteritis nodosa, childhood Wegener granulomatosis and childhood Takayasu arteritis: Ankara 2008. Part II: final classification criteria. Ann Rheum Dis. 2010;69(5):798–806.

    Article  PubMed  Google Scholar 

  9. Jiang L, Liu G, Lv J, Huang C, Chen B, Wang S, et al. Concise semiquantitative histological scoring system for immunoglobulin A nephropathy. Nephrol (Carlton). 2009;14(6):597–605.

    Article  Google Scholar 

  10. Lv Y, Fu R, Peng XJ, Wang Y, Yin TT, Deng YQ. Comparative study on clinicopathological features and prognosis of IgA vasculitis nephritis and IgA nephropathy in children. BMC Pediatr. 2023;23(1):423.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Pozzi C. Treatment of IgA nephropathy. J Nephrol. 2016;29(1):21–5.

    Article  CAS  PubMed  Google Scholar 

  12. Coppo R, Troyanov S, Bellur S, Cattran D, Cook HT, Feehally J, et al. Validation of the Oxford classification of IgA nephropathy in cohorts with different presentations and treatments. Kidney Int. 2014;86(4):828–36.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Stamellou E, Seikrit C, Tang SCW, Boor P, Tesař V, Floege J, et al. IgA nephropathy. Nat Rev Dis Primers. 2023;9(1):67.

    Article  PubMed  Google Scholar 

  14. Lutz J, Menke J, Sollinger D, Schinzel H, Thürmel K. Haemostasis in chronic kidney disease. Nephrol Dial Transplant. 2014;29(1):29–40.

    Article  CAS  PubMed  Google Scholar 

  15. Troyanov S, Hladunewich MA, Reich HN. How should Pathology findings Influence Treatment in IgA Nephropathy? Kidney Int Rep. 2022;7(1):3–5.

    Article  PubMed  Google Scholar 

  16. Hahn D, Hodson EM, Craig JC. Interventions for preventing and treating kidney disease in IgA vasculitis. Cochrane Database Syst Rev. 2023;2(2):Cd005128.

    PubMed  Google Scholar 

  17. Wakabayashi I, Masuda H. Association of D-dimer with microalbuminuria in patients with type 2 diabetes mellitus. J Thromb Thrombolysis. 2009;27(1):29–35.

    Article  CAS  PubMed  Google Scholar 

  18. Yu G, Jiang Y, Xu Z, Cheng J, Li H, Li X, et al. Plasma D-dimer as a potential predictor of progression in IgA nephropathy: a cohort study. Ren Fail. 2023;45(2):2251587.

    Article  PubMed  PubMed Central  Google Scholar 

  19. Nie YL, Song ZX, Tao J, Han X, Yang L. Correlations of serological markers with development of systemic involvement in adult immunoglobulin a vasculitis: a retrospective study of 259 patients in Central China. Curr Med Sci. 2021;41(5):888–93.

    Article  CAS  PubMed  Google Scholar 

  20. Mosakowska M, Kania DB, Szamotulska K, Rymarz A, Niemczyk S. Assessment of the correlation of commonly used laboratory tests with clinical activity, renal involvement and treatment of systemic small-vessel vasculitis with the presence of ANCA antibodies. BMC Nephrol. 2021;22(1):290.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Sörensen I, Susnik N, Inhester T, Degen JL, Melk A, Haller H, et al. Fibrinogen, acting as a mitogen for tubulointerstitial fibroblasts, promotes renal fibrosis. Kidney Int. 2011;80(10):1035–44.

    Article  PubMed  Google Scholar 

  22. Qin A, Wang S, Dong L, Jiang Z, Yang D, Tan J et al. Prognostic value of the albumin-to-fibrinogen ratio (AFR) in IgA nephropathy patients. Int Immunopharmacol. 2022;113(Pt A):109324.

  23. Wang F, Huang L, Tang H, Li X, Zhu X, Wang X. Significance of glomerular fibrinogen deposition in children with Henoch-Schönlein purpura nephritis. Ital J Pediatr. 2018;44(1):97.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Hong J, Yang HR. Laboratory markers indicating gastrointestinal involvement of henoch-schönlein purpura in children. Pediatr Gastroenterol Hepatol Nutr. 2015;18(1):39–47.

    Article  PubMed  PubMed Central  Google Scholar 

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Funding

This study was supported by the Shaanxi Province Foundation for Key R&D Projects (2020SF-158).

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Author notes

  1. Yinhong Wang, Hao Wang authors contributed equally to this work.

Authors and Affiliations

  1. Department of Nephropathy, the Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China

    Yinhong Wang, Xiaotao Ma, Rongguo Fu & Lining Jia

  2. Department of Nephropathy, Xi’an No 3 Hospital, the Affiliated Hospital of Northwest University, Xi’an, China

    Hao Wang

  3. Department of Computer Science, School of Computing & Department of Electrical and Computer Engineering, National University of Singapore, Singapore, Singapore

    Zikun Zhu

  4. Section of Nephrology, Department of Internal medicine, Yale University School of Medicine, New Haven, CT, USA

    Xuefei Tian

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Contributions

Y.W. completed all data analysis and wrote the paper. H.W., X.M., and Z.Z. performed the study and completed the data collection. L.J. and R.F. designed research. L.J., R.F.,and X.T. reviewed and edited the manuscript. All authors reviewed the manuscript, and approved the final manuscript.

Corresponding authors

Correspondence to Rongguo Fu or Lining Jia.

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Ethics approval and consent to participate

This study was approved by the ethics committee of the Second Affiliated Hospital of Xi’an Jiaotong University and conducted according to the declaration of Helsinki. All study participants were informed of the study’s purpose, and written informed consent was obtained from the patients or their legal representatives.

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Not applicable.

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The authors declare no competing interests.

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Wang, Y., Wang, H., Ma, X. et al. Characteristics of renal pathology and coagulation function in IgA nephropathy and IgA vasculitis associated nephritis. BMC Nephrol 25, 35 (2024). https://doi.org/10.1186/s12882-024-03465-6

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BMC Nephrology

ISSN: 1471-2369

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