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Risk factors for relapse and aggravation in membranous nephropathy after COVID-19 infection

BMC Nephrology volume 26, Article number: 71 (2025) Cite this article

Abstract

Background

Relapse of membranous nephropathy (MN) and other glomerular diseases has been observed after COVID-19 infection. The risk factors contributing to disease progression in MN patients after contracting COVID-19 remain unclear.

Methods

This retrospective study included 656 consecutive patients with biopsy-proven primary MN who received treatment and were regularly followed up for over six months. Logistic regression analyses were conducted to identify risk factors for disease progression.

Results

Among the cohort, 555 patients (84.6%) contracted COVID-19 from November 11th, 2022, to February 22nd, 2023. Of them, 112 patients (20.2%) experienced a > 50% increase in proteinuria, including 30 patients (5.4%) who experienced nephrotic syndrome relapse. Sixteen patients (2.9%) showed immune aggravation with elevated anti-PLA2R antibody levels, and five patients (0.9%) had immune relapse characterized by antibody reoccurrence. Kidney dysfunction, defined as an eGFR reduction > 30% from baseline, occurred in 10 patients (1.8%), with two patients (0.4%) progressing to ESKD. Four patients (0.7%) died of respiratory failure. Overall, 132 patients (24.0%) experienced disease progression after COVID-19 infection. Multivariate logistic regression identified longer fever duration (OR 1.118, 95% CI 1.029–1.356, P = 0.018), withdrawal of immunosuppressants and/or steroids (OR 2.571, 95% CI 1.377–4.799, P = 0.003) and extended drug cessation (OR 1.113, 95% CI 1.045–1.186, P = 0.001) as independent risk factors for MN progression.

Conclusions

These findings suggest prompt antiviral treatment and minimizing the duration of immunosuppressant withdrawal to optimize kidney outcomes in MN patients with COVID-19.

Peer Review reports

Introduction

Membranous nephropathy (MN) is the leading cause of nephrotic syndrome in adults and is characterized by autoimmune-mediated thickening of the glomerular basement membrane due to immune complex deposition [1]. The identification of phospholipase A2 receptor (PLA2R) as the major antigen has revolutionized the diagnosis and monitoring of MN, with additional antigens subsequently identified [1,2,3,4]. The clinical course of MN is chronic and variable, often marked by cycles of relapse and remission [2, 5]. Understanding the risk factors contributing to relapse and disease aggravation is crucial for improving patient outcomes.

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected millions worldwide, presenting a global health challenge [6, 7]. Beyond respiratory complications such as pneumonia and acute respiratory distress syndrome [6,7,8,9,10], COVID-19 has been implicated in multiple-organ injuries, including kidney, cardiovascular, and central nervous system damage [6,7,8,9,10,11,12,13,14]. Patients with COVID-19 have exhibited a wide spectrum of glomerular and tubular abnormalities, including acute kidney injury and nephrotic-range proteinuria, with histopathologic diagnoses such as collapsing glomerulopathy, minimal change disease, MN, crescentic transformation of lupus nephritis, anti-glomerular basement membrane nephritis, and isolated acute tubular injury [15,16,17,18].

Despite several studies on the renal complications of COVID-19, data on its impact on pre-existing kidney diseases, including MN, remain limited. MN was selected as the focus of this study due to its high prevalence as a leading cause of nephrotic syndrome in adults, its chronic nature with frequent relapses, and the widespread use of immunosuppressive therapy among patients. These factors render MN particularly vulnerable to the effects of COVID-19 infection.

This study aimed to evaluate the clinical features and risk factors associated with adverse outcomes in MN patients who were regularly followed up at our hospital during the COVID-19 pandemic from late 2022. These findings provide insights into the clinical management of MN in the context of COVID-19 and may help improve patient outcomes in similar scenarios in the future.

Methods

Participants

This study enrolled 656 consecutive patients with kidney biopsy-proven primary MN who had been treated and followed up for at least six months at Peking University First Hospital. Patients with known secondary MN, such as those due to hepatitis B/C virus infection, lupus, malignancy, rheumatoid arthritis, medication use, or heavy metal poisoning, were excluded. Clinical data were obtained from medical records at diagnosis and during follow-up.

The study was approved by the Ethics Committee of Peking University First Hospital and conducted in accordance with the principles of the Declaration of Helsinki. Written informed consent was obtained from all participants.

Patients or the public were not involved in the design, conduct, reporting, or dissemination of this research.

COVID-19 infections

From November 2022 to April 2023, participants were surveyed regarding COVID-19 infections either in person or by phone. Active surveillance included symptoms such as fever, chills, cough, shortness of breath, sore throat, diarrhea, muscle aches, and changes in smell or taste. COVID-19 diagnosis was based on the presence of symptoms and/or positive test results from RT-qPCR tests or rapid antigen tests using nasopharyngeal or throat swabs. The survey collected details on symptom onset, symptoms type, fever duration, days bedridden, medical care received, and symptom resolution.

Outcomes

Complete remission was defined as urinary protein < 0.3 g/24 h or protein creatinine ratio < 0.3 g/g [2]. Partial remission was defined as urinary protein reduction > 50% from baseline and < 3.5 g/24 h or 3.5 g/g, with stable eGFR. Patients who did not reach remission were considered as no-remission. Relapse was defined as recurrence of proteinuria > 3.5 g/24 h or 3.5 g/g after a period of remission. Aggravation was defined as urinary protein increase > 50% from baseline. Immune relapse was defined as reappearance of anti-PLA2R antibodies after a period of clearance. Immune aggravation was defined as increased anti-PLA2R antibody levels. Primary endpoint was ESKD defined as eGFR [19] < 15 ml/min/1.73m2 or the need for dialysis. Secondary endpoint was eGFR reduction > 30% from baseline.

Statistical analysis

Statistical analysis was performed using SPSS 26.0 (IBM, New York, NY, USA). Categorical variables were presented as frequencies (n, %) and analyzed using the chi-squared test or Fisher’s exact test. Continuous variables were described as median (interquartile range, IQR) for non-normally distributed data and mean ± standard deviation (SD) for normally distributed data. Comparisons were conducted using Student’s t test or one-way ANOVA for normally distributed variables and the Kruskal-Wallis test or Mann-Whitney U test for non-normally distributed variables. Univariate logistic regression was used to identify potential risk factors associated with MN progression following COVID-19 infection. Variables with P < 0.05 in the univariate analysis were included in the multivariate logistic regression models. Odds ratios (OR) and 95% confidence intervals (CIs) were reported for covariates. Statistical significance was defined as P < 0.05 (two-tailed tests).

Results

COVID-19 infection

Of the 656 consecutive biopsy-proven primary MN patients treated and followed up for more than six months, 555 (84.6%) contracted COVID-19 between November 11, 2022, and February 22, 2023, while 101 (15.4%) remained uninfected (Fig. 1A). The cohort characteristics are summarized in Table 1.

Table 1 Characters of patients with primary MN
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Fig. 1
figure 1

Composition and Clinical Outcomes of Primary Membranous Nephropathy Patients with and without COVID-19 Infection. (A) Among the 656 patients, 555 (84.6%) were infected with COVID-19, while 101 (15.4%) remained uninfected. (B) Of the 555 infected patients, 419 (75.5%) exhibited stable MN, 132 (23.8%) experienced disease progression, and 4 (0.7%) died from pneumonia. (C) Within the 132 patients with disease progression, 112 (20.2%) had proteinuria aggravation (> 50% increase from baseline), including 30 (5.4%) with proteinuria relapse. Additionally, 16 (2.9%) exhibited immune aggravation, 5 (0.9%) experienced immune relapse, and 10 (1.8%) developed kidney dysfunction, with 2 (0.4%) progressing to ESKD. (D) Among the 551 surviving patients, 132 (24.0%) experienced disease progression, a rate significantly higher than the 8.9% in the 101 uninfected patients (P < 0.001). *P < 0.05, **P < 0.01, ***P < 0.001

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The median age of the infected group was 54.9 ± 14.7 years, consisting of 340 males and 215 females. The median date of infection onset was December 13, 2022. Symptoms persisted for 1–4 weeks, with most patients (508/555, 91.5%) experiencing mild symptoms such as fever, cough, sore throat, and malaise. Severe pneumonia occurred in 7.7%, and 0.7% developed critical illness, leading to death from respiratory failure. Fever was reported in 78.4% of patients, lasting 1–10 days, with a median duration of 2 days (IQR 1–3) and a maximum temperature of 38.5 °C (range: 38–39 °C).

Among the infected patients, 45.0% (250/555) took NSAIDs, 0.9% (5/555) received antiviral agents, and 6.5% (36/555) were treated with antibiotics for secondary bacterial pneumonia. Additionally, 42.5% (236/555) used traditional Chinese medicine.

Outcomes of MN after COVID-19 infection

Of the 555 infected MN patients, 112 (20.2%) experienced proteinuria aggravation (increase > 50% from baseline), including 30 (5.4%) who had proteinuria relapse. Immune aggravation, defined by increased anti-PLA2R levels, occurred in 16 patients (2.9%), including 6 with proteinuria aggravation and 5 experienced relapses. Immune relapse, marked by the recurrence of anti-PLA2R antibodies, was observed in 5 patients (0.9%), 2 of whom had proteinuria aggravation and 1 with relapse. Kidney dysfunction, defined as an eGFR reduction > 30% from baseline, occurred in 10 patients (1.8%), including 2 to ESKD. Four patients (0.7%) died due to respiratory failure from pneumonia.

Among the 551 surviving patients, 132 (24.0%) experienced disease progression, including proteinuria aggravation, immune aggravation or relapse, and kidney dysfunction or ESKD (Fig. 1B and C). The progression rate was significantly higher in the COVID-19 infected group than in the uninfected group (24.0% vs. 8.9%, P < 0.001) (Fig. 1D).

Comparisons between MN progression and stable patients

The 551 infected patients were divided into two groups: a stable group (n = 419, 76.0%) and a progressive group (n = 132, 24.0%). Baseline characteristics were similar between the two groups (P > 0.05). The progression group had a significantly longer median fever duration [2 (1–4) vs. 2 (1–3) days, P = 0.001]. More patients in the progression group discontinued immunosuppressants and/or steroids during infection (15.9 vs. 6.2%, P = 0.001), and the median duration of treatment withdrawal was significantly longer [10 (7–23) vs. 3 (2–7) days, P < 0.001] (Table 2).

Table 2 Comparisons between MN patients with disease progression and those with stable condition after COVID-19 infections
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Risk factors for MN progression

We performed logistic regression analysis to explore the risk factors for disease progression after COVID-19 infection (Table 3).

Table 3 Risk factors of MN progression following COVID-19 infections
Full size table

Fever duration and disease progression

Univariate logistic regression analysis showed that a longer fever duration was associated with MN disease progression. Multivariate logistic regression further confirmed fever duration as an independent risk factor (OR 1.181, 95% CI 1.029–1.356; P = 0.018), indicating an 18% increased risk of MN progression for each additional day of fever.

Using the maximum selection test, the fever duration threshold for predicting MN progression was determined to be 3.5 days. Among patients with fever > 3 days, 71% experienced disease progression, compared to 19% of those with fever ≤ 3 days (P < 0.001) (Fig. 2A). Patients with fever lasting > 3 days had a significantly higher risk of MN progression (OR 10.367, 95% CI 4.925–21.823; P < 0.001).

Withdrawal of immunosuppressive therapy and MN progression

The withdrawal of immunosuppressants and/or steroids was another significant risk factor for MN progression after COVID-19 (OR 1.107, 95% CI 1.009–1.214; P = 0.032). Disease progression occurred in 45% of patients who discontinued immunosuppressive treatment, compared to 22% of those who continued treatment (P < 0.001) (Fig. 2B). Multivariate logistic regression identified treatment withdrawal as an independent risk factor (OR 2.571, 95% CI 1.377–4.799; P = 0.003).

Duration of treatment cessation and MN progression

A longer duration of treatment cessation was associated with a higher risk of MN progression (OR 1.113, 95% CI 1.045–1.186; P = 0.001). The maximum selection test identified 6.5 days as the threshold for increased risk. Among patients who discontinued immunosuppressants and/or steroids for ≥ 7 days, 68% experienced disease progression, compared to only 18% of those who stopped treatment for < 7 days (P < 0.001) (Fig. 2C). Patients who ceased treatment for ≥ 7 days had a significantly higher risk of MN progression (OR 9.562, 95% CI 2.427–37.673; P = 0.001).

Fig. 2
figure 2

Risk factors for MN disease progression after COVID-19 Infections. (A) Disease progression stratified by fever duration, showing a significantly higher progression rate in patients with fever lasting > 3 days. (B) Disease progression based on the withdrawal of immunosuppressants and/or corticosteroids, with a significantly increased progression rate in patients who discontinued treatment. (C) Disease progression stratified by the duration of immunosuppressant and/or corticosteroid withdrawal, showing a markedly higher progression rate in patients whose withdrawal lasted ≥ 7 days. * P < 0.05, ** P < 0.01, *** P < 0.001

Full size image

Risk factors for proteinuria, anti-PLA2R antibodies, and kidney dysfunction

Further analyses explored risk factors for specific outcomes, including proteinuria aggravation, anti-PLA2R antibody levels, and kidney dysfunction (Supplementary Tables 1–6). Rituximab treatment was associated with a reduced risk of proteinuria aggravation. Immunosuppressant withdrawal and prolonged cessation durations were linked to increased risks. Longer fever duration was independently associated with proteinuria relapse, immune aggravation, and immune relapse. Higher fever temperatures were associated with kidney dysfunction.

COVID-19 vaccination

Among the cohort, 340 patients (51.8%) had received a COVID-19 vaccine prior to infection, including 26 (4.0%) who received a single dose, 95 (14.5%) who received two doses, and 219 (33.4%) received three doses. Comparisons between vaccinated and unvaccinated patients revealed no significant difference in infection rates or overall disease progression rates (P > 0.05). However, unvaccinated patients exhibited a higher frequency of eGFR reduction > 30% (2.8% vs. 0.3%, P = 0.019). Notably, all four recorded deaths occurred in unvaccinated patients (Supplementary Table 7).

Discussion

This study evaluated the impact of COVID-19 infection on a cohort of 656 patients with biopsy-proven MN. The findings demonstrated that disease progression was more common in infected patients, with proteinuria aggravation being the primary manifestation. Severe complications such as ESKD and immune relapse were rare. Three independent risk factors for MN progression post-COVID-19 infection were identified: longer duration of fever, withdrawal of immunosuppressive treatments, and extended cessation of MN therapy. To our knowledge, this is the first study to systematically examine risk factors for MN relapse or exacerbation after COVID-19 infection, providing crucial insights for the management of MN patients during viral infections.

The high prevalence of COVID-19 in our cohort (84.6%) is likely attributable to the increased susceptibility of MN patients to infections, a result of immunosuppressive conditions and impaired responses to vaccine due to immunosuppressive treatments. This vulnerability was particularly relevant during the late 2022 Omicron variant wave, characterized by higher transmissibility but reduced severity compared to the Delta variant [20,21,22,23,24]. Despite the high infection rate, 91.5% of our patients experienced mild symptoms, and the mortality rate (0.7%) was significantly lower than those reported in ESKD patients (18.1%) and the global average (5.0%) [25]. This suggests that MN patients predominantly experienced mild disease courses of COVID-19 infections, likely due to Omicron’s reduced virulence and a lower baseline case fatality rate.

Disease progression occurred in 24.0% of our MN patients following COVID-19 infection, which was significantly higher than in those without infection (8.9%). Notably, disease progression was not associated with the severity of COVID-19 but was independently linked to a longer duration of fever, particularly when fever lasted for more than 3 days. Pathological analyses [26, 27] have provided evidence against direct viral infection within the kidneys. Instead, they suggest that cytokine-mediated effects and heightened adaptive immune responses contribute to MN progression. This highlights the potential benefits of early intervention to shorten the infection course in these patients.

During COVID-19 infection, some patients discontinued their immunosuppressants and/or steroids due to concerns about immunosuppression. Our study identified treatment withdrawal as an independent risk factor for MN progression, with a significantly higher risk observed when treatment cessation exceeded 7 days. Prior to COVID-19 infection, 59.1% of our patients were receiving immunosuppressive therapy, with calcineurin inhibitors (CNIs), either alone or in combination with corticosteroids, being the most common regimen (77.1%). Both cyclosporine and tacrolimus have been shown to reduce proteinuria in 70–80% of MN patients [28]. However, high relapse rates have been reported following CNI discontinuation, ranging from 43 to 80% after cyclosporine withdrawal [29,30,31] and approximately 50% after tacrolimus cessation [32]. This may explain the elevated risk of disease progression in our patients following the discontinuation of immunosuppressants, as well as the positive correlation between longer treatment cessation and increased risk of MN progression. Notably, subgroup analysis of proteinuria aggravation outcomes identified rituximab use as an independent protective factor. This aligns with previous evidence indicating that remissions achieved with rituximab are more sustained compared to CNIs [2].

Our findings revealed no significant differences in infection rates or disease progression between vaccinated and unvaccinated MN patients. However, vaccinated patients exhibited lower rates of eGFR reduction and mortality, consistent with previous studies [33]. This could be attributed to the large-scale infection environment during the Omicron wave, potentially diminishing vaccine efficacy. Additionally, the influence of immunosuppressive therapy and the timing of vaccination may have impacted the protective effects of the vaccine.

Several limitations should be acknowledged. First, the reliance on self-reported data for COVID-19 symptoms introduces potential recall bias and inaccuracies. Future studies should incorporate objective measures, such as medical records or diagnostic testing, to enhance data reliability. Moreover, this study did not investigate the biological mechanisms underlying MN progression post-COVID-19 infection. Both conditions involve immune dysregulation and inflammatory cytokines, which may exacerbate MN. Another limitation is the relatively short follow-up period. Longer-term studies are needed to evaluate whether disease progression stabilizes, improves, or worsens over time, providing a more comprehensive understanding of the sustained effects of COVID-19 on MN.

Our findings highlight critical risk factors for MN progression during COVID-19 infection, emphasizing the need for careful management of immunosuppressive therapy. Continuation of treatment during mild infections or limiting suspension to less than seven days could mitigate disease progression. Timely antiviral therapy and adjunctive use of NSAIDs may further support favorable outcomes. These insights are particularly relevant for formulating clinical management strategies and public health policies, such as optimizing vaccination protocols for immunosuppressed populations.

Conclusions

This study underscores the relatively mild severity but high prevalence of COVID-19 in MN patients. The identification of modifiable risk factors for MN progression offers actionable guidance for clinicians and policymakers, aiming to improve outcomes in this vulnerable population.

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Abbreviations

MN:

Membranous Nephropathy

COVID-19:

Coronavirus Disease 2019

eGFR:

Estimated Glomerular Filtration Rate

ESKD:

End-Stage Kidney Disease

OR:

Odds Ratio

CI:

Confidence Interval

NSAIDs:

Nonsteroidal Anti-Inflammatory Drugs

RT-qPCR:

Reverse Transcription Quantitative Polymerase Chain Reaction

PLA2R:

Phospholipase A2 Receptor

CNI:

Calcineurin Inhibitors

SD:

Standard Deviation

IQR:

Interquartile Range

ANOVA:

Analysis of Variance

SPSS:

Statistical Package for the Social Sciences

IBM:

International Business Machines

SARS-CoV-2:

Severe Acute Respiratory Syndrome Coronavirus 2

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Acknowledgements

The technical support by Yao Yao was greatly appreciated.

Funding

This work was supported by the National High Level Hospital Clinical Research Funding (High Quality Clinical Research Project of Peking University First Hospital, 2023HQ07), the National Natural Science Foundation of China (82090021), and the Peking University First Hospital Cross-Research Project (2023IR19).

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Author notes

  1. Yue Shu Jing Huang contributed equally to this work.

Authors and Affiliations

  1. Renal Division, Institute of Nephrology, Key Laboratory of Renal Disease, Key Laboratory of CKD Prevention and Treatment, Peking University First Hospital, Peking University, Ministry of Health of China, Ministry of Education of China, Beijing, China

    Yue Shu, Jing Huang, Yi-miao Zhang, Fang Wang, Xin Wang, Li-qiang Meng, Xu-yang Cheng, Gang Liu, Ming-hui Zhao & Zhao Cui

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  1. Yue Shu
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Contributions

All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Yue Shu. The first draft of the manuscript was written by Yue Shu and Zhao Cui commented on previous versions of the manuscript. All authors read and approved the final manuscript.

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Correspondence to Zhao Cui.

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The study was approved by the Ethics Committee of Peking University First Hospital and followed the purpose of the Declaration of Helsinki.

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Shu, Y., Huang, J., Zhang, Ym. et al. Risk factors for relapse and aggravation in membranous nephropathy after COVID-19 infection. BMC Nephrol 26, 71 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12882-025-04000-x

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  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12882-025-04000-x

Keywords

BMC Nephrology

ISSN: 1471-2369

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