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World J Nephrol. Jun 25, 2026; 15(2): 118214
Published online Jun 25, 2026. doi: 10.5527/wjn.v15.i2.118214
Post vaccination acute kidney injury and other renal complications after COVID-19 and influenza vaccination
Yunn Honey Aye Kyaw, Pierre Yip, Yong Loo Lin School of Medicine, National University of Singapore, 117597, Singapore
Kay Choong See, Division of Respiratory and Critical Care Medicine, Department of Medicine, National University Hospital, 119228, Singapore
ORCID number: Yunn Honey Aye Kyaw (0009-0005-5970-6985); Pierre Yip (0009-0005-2067-8841); Kay Choong See (0000-0003-2528-7282).
Co-first authors: Yunn Honey Aye Kyaw and Pierre Yip.
Author contributions: Aye Kyaw YH, Yip P and See KC designed the research study; Aye Kyaw YH and Yip P, performed the research; Aye Kyaw YH and Yip P curated the data and performed the investigation; See KC provided supervision; Aye Kyaw YH and Yip P prepared the figures and visualizations; Aye Kyaw YH and Yip P wrote the original draft; Aye Kyaw YH, Yip P and See KC reviewed and edited the manuscript; Aye Kyaw YH and Yip P contributed equally to this manuscript and are co-first authors. All authors have read and agreed to the published version of the manuscript.
Conflict-of-interest statement: See KC declares receipt of personal fees for lectures and advisory board participation from Bavarian Nordic, GlaxoSmithKline, Moderna, and Pfizer, outside the submitted work. The other authors declare no conflict of interest with the submitted work.
PRISMA 2009 Checklist statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Checklist.
Corresponding author: Yunn Honey Aye Kyaw, Yong Loo Lin School of Medicine, National University of Singapore, 10 Medical Dr, 117597, Singapore. e0974487@u.nus.edu
Received: December 28, 2025
Revised: January 14, 2026
Accepted: March 3, 2026
Published online: June 25, 2026
Processing time: 170 Days and 18.2 Hours

Abstract
BACKGROUND

Vaccination remains a cornerstone of public health, yet concerns regarding serious adverse events continue to contribute to vaccine hesitancy. While systemic and local vaccine reactions are well described, renal complications such as acute kidney injury (AKI) and immune-mediated glomerular disease are less well characterised. With widespread and sustained use of coronavirus disease 2019 (COVID-19) and influenza vaccines, a comprehensive synthesis of reported renal adverse outcomes is needed.

AIM

To synthesise and critically evaluate the existing evidence on AKI and other renal manifestations reported following influenza and COVID-19 vaccination. Specifically, it aims to characterise the spectrum of reported renal presentations, summarise clinical features and timelines described in case reports and case series, and contextualise these findings using population-level observational and pharmacovigilance data to assess the overall renal safety profile of these vaccines.

METHODS

We conducted a systematic review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines. PubMed and EMBASE were searched from inception to 6 December 2025 for studies reporting renal outcomes following COVID-19 or influenza vaccination. Eligible studies included observational studies, pharmacovigilance analyses, case reports, and case series. Data on incidence, clinical presentation, timing of onset, management, and outcomes were extracted and synthesised narratively due to heterogeneity. Risk of bias in observational studies was assessed using the Risk Of Bias In Non-randomised Studies - of Interventions (ROBINS-I) tool.

RESULTS

A total of 255 COVID-19 vaccine-related studies and 73 influenza vaccine-related studies met the inclusion criteria, supplemented by additional studies identified through reference screening. Population-level observational studies consistently demonstrated a low absolute risk of renal adverse outcomes following vaccination, with several studies reporting reduced AKI-related risk among vaccinated individuals. In contrast, pharmacovigilance analyses and case reports described serious instances of de novo or relapsing renal disease, including minimal change disease, immunoglobulin A nephropathy, membranous nephropathy, pauci-immune glomerulonephritis, and systemic inflammatory syndromes with secondary renal involvement. Symptom onset typically occurred within days to weeks of vaccination. Most cases responded favourably to supportive or disease-specific therapy, with recovery observed over weeks to months; irreversible renal outcomes were uncommon.

CONCLUSION

Current evidence indicates that both COVID-19 and influenza vaccines are associated with a low population-level risk of adverse renal outcomes. Serious immune-mediated renal events have been reported in temporal association with vaccination, likely reflecting idiosyncratic immune responses or unmasking of pre-existing disease rather than a widespread nephrotoxic effect. The overall benefits of vaccination substantially outweigh potential renal risks. Ongoing surveillance and well-designed population-based studies remain essential to refine risk estimates and identify susceptible subgroups.

Key Words: COVID-19 vaccination; Influenza vaccination; Adverse renal effects; Acute kidney injury; Glomerulonephritis; Immune-mediated renal disease; Vaccine safety

Core Tip: Renal adverse events following coronavirus disease 2019 and influenza vaccination are rare at the population level. While case reports describe immune-mediated kidney diseases occurring in temporal association with vaccination, large observational studies consistently demonstrate a low absolute risk of acute kidney injury and other renal outcomes. Clinicians should remain vigilant for unusual renal presentations after vaccination, particularly in high-risk individuals, while continuing to advocate vaccination given its substantial overall benefits.



INTRODUCTION

Vaccines have been commonly heralded as a key cornerstone of global public health. Between 2021 and 2030, an estimated 51.0 million [95% confidence interval (CI): 48.5-53.7] deaths are expected to be averted due to vaccinations - a staggering testament to the potential of immunisation in positively impacting our global health landscape[1]. Notable achievements include the eradication of smallpox and rinderpest, near-eradication of poliomyelitis, and major declines in measles, neonatal tetanus, and other childhood infections following the global expansion of vaccination programmes[2]. With growing evidence supporting vaccine efficacy, vaccination has become an indispensable tool utilised by healthcare systems and institutions worldwide to improve public health. This is reflected in the World Health Organisation’s Immunisation Agenda 2030, which advocates for the benefits of vaccines and strives to achieve equal access to vaccines across nations[3]. The crucial role of vaccines was further highlighted during the recent coronavirus disease 2019 (COVID-19) pandemic, whereby vaccines were found to greatly decrease the risk of mortality from severe COVID-19 infection[4]. This has thus reinforced emphasis on COVID-19 vaccination distribution, with the most recent data finding that 70.7% of the world's population has received at least one dose of the COVID-19 vaccine[5].

However, with the increased prevalence of vaccines in this post-pandemic era, vaccines targeting respiratory viruses, particularly COVID-19 and influenza, have come under increased public and clinical scrutiny[6,7]. While COVID-19 vaccinations are relatively new, influenza vaccines have long been administered on a population-wide scale - together representing some of the most frequently delivered vaccines targeting respiratory diseases worldwide[8,9]. Among the side effects of these vaccines that have been explored, adverse renal complications, including acute kidney injury (AKI) and glomerulopathies, have received comparatively limited attention in recent literature. This review thus aims to collate the newest studies on renal effects, providing an up-to-date review of the current literature and summarising the signs, symptoms, and timelines reported in past case reports, to guide clinicians in the management of vaccine-associated renal injury.

MATERIALS AND METHODS
Methods

This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines.

Search strategy

We conducted a comprehensive search of PubMed and EMBASE from inception to 6 December 2025. Searches were performed separately for COVID-19 and influenza vaccines. For COVID-19, the search terms used for PubMed were [“COVID-19 Vaccines” (MeSH) OR “COVID-19 vaccine” OR “SARS-CoV-2 vaccine” OR “RNA-1273” R “NT162b2” OR “Pfizer-BioNTech” OR “Moderna” OR “ChAdOx1 nCoV-19” OR “AZD1222” OR “AstraZeneca” OR “Johnson & Johnson” OR “inactivated vaccine” OR “Sinovac” OR “CoronaVac” OR “Sinopharm”] AND [“Kidney Diseases” (MeSH) OR “acute kidney injury” OR AKI OR “glomerulonephritis” OR “nephrotic syndrome” OR “renal impairment” OR “renal dysfunction” OR “proteinuria” OR “hematuria” OR “tubulointerstitial nephritis” OR “renal vasculitis” OR “minimal change disease” OR “rhabdomyolysis” OR “atypical hemolytic uremic syndrome”] AND [“adverse effects” (Subheading) OR “vaccine-related adverse events” OR “autoimmune response” OR “immune-mediated kidney injury” OR “drug-induced kidney injury” OR “immune complex deposition” OR “molecular mimicry” OR “vaccine reaction”]. The search terms used for EMBASE were (“covid-19 vaccine”/exp OR “covid-19 vaccine” OR “sars-cov-2 vaccine” OR “mrna-1273” OR “bnt162b2” OR “pfizer-biontech” OR “moderna” OR “chadox1 ncov-19” OR “azd1222” OR “astrazeneca” OR “johnson & johnson” OR “inactivated vaccine” OR “Sinovac” OR “coronavac” OR “Sinopharm”) AND (“kidney disease”/exp OR “acute kidney injury” OR “aki” OR “glomerulonephritis” OR “nephrotic syndrome” OR “renal impairment” OR “renal dysfunction” OR “proteinuria” OR “hematuria” OR “tubulointerstitial nephritis” OR “renal vasculitis” OR “minimal change disease” OR “rhabdomyolysis” OR “atypical hemolytic uremic syndrome” OR “hemolytic uremic syndrome”) AND (“adverse drug reaction”/exp OR “vaccine-related adverse events” OR “autoimmune response” OR “immune-mediated kidney injury” OR “drug-induced kidney injury” OR “immune complex deposition” OR “molecular mimicry” OR “vaccine reaction”).

For influenza, the search terms used for PubMed were [“influenza vaccines” (MeSH Terms) OR “influenza vaccine” OR “flu vaccine” OR “flu immunization” OR “inactivated influenza” OR “live attenuated influenza” OR “recombinant influenza”] AND [“acute kidney injury” (MeSH Terms) OR “kidney diseases” OR “acute kidney injury” OR “AKI” OR “acute renal failure” OR “renal injury” OR “nephritis” OR “glomerulonephritis” OR “nephrotic syndrome” OR “renal impairment” OR “renal dysfunction” OR “proteinuria” OR “hematuria” OR “renal vasculitis” OR “interstitial nephritis” OR “minimal change disease” OR “rhabdomyolysis” OR “vaccine-related adverse events” OR “immune-mediated kidney injury” OR “drug-induced kidney injury” OR “immune complex deposition”]. The search terms used for Embase were (“influenza vaccine”/exp OR “influenza vaccine”: Ti,ab OR “flu vaccine”: Ti,ab OR “flu immunization”: Ti,ab OR “flu immunization”: Ti,ab OR “inactivated influenza”: Ti,ab OR “live attenuated influenza”: Ti,ab OR “recombinant influenza”: Ti,ab) AND (“acute kidney injury”/exp OR “acute kidney injury”: Ti,ab OR AKI: Ti,ab OR “kidney disease”/exp OR “kidney diseases”: Ti,ab OR “acute renal failure”: Ti,ab OR “renal injury”: Ti,ab OR nephritis: Ti,ab OR “glomerulonephritis”/exp OR glomerulonephritis: Ti,ab OR “nephrotic syndrome”/exp OR “nephrotic syndrome”: Ti,ab OR “renal impairment”: Ti,ab OR “renal dysfunction”: Ti,ab OR proteinuria: Ti,ab OR hematuria: Ti,ab OR “renal vasculitis”: Ti,ab OR “interstitial nephritis”: Ti,ab OR “minimal change disease”: Ti,ab OR rhabdomyolysis: Ti,ab OR “vaccine-related adverse events”: Ti,ab OR “immune-mediated kidney injury”: Ti,ab OR “drug-induced kidney injury”: Ti,ab OR “immune complex deposition”: Ti,ab).

Study selection

Title and abstract screening were conducted independently using Rayyan reference management software by Aye Kyaw YH and Yip P. English-language case reports, case series, pharmacovigilance studies, and observational studies involving individuals who had received either a COVID-19 or influenza vaccine and reported AKI were included. Systematic reviews, literature reviews, narrative reviews, and commentaries were excluded. Full-text articles were subsequently assessed for eligibility. Discrepancies were resolved through discussion and consensus.

Data extraction and synthesis

Data extraction was performed independently by 2 reviewers using a standardized data extraction form. Data on incidence and effect estimates, including hazard ratios and risk ratios, were extracted from observational studies where reported by Aye Kyaw YH and Yip P. For case reports and case series, clinical presentation, signs and symptoms, and time interval between vaccination and onset of kidney injury were extracted by Aye Kyaw YH and Yip P. Due to heterogeneity in study design and outcome definitions, findings were synthesised narratively. Risk of bias for observational studies was assessed using the ROBINS-I framework by Aye Kyaw YH and Yip P. Discrepancies were resolved through discussion with the senior author, See KC.

RESULTS
Results - study selection

After removal of duplicates, 812 unique records related to COVID-19 vaccination and 1062 unique records related to influenza vaccination were identified (PRISMA flow diagram reported in Figure 1). Following title and abstract screening, 416 COVID-19 studies and 171 influenza studies were retrieved for full-text eligibility assessment. At the full-text stage, studies were excluded primarily due to the absence of renal adverse outcomes. Ultimately, 255 COVID-19 studies and 74 influenza studies met the inclusion criteria and were included in the analysis. In addition, 6 COVID-19 studies and four influenza studies were identified through reference list screening of included articles and were incorporated into the final analysis. The number of cases reported, clinical signs, symptoms, and timelines reported in case reports and case series are summarised in the Supplementary material.

Figure 1
Figure 1 Preferred Reporting Items for Systematic Reviews and Meta-Analyses flow diagram. COVID-19: Coronavirus disease 2019.

Risk of bias assessment: The risk of bias of included studies was assessed using the ROBINS-I framework, which evaluates bias across seven domains. The full assessment is summarized in Table 1[10-55]. Risk of bias in observational studies was assessed using the ROBINS-I tool. 26 studies were judged to have a moderate risk of bias, 8 studies a low risk of bias, and 13 studies a serious risk of bias. No studies were assessed as having a critical risk of bias. The most common sources contributing to serious risk judgements were residual confounding and selection of participants, particularly in studies lacking a control or comparator group, while the remaining ROBINS-I domains were predominantly rated as low risk.

Table 1 Risk of bias assessment of included studies using the risk of bias in non-randomised studies - of interventions tool.
Ref.
Vaccine
Confounding
Selection of participants
Exposure classification
Deviations from intended interventions
Missing data
Outcome measurement
Selection of reported results
Overall risk of bias
Kamei et al[10], 2023COVID-19SeriousModerateLowModerateLowLowModerateSerious
Waldman et al[11], 2023COVID-19SeriousSeriousLowLowModerateLowModerateSerious
Sanders et al[12], 2022COVID-19SeriousModerateLowLowModerateLowModerateSerious
Wan et al[13], 2022, COVID-19LowModerateLowLowModerateModerateLowModerate
Yechezkel et al[14], 2023COVID-19ModerateModerateLowLowModerateModerateLowModerate
Choi et al[15], 2024COVID-19ModerateLow LowLowLowSeriousModerateModerate
Lionaki et al[16], 2024COVID-19ModerateModerateLowLowLowModerateLowModerate
Poster Abstracts[17], 2022 COVID-19SeriousModerateLowLowModerateLowModerateSerious
Carrillo et al[18], 2023COVID-19ModerateModerateLowLowModerateLowModerateModerate
Chen et al[19], 2023COVID-19ModerateModerateLowLowModerateLowModerateModerate
Diebold et al[20], 2022COVID-19LowLowLowLowLowLowLowLow
Canney et al[21], 2022COVID-19LowLowLowLowLowLowLowLow
Ota et al[22], 2023COVID-19ModerateModerateLowLowModerateLowModerateModerate
Wang et al[23], 2024COVID-19LowLowLowLowLowLowLowLow
Sun et al[24], 2024COVID-19ModerateModerateLowLowModerateLowModerateModerate
Nagatsuji et al[25], 2024COVID-19ModerateModerateLowLowModerateLowModerateModerate
Aoki et al[26], 2024COVID-19SeriousSeriousLowLowModerateLowModerateSerious
Zhang et al[27], 2024COVID-19ModerateModerateLowLowModerateLowLowModerate
Mazza et al[28], 2025COVID-19ModerateModerateLowLowLowLowLowModerate
Thepveera et al[29], 2025COVID-19ModerateModerateLowLowModerateLowModerateModerate
Tsai et al[30], 2025COVID-19ModerateLowLowLowLowModerateLowModerate
Huang et al[31], 2025COVID-19ModerateLowLowLowLowModerateLowModerate
Ishimori et al[32], 2023InfluenzaModerateModerateLowLowLowLowLowModerate
Hao et al[33], 2023InfluenzaModerateLowLowLowModerateModerateModerateModerate
Moghaddasi et al[34], 2013InfluenzaSeriousSeriousLowLowModerateLowModerateSerious
Fernández-Ruiz et al[35], 2015InfluenzaSeriousModerateLowLowModerateLowModerateSerious
Cohet et al[36], 2016InfluenzaLowLowLowLowLowModerateLowLow
Dos Santos et al[37], 2016InfluenzaLowLowLowLowModerateLowLowLow
Miskulin et al[38], 2018InfluenzaModerateLowLowLowModerateLowModerateModerate
Klifa et al[39], 2019InfluenzaSeriousSeriousModerateLowModerateModerateModerateSerious
Ishimori et al[40], 2021InfluenzaModerateModerateLowLowModerateModerateLowModerate
Kumar et al[41], 2023InfluenzaModerateModerateLowLowModerateLowLowModerate
Levison et al[42], 2022InfluenzaLowLowLowLowLowLowLowLow
Shih et al[43], 2018InfluenzaModerateLowLowLowLowLowLowModerate
Cho et al[44], 2024InfluenzaLowLowLowLowLowLowLowLow
Zhuo et al[45], 2026InfluenzaModerateLowLowLowLowModerateLowModerate
Chen et al[46], 2025InfluenzaModerateLowLowLow Low ModerateLowModerate
Liao et al[47], 2022InfluenzaModerateLowLowLowLowLowLowModerate
Sheth et al[48], 1979InfluenzaSeriousSeriousLowModerateModerateModerateModerateSerious
Jeffs et al[49], 2015InfluenzaLowLowLowModerateLowLowLowLow
Chen et al[50], 2022InfluenzaModerateLowLowLowLowModerateLowModerate
Pabico et al[51], 1974InfluenzaSeriousModerateLowModerateLowLowModerateSerious
Reynales et al[52], 2012InfluenzaSeriousModerateLowLowLowModerateLowSerious
Gwynn et al[53], 2020InfluenzaSeriousModerateLowModerateLowModerateModerateSerious
Ishimori et al[54], 2020InfluenzaModerateModerateLowModerateLowLowLowModerate
Zawiasa-Bryszewska et al[55], 2025InfluenzaModerateModerateLowModerateModerateModerateLowModerate
COVID-19 vaccine results

The included studies assessed different types of COVID-19 vaccines, including mRNA (e.g. BNT162b2, mRNA-1273), viral vector-based (e.g. ChAdOx1 nCoV-19, Ad26.COV2.S), inactivated vaccine (e.g. CoronaVac, Covaxin) and Recombinant Protein Nanoparticle Vaccine (e.g. GBP510) types. In total, 23 observational studies and 27 pharmacovigilance studies examined the association between COVID-19 vaccination and renal outcomes. In addition, 211 published case reports and case series described renal adverse events occurring after COVID-19 vaccination. A summary of the included studies is presented in Table 2[10-31,56-78].

Table 2 Population-level renal outcomes reported following coronavirus disease 2019 vaccination1.
Ref.
Type of vaccine
Associated kidney injury
Incidence
Wan et al[13], 2022; Yechezkel et al[14], 2023; Lee et al[56], 2022; Kim et al[57], 2022; Kim et al[58], 2022; Kim et al[59], 2023; Luo et al[60], 2022; Hwang et al[61], 2025; Yan et al[62], 2022; Yoon et al[63], 2023mRNA vaccineUnspecified acute kidney injury (AKI)1.17/100000 doses (0.21, 3.41), 2.21/100000 persons (0.46, 6.46), and the incidence rate was 20.94/100000 person-years (6.75, 64.92); The risk difference reported after the second booster is 1.68/100000 people (-3.37 to 6.74), and risk difference of second boosters vs first boosters is 3.93/100000 (-0.56 to 8.42) although both results were found to be not statistically significant; 17 cases of AKI out of 153183 adverse events; 4 cases/100000 people for 12-17 years old, 4 cases/100000 for 5-17 years old; 0.1/100000 persons incidence of AKI for 18 years old and above; Pfizer: AKI reporting odds ratio (ROR) of 2.15 (1.97, 2.36), proportional reporting ratio (PRR) of 2.15 (χ2 = 290.75), and an Information component (IC) of 0.9 (IC025 = 0.82), Empirical Bayes Geometric Mean (EBGM) of 1.87 (EBGM05 = 1.73); Moderna: AKI ROR of 1.25 (1.13-1.39), PRR of 1.25 (χ2 =17.97) and IC of 0.27 (IC025 = 0.24) and a EBGM of 1.21 (EBGM05 = 1.11); disproportionate signal of AKI with ROR of 2.38 (2.30-2.46) and IC of 1.14 (IC025 = 1.09); BNT162b2 mRNA: AKI ROR of 5.41 (4.54-6.43); mRNA-1273: AKI ROR of 2.48 (2.05, 3.00); In a Vigibase analysis of the WHO pharmacovigilance database, COVID-19 mRNA vaccines were solely associated with higher reporting of AKI (IC025 = 1.09) and tubular interstitial nephritis (TIN) (IC025 = 0.48) compared to other types of vaccines
Waldman et al[11], 2023; Diebold et al[20], 2022; Kronbichler et al[64], 2022Minimal change disease (MCD)In a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 28.6% (28/98) of patients presented with MCD, with 75% of MCD due to mRNA vaccines; risk ratio between MCD and COVID-19 vaccine is 1.72 (95%CI: 0.46-6.38); MCD after Pfizer/BioNTech mRNA vaccine: IC/IC025 of 0.88/0.37 with 36 cases out of 770304 individual case safety reports (ICSR) reported
Kamei et al[10], 2023; Mazza et al[28], 2023; Kronbichler et al[64], 2022Unspecified nephrotic syndrome In 40 patients with childhood-onset nephrotic syndrome using immunosuppressive agents, 3 (7.5%) patients suffered from a relapse of nephrotic syndrome (2 and 3 days after the first dose and 8 days after 2nd dose), and 2 patients suffered from transient proteinuria after COVID-19 vaccination; in 95 patients with relapsing nephrotic syndrome, 17 (18%) patients had ≥ 1 relapse post vaccination, with no significant difference in the risk of relapse after vs before vaccination (odds ratio = 0.43, P-value = 0.08), and no significant difference in relapse rates after vs before vaccination (mean difference 008 per 100 patient-days, P-value = 0.39); 5 patients had new onset nephrotic syndrome presenting within 60 days of taking the vaccine; nephrotic syndrome after Pfizer/BioNTech mRNA vaccine: IC/IC025 of 0.60/0.31 with 103 cases out of 770304 ICSRs
Waldman et al[11], 2023; Diebold et al[20], 2022; Ota et al[22], 2023; Kronbichler et al[64], 2022; Aoki et al[65], 2023; Poster Abstracts[66], 2022; Nakao et al[67], 2023IgA nephropathyIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID vaccine, 26.5% (26/98) of patients presented with IgA nephropathy, with 73.1% of IgA Nephropathy due to mRNA vaccines, with most patients (38.5%) presenting within 1-2 days after the vaccine; in a retrospective cohort study using a cohort representing the entire adult Swiss population, they found the risk ratio between IgA nephropathy to COVID-19 vaccine = 1.14 (95%CI: 0.67-1.97); in IgA nephropathy histopathology, acute lesions were found to be associated with renal events, and E lesions were associated with worsening haematuria; IgA nephropathy after moderna vaccine: IC/IC025 of 1.51/0.71 with 19 out of 286467 ICSRs; in 82 patients who presented with gross haematuria after COVID-19 vaccination, 42 patients have a new diagnosis of IgA nephropathy (n = 41); in an analysis of 20 cases of post-vaccine IgA nephropathy, the mean time to onset was 3.18 days (1-31 days), where 60% of the cases came from COMIRNATY vaccine, and 40% came from SPIKEVAX; additionally, the study found that macroscopic haematuria was the most revealing symptom, and 35% of patients in the study had AKI; ROR of IgA nephropathy to COVID-19 mRNA vaccines is 6.49, 95%CI: 4.38-9.61, IC of 2.27, 95%CI: 1.70-2.83), showing a significant increase in reported number from baseline after COVID-19 vaccine; time to onset of IgA nephropathy from vaccine is 2 patients on the same day, 5 patients 1 day later, 4 patients 2 days later, 3 patients 3-28 days later and 2 patients more than 28 days later
Aoki et al[65], 2023IgA nephropathy relapse 22 out of 82 patients who presented with gross haematuria after COVID-19 vaccination had a prior diagnosis of IgA nephropathy or IgA vasculitis
Aoki et al[65], 2023IgA vasculitis 42 out of 82 patients who presented with gross haematuria after COVID-19 vaccination have a new diagnosis of IgA vasculitis
Aoki et al[65], 2023IgA vasculitis relapse 22 out of 82 patients who presented with gross haematuria after COVID-19 vaccination had a prior diagnosis of IgA nephropathy or IgA vasculitis
Thepveera et al[29], 2025Lupus nephritis Out of 69 vaccinated adolescents with SLE; 24 (34.8%) experienced SLE flares; 14 (20.3%) out of the 69 patients experienced a new or worsened renal flare, including 13 (27.7%) of 47 patients who have had previous lupus nephritis; 5 (7.2%) renal flares occurred within the first month, 1 (1.4%), 4 (5.8%) and 4 (5.8%) patients at the 3-, 6- and 12-month follow-ups, respectively; 4 (8.7%) out of 46 of the patients had their renal flares occurred after they were administered the third vaccine dose; manifestations of renal flares include increased proteinuria (71.4%), abnormal urine sediment (42.9%) and decreased renal function (28.6%)
Waldman et al[11], 2023; Diebold et al[20], 2022Membranous nephropathyIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 10.2% (10/98) of patients presented with membranous nephropathy, with 80% of membranous nephropathy due to mRNA vaccines, with most patients (30%) presenting within 5-7 days after vaccine; risk ratio between membranous nephropathy to COVID-19 vaccine = 1.17 (95%CI: 0.43-3.23)
Waldman et al[11], 2023; Diebold et al[20], 2022Crescentic glomerulonephritis: Pauci-immuneIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 17.3% (17/98) of patients presented with pauci-immune crescentic glomerulonephritis, with 94.1% due to mRNA vaccines, with most patients (35.3%) presenting 2 weeks after the vaccine; risk ratio between pauci-immune necrotising glomerulonephritis and COVID-19 vaccine = 0.54 (95%CI: 0.26-1.15)
Waldman et al[11], 2023Crescentic glomerulonephritis: Anti-GBMIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 5.1% (5/98) of patients presented with anti-GBM, with 40% of MCD due to mRNA vaccines, with most patients (60%) presenting 2 weeks after vaccine
Ota et al[22], 2023; Hwang et al[61], 2025Unspecified glomerulonephritisOut of 111 adults with diagnosed glomerulonephritis, 22.5% developed a renal event (increased proteinuria, haematuria or 1.5x increase in serum creatinine) post 2 doses of COVID-19 vaccination, with only 0.9% requiring temporary haemodialysis and 1.8% requiring additional immunosuppressive treatment; ROR of 13.41 (12.62-14.26) and IC of 2.98 (IC025 = 2.90)
Hwang et al[61], 2025Acute tubulointerstitial nephritisROR of 2.43(2.11-2.81) and IC of 1.22 (IC025 = 0.99)
Lee et al[68], 2023Immune thrombotic thrombocytopenic purpura leading to AKI ROR of 0.81 (0.79-0.83) and IC: -0.28 (IC025: -0.31)
Wan et al[13], 2022Rhabdomyolysis leading to AKIIncidence of 0.75/100000 doses (0.09, 2.71); 1.42/100000 persons (0.17, 5.13), and the incidence rate was 13.48/100000 person-years (3.37, 53.88)
Sanders et al[12], 2022; HK et al[17], 2022Renal transplant rejection or pathological change1 out of 159 patients faced kidney transplant rejection; 40.1% of kidney transplant recipients showed a rise in creatinine, proteinuria, or new microscopic haematuria
Lee et al[56], 2022; Luo et al[60], 2022Vector vaccineUnspecified AKIOut of 153183 adverse events following COVID-19 vaccination, 62 cases of AKI were reported in patients who took AZD1222 vaccines and 6 cases in patients who took JNJ-78436735; ROR of AKI and Jannsen: ROR of 1.04 (0.84, 1.28), PRR of 1.04 (χ2 = 0.12), and an IC of 0.5 (IC025 = 0.04), EBGM of 1.04 (EBGM05 = 0.87)
Waldman et al[11], 2023MCDIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 28.6% (28/98) of patients presented with MCD, with 14.3% of MCD due to Vector vaccines, with most patients (35.7%) presenting within 5-7 days after the vaccine
Waldman et al[11], 2023Crescentic glomerulonephritis pauci-immuneIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 17.3% (17/98) of patients presented with pauci-immune crescentic glomerulonephritis, with 5.9% due to Vector vaccines, with most patients (35.3%) presenting 2 weeks after the vaccine
Waldman et al[11], 2023Collapsing glomerulopathy In a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 5.1% (5/98) of patients presented with collapsing glomerulonephritis, with 20% of collapsing glomerulonephritis due to Vector vaccines, with most patients (60%) presenting within 5-7 days after the vaccine
Hwang et al[61], 2025Unspecified glomerulonephritis Disproportionate signal with ROR of 3.12 (2.73-3.56) and IC of 1.58 (IC025 = 1.36)
Lee et al[68], 2024Thrombotic thrombocytopenia leading to AKI ROR of 1.64 (1.59-1.68) and IC: 0.69 (IC025: 0.64)
Wan et al[13], 2022Inactivated vaccine Unspecified AKIIncidence for AKI post CoronaVac inactivated vaccine was 1.41/100000 doses (0.46, 3.28), 2.51/100000 persons (0.81, 5.85), and the incidence rate was 25.42/100000 person-years (10.58, 61.08)
Zhang et al[27], 2024Membranous nephropathyNo difference in the rate of relapse or worsening between the two groups, with 10 (13%) in the vaccinated group and 11 (15%) in the unvaccinated group (hazard ratio = 0.98, 95%CI: 042-2.33)
Waldman et al[11], 2023 Anti-GBM diseaseIn a retrospective cohort study that included subjects with de novo glomerulonephritis presenting 3 months after the COVID-19 vaccine, 5.1% (5/98) of patients presented with anti-GBM, with 60% of MCD due to inactivated vaccines, with most patients (60%) presenting 2 weeks after the vaccine
Song et al[69], 2023 Recombinant protein nanoparticle vaccineAKI, rapidly proliferative glomerulonephritis, cutaneous vasculitis3 cases of systemic adverse events were reported in the GBP510 group, with the cases being AKI, rapidly progressive glomerulonephritis and cutaneous vasculitis
Choi et al[15], 2024; Lionaki et al[16], 2024; Chen et al[19], 2023; Aoki et al[26], 2024; Tsai et al[30], 2025; Abdel-Qader et al[70], 2022; Hu et al[71], 2024; Nurminen et al[72], 2025; Lichtbroun et al[73], 2024; Anastassopoulo et al[74], 2023; Cullen et al[75], 2023; Tavakoli et al[76], 2021Unspecified vaccineUnspecified AKIAbsolute risk difference for AKI per 100000 persons was reported as 0.06, with the incidence rate ratio reported as 0.67 (0.11-3.99), and hence it was not statistically significant; 23 out of 255 patients (9%) experienced a glomerular disease relapse after vaccination, with the average time to relapse from vaccination being 2.5 months; 27 cases out of 1897 COVID-vaccinated adults were found to develop COVID-19 vaccine related acute kidney disease; in a study of patients presenting with gross haematuria after the COVID-19 vaccine, none of the patients in the cohort developeda 15-fold increase in serum creatinine from baseline, proteinuria also only temporarily increased after the vaccinations; out of 127 patients who presented with gross haematuria, 37 patients had kidney biopsy done before where 35 patients were previously diagnosed with IgA nephropathy, 1 patient with IgA vasculitis and one patient with proliferative glomerulonephritis with monoclonal IgG deposits; out of the 90 patients who did not have prior kidney biopsy, 70 patients went for post-gross haematuria biopsy, with 67 of them being diagnosed with IgA nephropathy, 2 of them diagnosed with IgA vasculitis and 1 patient with non-IgA proliferative glomerulonephritis using the biopsy; 71% of these patients have had pre-vaccination abnormal urinary findings; COVID-19 is hypothesised to have manifested the subclinical IgA nephropathy; vaccinated individuals were found to have a higher incidence of AKI (HR = 1.20, 95%CI: 1.18-1.23) and dialysis initiation (HR = 1.84, 95%CI: 1.68-2.01) compared with unvaccinated individuals; at one year of follow-up, there were 7693 deaths in the vaccinated group and 7364 deaths in the unvaccinated group; mortality risk was significantly lower among vaccinated individuals (HR = 0.88, 95%CI: 0.85-0.91); cumulative incidence curves demonstrated higher rates of AKI and dialysis in the vaccinated cohort, whereas the probability of death was significantly lower in vaccinated compared with unvaccinated individuals (P-value < 0.001); in a prospective observational study in Jordan, 129 AKI events were reported after the COVID-19 vaccine; with 19.7 events/100000 persons reported in the study; in a Taiwanese VAERS analysis, there were 12 cases of AKI reported after COVID vaccine with the time of onset falling between 1-70 days; renal failure is reported in 13 cases out of 456 COVID-19 vaccine related adverse drug reaction reports with fatal outcomes; 12 cases were associated with cominarty vaccine and 1 case associated with Spikevax vaccine; there were 1572 cases of Haematuria were reported in a VAERS study with 13568650 COVID-19 vaccine associated symptoms reported, with the adverse event rate of haematuria being (0.012%); overall reporting rate for AKI post COVID-19 vaccine was 3.03 reports per 1 million doses and the reporting rate of renal failure post COVID-19 vaccine was 1.11 reports per million doses; potential side effects were elevated following vectored vaccines rather than mRNA vaccines (RR of AKI post AD26.COV2.S vaccine is 12.24, 95%CI: 10.66-13.81; while the reporting rate of renal failure post AD26.COV2.S vaccine is 3.17 95%CI: 2.36-3.97); there were 1312 deaths possibly associated with AKI (RR = 0.94, 95%CI: 0.89-0.99) and 460 deaths possibly associated with renal failure (RR = 0.33, 95%CI: 0.30-0.36) per million vaccine doses; the odds of a ≥ 65 years male reporting AKI post COVID vaccine is 7.23 times (95%CI: 6.63-7.88, P-value = 0.000) compared to 18-64 years old; the odds of a ≥ 65-year-old male reporting renal failure post COVID vaccine is 4.74 times (95%CI: 3.99-5.63, P-value < 0.001) compared to 18-64 years old; IR of acute renal failure during the pandemic period [449.8 (CI: 442.9-456.7)] was lower than the pre-pandemic period [478.4 (CI: 475.8-481)]; 8 cases of renal side effects (0.0007% of the targeted population), with 4 cases being proteinuria, 2 cases being haematuria and 2 being renal dysfunction
Huang et al[31], 2025 Safety in chronic kidney diseaseVaccinated cohort demonstrated a significantly reduced risk of major adverse kidney events or death (HR = 0.637, 95%CI: 0.581-0.689), major adverse kidney events alone (HR = 0.792, 95%CI: 0.698-0.898), and all-cause mortality (HR = 0.549, 95%CI: 0.484-0.622)
Lionaki et al[16], 2024; Carrillo et al[18], 2023; Canney et al[21], 2022 MCD6 patients out of 29 patients experienced a relapse of MCD after COVID-19 vaccination; the incidence of MCD was significantly higher post-Spanish vaccine (n = 20) (COVID-19 vaccine) than pre-Spanish vaccine (n = 13) (P-value=0.002); absolute increase in risk of a disease flare associated with a second or third dose of a COVID-19 vaccine varied from 1% to 2% in those with MCD
Lionaki et al[16], 2024; Carrillo et al[18], 2023Focal segmental glomerulosclerosis (FSGS)2 out of 38 patients experienced a relapse of focal segmental glomerulosclerosis after COVID-19 vaccination; the absolute increase in risk of a disease flare associated with a second or third dose of a COVID-19 vaccine varied from 1% to 2% in those with focal segmental glomerulosclerosis
Carrillo et al[18], 2023Idiopathic nephrotic syndrome In a retrospective observational cohort study, the incidence of idiopathic nephrotic syndrome was significantly higher post-Spanish vaccine (n = 18,10.7%) (COVID-19 vaccine) than pre-Spanish vaccine (n = 11, 5%) (P-value =0.036)
Lionaki et al[16], 2024; Canney et al[21], 2022IgA nephropathy 7 patients out of 41 patients experienced a relapse of IgA nephropathy after COVID-19 vaccination; the absolute increase in risk of a disease flare associated with a second or third dose of a COVID-19 vaccine varied from 3% to 5% in those with IgA nephritis
Sun et al[24], 2024; Nagatsuji et al[25], 2024IgA nephropathy relapse Significant decrease in eGFR in IgA nephropathy patients with 30 ≤ eGFR < 60 post second dose (n = 18, P = 0.01); however, there was a trend towards a decrease in eGFR after 6-month follow-up in vaccinated patients, although this difference was not significant (P = 0.06); the study also reported that there were 10 patients who displayed worsening proteinuria post vaccination; no significant changes in renal function or proteinuria before vs after vaccination in patients with gross haematuria, however, evaluation of the rate of change in eGFR showed that three of 16 patients with gross haematuria had an eGFR decrease of more than 10% after approximately 1 year; in addition, in four of the patients, renal biopsy was performed and showed Crescent formation in the glomerulus in three of the patients
Lionaki et al[16], 2024; Canney et al[21], 2022; Kim et al[77], 2024 Lupus nephritis 0 patients out of 69 patients experienced a relapse of lupus nephritis after COVID-19 vaccination; absolute increase in risk of a disease flare associated with a second or third dose of a COVID-19 vaccine varied from 3% to 5% in those with lupus nephritis; 16 cases of lupus nephritis after COVID-19 vaccine reported, with a cumulative incidence rate of 0.007/100000 person years (P-value = 0.021)
Canney et al[21], 2022Membranous nephropathy The absolute increase in risk of a disease flare associated with a second or third dose of a COVID-19 vaccine varied from 1% to 2% in those with membranous nephropathy
Carrillo et al[18], 2023 Autoimmune glomerulonephritis Incidence of autoimmune glomerulopathy was significantly higher post-Spanish vaccine (COVID-19 vaccine) (n = 85, 50.6%) than pre-Spanish vaccine (n = 86, 39.4%) (P-value=0.029), a total of 17 (20%) took place in the first 6 weeks after SARS-CoV-2 vaccine
Canney et al[21], 2022ANCA-associated glomerulonephritis The absolute increase in risk of a disease flare associated with a second or third dose of a COVID-19 vaccine varied from 1% to 2% in those with ANCA-glomerulonephritis
Canney et al[21], 2022; Wang et al[23], 2024 Unspecified glomerulonephritisHazard ratio of the second and third dose to glomerular disease was significant at 2.16 (1.03-4.51, P-value = 0.04), the hazard ratio for the first dose was less significant at 0.65 (0.32-1.32); vaccination did not associate with higher risk of subsequent glomerulonephritis disease worsening (HR = 1.02, 95%CI: 0.79-1.33); furthermore, COVID-19 vaccination was not associated with decline in eGFR following vaccination
Kim et al[77], 2024Renal vasculitis 3 cases of renal vasculitis after COVID-19 vaccine reported, with a cumulative incidence rate of 0.001/100000 person years
Chen et al[78], 2023Atypical haemolytic uraemic syndrome (aHUS) Out of 21 patients, only 1 patient had transient aHUS disease instability, but it was self-limited
Kim et al[77], 2024Immune thrombotic thrombocytopenic purpura leading to AKI13 cases of thrombotic thrombocytopenia purpura after COVID-19 vaccine reported, with a cumulative incidence rate of 0.006/100000 person years

For several renal outcomes, no population-level or observational studies were identified. However, isolated case reports describing these conditions following COVID-19 or influenza vaccination were captured in the Supplementary material. For all case reports and case series, clinical signs, symptoms, and recovery timelines were collated, summarised, and are presented in the Supplementary material. The various renal complications have been split across 8 main categories: Unspecified AKI, podocytopathies, immune-complex glomerulonephritis, crescentic/rapidly progressive glomerulonephritis, other glomerular entities, tubulointerstitial and vascular renal disorders, systemic/multiorgan inflammatory syndromes with renal involvement and transplant-related renal outcomes.

AKI in general across all vaccine platforms: Across studies evaluating all COVID-19 vaccine platforms, renal outcomes were variably reported across observational, pharmacovigilance, and population-level analyses. Of the 3 observational and cohort studies reported, a temporal association between COVID-19 vaccination and AKI or acute kidney disease. Abdel-Qader et al[70] observed 19.7 AKI events per 100000 vaccinated persons, while Chen et al[19] identified 27 AKI cases among 1897 vaccinated adults. In a global retrospective cohort, Tsai et al[30] reported a higher incidence of AKI [hazard ratio (HR) = 1.20, 95% confidence interval (CI): 1.18-1.23] and dialysis initiation (HR = 1.84, 95%CI: 1.68-2.01) in vaccinated individuals compared with unvaccinated controls. Of the 3 population-level cohort studies, however, reported no statistically significant association between COVID-19 vaccination and AKI. Choi et al[15] identified five AKI events, with an incidence rate ratio of 0.67 (95%CI: 0.119-3.99), while Tavakoli et al[76] reported renal adverse events in 0.0007% of vaccinated Iranian adolescents. Of the 4 pharmacovigilance studies based on spontaneous reporting systems, signals for renal adverse events following COVID-19 vaccination were identified. Anastassopoulou et al[74] reported AKI and renal failure reporting rates of 3.03 and 1.11 cases per million vaccine doses, respectively, while Nurminen et al[72] reported renal failure in 13 of 456 vaccine-related adverse drug reaction reports with fatal outcomes.

Relapse of pre-existing renal disease following vaccination was reported in observational cohorts, with Lionaki et al[16] noting glomerular disease relapse in 23 of 255 patients (9%). However, among individuals with chronic kidney disease (CKD), Huang et al[31] reported lower risks of major adverse kidney events and all-cause mortality in vaccinated patients. Observational studies reported both de novo disease and relapse of podocytopathies following vaccination. Carrillo et al[18] reported a significant increase in the incidence of minimal change disease (MCD) (from 13 cases to 20 cases, P-value = 0.002) and idiopathic nephrotic syndrome [from 11 (5%) to 18 (10.7%)], P-value = 0.036). Regarding relapse, Lionaki et al[16] reported relapse in 6 of 29 patients with MCD and 2 of 38 patients with focal segmental glomerulosclerosis (FSGS), while Canney et al[21] reported an increase in flare risk of 1%-2% following a second or third vaccine dose in patients with FSGS.

Multiple studies reported de novo disease or relapse of immune-complex glomerulonephritis following vaccination. For membranous nephropathy, Canney et al[21] reported an absolute increase in relapse risk of 1%-2% following second or third vaccine doses. Carrillo et al[18] also reported a statistically significant increase in membranous nephropathy incidence between pre-vaccination and post-vaccination periods (P-value = 0.029). Lionaki et al[16] reported relapse in 7 of 41 patients with immunoglobulin A nephropathy (IgAN), while Canney et al[21] reported an absolute flare risk increase of 3%-5% after second or third vaccine doses. Sun et al[24] reported a significant decline in epidermal growth factor receptor (EGFR) among vaccinated IgAN patients after the second dose (P-value = 0.01), as well as worsening proteinuria in 10 patients. In contrast, Nagatsuji et al[25] reported no significant changes in renal function or proteinuria before vs after vaccination overall, although 3 of 16 patients with gross haematuria experienced an eGFR decline greater than 10% at one year.

For lupus nephritis, relapse rates were generally uncommon. Canney et al[21] reported an absolute flare risk of 3%-5% after second or third doses, Kim et al[77] identified 16 cases in a Vaccine Adverse Event Reporting System (VAERS) analysis (0.007 per 100000 person-years), and Lionaki et al[16] reported no relapses among 69 biopsy-proven patients. Evidence regarding glomerulonephritis relapse overall was mixed. For anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis, Canney et al[21] reported an absolute increase in flare risk of 3%-5% following the second or third vaccine dose. Canney et al[21] also reported a higher hazard of glomerulonephritis relapse following second and third vaccine doses (HR = 2.16, 95%CI: 1.03-4.51), whereas Wang et al[23] reported no association between vaccination and disease worsening (HR = 1.02, 95%CI: 0.79-1.33) or significant eGFR decline.

Evidence for tubulointerstitial and vascular renal disorders following COVID-19 vaccination was limited. In a VAERS analysis, Kim et al[77] reported three cases of renal vasculitis (incidence 0.001 per 100000 person-years) and 13 cases of thrombotic thrombocytopenic purpura (incidence 0.006 per 100000 person-years) following vaccination. In addition, a Taiwanese cohort of patients with atypical haemolytic uraemic syndrome reported transient disease instability in 1 of 21 patients, which stabilised following a switch from mRNA-1273 to BNT162b2[78].

mRNA vaccines: Across 199 case reports and case series, 350 patients were described to have a wide range of renal manifestations following the mRNA vaccine. Following mRNA vaccination, symptom onset ranged from 6 hours to 6 months, with most cases occurring within 1 day to 6 weeks. Symptoms most commonly reported after mRNA vaccination included peripheral oedema, foamy urine, reduced urine output, fatigue, and weight gain. Clinical signs and laboratory findings included new-onset or worsening proteinuria, hypoalbuminemia, AKI with elevated serum creatinine, and microscopic or macroscopic haematuria, particularly in cases of IgA nephropathy or crescentic glomerulonephritis. The most frequently reported adverse renal effect included MCD, IgA nephropathy (both de novo and relapse), IgA vasculitis, membranous nephropathy, and pauci-immune crescentic glomerulonephritis. Management predominantly involved corticosteroid therapy, where a common regimen would be high-dose methylprednisolone pulse therapy followed by prednisone/prednisolone taper. This is alongside supportive measures such as renin-angiotensin system blockade and diuretics. Additional immunosuppressive agents, such as cyclophosphamide or renal replacement therapy, were required in a minority of severe cases; 29 patients required dialysis treatment, while 1 underwent renal replacement therapy. Cases of spontaneous recovery without treatment were reported as well. Recovery was generally observed within weeks to months, depending on disease severity. Notably, 3 fatalities were reported, attributed to rhabdomyolysis-associated multiorgan failure, thrombocytopenia, anasarca, fever, reticulin myelofibrosis, renal dysfunction, and organomegaly syndrome, and severe lupus nephritis flare, respectively.

While 5 population-based[13,56-59] and 1 cohort study[14] reported a temporal association of AKI following mRNA vaccinations, the incidence rate was generally low. These studies consistently described incidence rates ranging from 0.1 cases per 100000 persons to 4 cases per 100000 persons, or similarly low rates per dose or person-year, with no statistically significant increase in risk in comparator analyses. In contrast, five pharmacovigilance and disproportionality analyses reported elevated reporting signals for AKI following COVID-19 vaccinations, with reported retinoic-acid-receptor-related orphan receptors (RORs) ranging from 1.25 to 5.41 and information component (IC) lower bounds consistently above zero[60-63,79].

Across multiple study designs, MCD and nephrotic syndrome were among the most frequently reported glomerular entities following COVID-19 vaccination. In a retrospective cohort, MCD accounted for 28.6% of de novo glomerulonephritis cases, mostly within 5-7 days post-vaccination[11]. Pharmacovigilance analyses from VigiBase reported disproportionality signals for MCD (36 cases; IC/IC025: 0.88/0.37) and nephrotic syndrome (103 cases; IC/IC025: 0.60/0.31) following Pfizer-BioNTech vaccination[64]. Among patients with pre-existing nephrotic syndrome, relapse rates after vaccination were comparable to pre-vaccination periods[28], while a prospective study in childhood-onset nephrotic syndrome reported relapse in 7.5% of patients following COVID-19 vaccination[10].

IgA nephropathy accounted for 26.5% of de novo glomerulonephritis cases, typically presenting within 1-2 days post-vaccination[11]. Disproportionality analyses identified signals for IgA nephropathy following Moderna (IC/IC025: 1.51/0.71) and mRNA vaccines overall (ROR 6.49, IC: 2.27)[64,67].

In the Waldman et al[11] cohort, membranous nephropathy (10.2%), pauci-immune crescentic glomerulonephritis (17.3%), anti-GBM disease (5.1%), and collapsing glomerulopathy (5.1%) were also reported following vaccination, predominantly after mRNA vaccines, with onset ranging from days to two weeks. However, Swiss population-based analyses found no statistically significant increased risk for MCD (RR = 1.72), membranous nephropathy (RR = 1.17), pauci-immune glomerulonephritis (RR = 0.54) or IgAN (RR = 1.14)[20]. Among adolescents with systemic lupus erythematosus (SLE), 34.8% experienced disease flares, with renal flares occurring in 20.3% overall and 27.7% of those with prior lupus nephritis. Renal manifestations included increased proteinuria, abnormal urine sediment, and reduced kidney function[29].

A large VigiBase pharmacovigilance analysis found disproportionate reporting signals for glomerulonephritis (ROR 13.41, IC 2.98) and tubulointerstitial nephritis (ROR = 2.43, IC: 1.22)[61]. In contrast, a VAERS analysis found no positive disproportionality signal for thrombotic thrombocytopenic syndromes (ROR = 0.81)[68]. Rhabdomyolysis with renal involvement was rare, with a self-controlled case series from Hong Kong reporting low incidence rates following BNT162b2 vaccination[13]. Among patients receiving kidney replacement therapy, renal complications were infrequent. In the RECOVAC prospective multicentre study, one case of kidney transplant rejection was reported among 159 dialysis patients who later underwent transplantation[12]. However, a separate single-centre prospective study reported transient renal abnormalities (creatinine rise, proteinuria, or haematuria) in 40.1% of kidney transplant recipients following vaccination[17].

Vector vaccines: Across 46 case reports and case series, 50 patients were described with renal manifestations following viral vector COVID-19 vaccination. Symptom onset typically occurred between 2 hours and 120 days after vaccination, with most cases presenting within 1-2 weeks. The most reported symptoms included peripheral oedema, reduced urine output, fatigue, and non-specific malaise. Reported clinical signs and laboratory abnormalities included proteinuria, AKI with elevated serum creatinine, reduced estimated glomerular filtration rate, and hypertension. Reported adverse renal effects most commonly included MCD and pauci-immune crescentic glomerulonephritis. Management was predominantly supportive, including optimisation of volume status using diuretics and renin-angiotensin system blockade. Other common modes of treatment include corticosteroids, with a regimen like that used for mRNA patients, and cyclophosphamide. The majority of patients experienced clinical improvement or recovery within weeks to months, and dialysis was used in 15 patients, and renal replacement therapy was used in 1 patient. Notably, 1 fatality occurred from cardiac arrest in a patient with systemic capillary leak syndrome.

Observational and pharmacovigilance data on Ad5-vectored COVID-19 vaccines suggest an overall low incidence of renal adverse events, though specific safety signals were identified in some analyses. A VAERS analysis of the Jannsen vaccine reported 89 cases of renal events; however, no statistically significant safety signal was observed (ROR = 1.04, 95%CI: 0.84-1.28; proportional reporting ratio = 1.04; IC025: 0.04)[60]. With respect to glomerulonephritis, a VigiBase pharmacovigilance study identified a disproportionate reporting signal following Ad5-vectored vaccines (ROR = 3.12, 95%CI: 2.73-3.56; IC: 1.58, IC025: 1.36)[63]. Thrombotic thrombocytopenic syndrome with associated AKI was reported in two case reports following vector vaccination. Supporting this, VAERS data documented 934 cases of thrombocytopenic syndrome after Ad5-vectored vaccines, with a modest disproportionality signal (ROR = 1.64, IC025: 0.64)[68].

Inactivated vaccines: Across 7 case reports and case series, 8 patients with renal manifestations following inactivated COVID-19 vaccines were reported. Symptom onset ranged from 4 hours to 2 weeks post-vaccination. Reported symptoms most commonly included peripheral oedema, foamy urine, and fatigue. Clinical signs and laboratory findings were commonly characterised by new-onset or worsening proteinuria, hypalbuminaemia, nephrotic-range proteinuria, and AKI with elevated serum creatinine. The most frequently described renal phenotypes involved relapse of pre-existing glomerular disease, particularly MCD and IgA nephropathy, as well as new-onset nephrotic syndrome. Renal recovery was seen in many patients within 2-8 weeks, particularly with immunosuppressive (corticosteroid) or supportive therapy. More severe cases, including thrombotic microangiopathy or severe glomerulonephritis, needed up to 3-5 months for renal recovery.

In an observational self-controlled case series study in Hong Kong for type 2 diabetes patients with COVID vaccinations, Wan et al[13] reported an incidence of AKI post COVID inactivated vaccine of 1.41/100000 doses (0.46, 3.28) with an incidence rate of 25.42/100000 person-years (10.58, 61.08). One retrospective cohort study with 253 patients with membranous nephropathy reported that there was no difference in the rate of relapse or worsening between vaccinated and non-vaccinated patients with membranous nephropathy, with a hazard ratio of 0.98 (95%CI: 0.42-3.23)[27].

Recombinant protein nanoparticle vaccine (GBP510): Evidence regarding renal safety for the recombinant protein nanoparticle COVID-19 vaccine (GBP510) is extremely limited. One randomised, active-controlled, observer-blinded, parallel group, phase 3 study reported only three systemic adverse events - including one case each of AKI, rapidly progressive glomerulonephritis, and cutaneous vasculitis[69].

Influenza vaccine results

The included studies assessed mainly two types of influenza vaccines, including the H1N1 pandemic vaccine and the inactivated seasonal vaccines. In total, 24 observational studies, 1 interventional study and 4 pharmacovigilance studies examined the association between influenza vaccination and renal outcomes. In addition, 49 published case reports and case series described renal adverse events occurring after influenza vaccinations. A summary of the included studies is presented in Table 3[32-47,49-55,61,68,80-82]. Signs, symptoms, as well as recovery timeline have been collated, summarised and made available under our Supplementary material.

Table 3 Population-level renal outcomes reported following influenza vaccination1.
Ref.
Type of vaccine
Associated kidney injury
Incidence
Hao et al[33], 2023; Miskulin et al[38], 2018; Liao et al[47], 2022Unspecified vaccinePatients with CKD or/and/or need haemodialysisRisk of CKD occurrence among vaccinated patients all season (adjusted hazard ratio: 0.38, 95%CI: 0.34-0.44); risk of haemodialysis after vaccination (aHR: 0.41, 95%CI: 0.33-0.51) all season; receipt of high dose trivalent vaccine was associated with a significant reduction in hospitalization compared to standard dose vaccines (hazard ratio = 0.93; 95%CI: 0.86-1.00; P-value=0.04); patients who had previous influenza vaccine had a lower risk of septicaemia (OR = 0.77, 95%CI: 0.68-0.87), need for intensive care (OR = 0.85, 95%CI: 0.75-0.96), and in-hospital mortality (OR = 0.56, 95%CI: 0.39-0.82) compared to people who did not take the influenza vaccine previously
Pabico et al[51], 1974; Hwang et al[61], 2025General glomerulonephropathiesCreatinine clearances remained relatively unchanged in all patients; patients with glomerulopathies had no adverse effects with influenza vaccination; VigiBase disproportionality analysis: ROR of Glomerulonephritis with influenza vaccine of 7.08 (6.32-7.93), with an IC of 2.78 (IC025: 2.59)
Shih et al[43], 2018; Cho et al[44], 2024; Zhuo et al[45], 2026; Hwang et al[61], 2025; Vesikari et al[80], 2011; Haber et al[81], 2014General acute kidney injury (AKI)Risk of hospitalization for AKI (aOR = 0.67, 95%CI: 0.63-0.72, P-value < 0.001) in vaccinated individuals; unvaccinated individuals who developed influenza infection also had higher AKI risk (aOR = 1.78, 95%CI: 1.57-2.01, P-value < 0.001); adjusted incidence rate ratios of AKI with influenza vaccination 0.83 (95%CI: 0.79-0.87) in the 2018-2019 season and 0.86 (95%CI: 0.82-0.90) in 2019-2020; incidence of AKI was 36.8 per 100000 person years in unvaccinated patients, incidence of AKI was 30.6 per 100000 person years in vaccinated patients, showing a hazard ratio of 0.83 (95%CI: 0.71-0.98) between influenza vaccine and AKI; VigiBase disproportionality analysis: ROR of AKI with influenza vaccine of 0.84 (0.76-0.93), with an IC of -0.25 (IC025: -0.42); one case of a renal and urinary tract disorder, 36-72 months after administration of the trivalent influenza vaccine without the MF59 adjuvant being reported; in a VAERS analysis of a trivalent live attenuated vaccine, there was one report of acute renal failure after vaccination
Hwang et al[61], 2025TINsVigiBase disproportionality analysis: ROR of TINs with influenza vaccine of 0.65 (0.46-0.93), with an IC of -0.61 (IC025: -1.21)
Ishimori et al[32], 2023; Ishimori et al[40], 2021; Kumar et al[41], 2023; Ishimori et al[54], 2020Inactivated seasonal vaccineNephrotic syndromeRelapse rate was not significantly different between the pre-vaccination period and the post vaccination period between the day of vaccination and 30 days after (0.38 times/person-year vs 0.19 times/person-year); children receiving the influenza vaccine showed a significantly lower RR for nephrotic syndrome relapse (RR: 0.22, 95%CI: 0.14-0.35) compared with unvaccinated children; among vaccinated children, there was a significantly lower risk for nephrotic syndrome relapse during the post-vaccination period (RR: 0.31, 95%CI: 0.17-0.56) compared with the pre-vaccination period; nephrotic syndrome relapses significantly reduced in the vaccinated children (P-value < 0.001), with the odds of them getting a nephrotic relapse after influenza vaccine being 0.29 (95%CI: 0.16-0.54); Incidence of nephrotic syndrome relapse is 1.19 times/person-year; comparing it with the various time periods post vaccination, risk ratio for post vaccination days 0-30 is 1.04 (95%CI: 0.82-1.89); risk ratio for days 31-60 is 1.33 (95%CI: 0.94-2.10); risk ratio for days 61-90 is 1.19 (95%CI: 0.94-2.10); risk ratio for days 91-120 is 1.19 (95%CI: 0.94-2.10); risk ratio for days 121-180 was 1.11 (95%CI: 0.98-1.76); steroid injection at first vaccination increases risk for NS relapses over all periods (RR: 3.01, 95%CI: 2.18-4.17)
Klifa et al[39], 2019Idiopathic nephrotic syndrome Relapse rates were reported to be not increased in vaccinated children compared to unvaccinated children; relapse rates were not increased in the 6 months following vaccination (1/14) compared to the 6 months before vaccinations (5/14)
Minimal change disease with acute tubular injury and acute interstitial nephritis No relevant statistics found
Gwynn et al[53], 2020Immune-mediated glomerulonephritis7 patients developed immune-mediated adverse events at the 60-day mark after influenza vaccine, with 1 of the patients (13%) developing grade 3 nephritis 57 days post inactivated influenza vaccine
Mixed-type cryoglobulinaemic glomerulonephritisNo relevant statistics found
Henoch-Schönlein purpura-associated nephritisNo relevant statistics found
Systemic lupus erythematosus-associated nephritisNo relevant statistics found
Relapsing membranous nephropathy with AKINo relevant statistics found
Jeffs et al[49], 2015Pauci-immune vasculitis-associated glomerulonephritisNo significant change in disease activity in vaccinated patients compared with non-vaccinated patients as measured by ANCA titre; no evidence of change in CRP, Birmingham Vasculitis Activity Score (BVAS) or serum creatinine; no significant change in the level of ANCA immune-fluorescence, ANCA IgG, anti-CCP, anti-dsDNA or RF among the vaccinated healthy individuals compared with their non-vaccinated counterparts at either day 7 or 28
Leukocytoclastic vasculitis-associated glomerulonephritisNo relevant statistics found
Polyarteritis causing glomerulonephritis with epithelial crescentsNo relevant statistics found
Focal segmental glomerulosclerosis in a patient with IgA nephropathyNo relevant statistics found
Acute renal failure due to acute tubule-interstitial nephropathy No relevant statistics found
Atypical haemolytic urinary syndrome causing AKINo relevant statistics found
Lee et al[68], 2023Thrombotic thrombocytopenic purpura causing acute renal failure VigiBase disproportionality analysis: ROR influenza vaccines related thrombotic thrombocytopenic syndrome of 0.82 (0.77-0.88) and IC: -0.28 (IC025: -0.39)
Milk alkali syndrome-associated AKI No relevant statistics found
Chen et al[46], 2025; Chen et al[50], 2022AKI due to rhabdomyolysisStatins use 1-30 days before the date of rhabdomyolysis was associated with a higher odds of rhabdomyolysis with the use of influenza vaccine within 1-7 days of the date of rhabdomyolysis, 1.67 (95%CI: 1.04-2.69, P-value = 0.034); individuals who developed rhabdomyolysis were less likely to have received an influenza vaccine within the preceding 28 days (OR = 0.65, 95%CI: 0.52-0.82)
Hemophagocytic lymphohistiocytosis complicated by Rhabdomyolysis, causing AKI No relevant statistics found
Septic shock after seasonal influenza vaccine leading to multiorgan failureNo relevant statistics found
Systemic capillary leak syndromeNo relevant statistics found
Acute disseminated encephalomyelitis after seasonal influenza vaccine leading to AKINo relevant statistics found
Levison et al[42], 2022; Souayah et al[82], 2007Nephrotic syndrome with Guillain-Barré syndrome (GBS)Influenza vaccination was linked to a mildly higher risk of GBS [OR = 1.94 (95%CI: 1.12-3.36)], particularly in the month following vaccination [OR = 2.9 (95%CI: 1.2-6.8)]; recent vaccination accounted for only 1.5% of GBS cases, corresponding to a population-attributable fraction of 0.4%; in a VAERS analysis in 2004, there were 31 cases of Guillain barre syndrome reported after influenza vaccine
GBS is causing renal salt-wasting syndromeNo relevant statistics found
Dos Santos et al[37], 2016; Zawiasa-Bryszewaska et al[55], 2025 Safety in patients with a kidney transplantRI of kidney rejection during the 30-day risk period was 0.59 (95%CI: 0.13-2.63), 1.28 (95%CI: 0.52-3.15), 0.98 (95%CI: 0.34-2.80) and 0.91 (0.44-1.87) in seasons 2006/07, 2007/08, 2008/09 and pooled seasons, respectively; corresponding RIs during the 60-day risk period were 050 (95%CI: 0.16-1.60), 0.82 (95%CI: 0.36-1.86), 0.42 (95%CI: 0.15-1.21) and 0.59 (95%CI: 0.32-1.08), respectively; no significant difference in eGFR before and after vaccine (Difference of eGFR from day of vaccine to 6 months after in vaccinated group [-1.0 (-5.0 to 2.0) mL/minute/1.73 m2] vs in non-vaccinated group, [1.0 (-3.0 to 5.0) mL/min/1.73 m2]; no significant difference in serum creatinine levels (difference in serum creatinine levels from day of vaccination to day 60 after vaccination in vaccinated group and non-vaccinated group, respectively, -1.27 (-1.71 to -0.90) vs -1.07 (-1.40 to -0.89) mg/dL; no significant difference in clinically significant proteinuria rates (Proteinuria rates from day 60 post vaccination in vaccinated vs non-vaccinated patients 7.4% vs 5.8%
Fernández-Ruiz et al[35], 2015Kidney graft rejection post-influenza vaccineOverall cumulative incidence of biopsy-proven acute graft rejection was 2 out of 37 (5.4%) patients who took the adjuvanted vaccine and 2 out of 28 (7.1%) patients who took the non-adjuvanted vaccine; the incidence rate was 0.22/1000 transplantdays for adjuvanted vaccinations and 0.18/1000 transplant days for non-adjuvanted vaccinations; the overall cumulative incidence of graft loss was 0 who took the adjuvanted vaccine and 2 out of 28 (7.1%) patients who took the non-adjuvanted vaccine; the incidence rate was 0.18/1000 ctransplant days for non-adjuvanted vaccinations
Reynales et al[52], 2012Inactivated H1N1 pandemic vaccineIncidence of renal and urinary disorders in MF59® adjuvanted cell culture-derived vaccineCumulative Incidence of urinary and renal disorders during the study is reported tobe 0.1% (CI: 0.0-0.3); however, 0 cases are reported to be possibly related to the vaccine and related to the vaccine
Relapse of nephrotic syndrome No relevant statistics found
Henoch-Schönlein purpura nephritis No relevant statistics found
Membranous glomerulonephritis causing nephrotic syndromeNo relevant statistics found
AKI due to rhabdomyolysisNo relevant statistics found
Multiorgan failure after influenza vaccineNo relevant statistics found
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome causing AKINo relevant statistics found
Serum sickness with AKI No relevant statistics found
Moghaddasi et al[34], 2013; Cohet et al[36], 2016Renal allograft function and transplant rejection The serum creatinine, creatinine clearance, and 24-hour urine proteinuria levels were not significantly different between before and 1 month after vaccination (1.3 ± 0.35 mg/dL vs 1.3 ± 0.5 mg/dL, 83 ± 28 mL/minute vs 78 ± 31 mL/minute, and 356 ± 437 mg vs 293 ± 307 mg, respectively); serum creatinine level did not differ significantly between before and 2.5 years after vaccination (1.3 ± 0.35 mg/dL vs 1.4 ± 0.39 mg/dL); the RI of acute transplant rejection adjusted for time since transplantation was 0.85 (95%CI: 0.38-1.90) within 30 days after vaccination and 0.68 (95%CI: 0.33-1.40) within 60 days after vaccination

AKI in general across all influenza vaccine platforms: Across multiple large observational studies, influenza vaccination was not associated with an increased risk of AKI, with several studies reporting lower AKI-related risk estimates among vaccinated individuals. Three observational studies evaluating unspecified AKI reported a lower risk among vaccinated individuals, including a hazard ratio of 0.83 (95%CI: 0.71-0.98) for AKI[45], an adjusted odds ratio of 0.67 (95%CI: 0.63-0.72; P-value < 0.001) for AKI-related hospitalisation[43], and adjusted incidence rate ratios of 0.83 (95%CI: 0.79-0.87) for the 2018-2019 season and 0.86 (95%CI: 0.82-0.90) for the 2019-2020 season[44]. Consistent with these findings, a large VigiBase pharmacovigilance analysis demonstrated no safety signal for AKI following influenza vaccination, with a ROR of 0.84 (95%CI: 0.76-0.93) and an IC of -0.25 (IC025: -0.42). No safety signal was identified for tubulointerstitial nephritis, with an ROR of 0.65 (95%CI: 0.46-0.93) and an IC of -0.61 (IC025: -1.21)[61]. Among patients with CKD, influenza vaccination was associated with a lower risk of CKD progression and dialysis initiation, with an adjusted hazard ratio of 0.41 (95%CI: 0.33-0.51) for incident CKD and 0.41 (95%CI: 0.33-0.51) for haemodialysis across influenza seasons[33]. Evidence relating to glomerulonephropathies was mixed. A VigiBase disproportionality analysis identified a reporting signal for glomerulonephritis following influenza vaccination (ROR = 7.08, 95%CI: 6.32-7.93; IC: 2.78, IC025: 2.59). In contrast, a cohort study of 21 patients with pre-existing glomerular disease reported no change in creatinine clearance following influenza vaccination[51].

Seasonal inactivated influenza vaccine: A total of 47 cases, reported as case reports and case series, described adverse renal effects temporally associated with inactivated seasonal influenza vaccination. The interval between vaccination and symptom onset ranged from 24 hours to 8 weeks, with most cases presenting within 3 weeks of vaccination. The most common presenting symptoms were oedema, fever, generalized weakness, myalgia, arthralgia, rash, and reduced urine output. Laboratory findings most frequently demonstrated AKI with elevated serum creatinine, accompanied by proteinuria and haematuria. Inflammatory markers, including C-reactive protein and erythrocyte sedimentation rate, were commonly elevated, with frequent anaemia and leucocytosis. Immunological abnormalities varied by disease subtype, including hypocomplementemia and cryoglobulinemia in immune-complex glomerulonephritis, ANCA positivity in pauci-immune glomerulonephritis, and antinuclear antibody or anti-double-stranded DNA positivity in lupus flares.

Reported renal manifestations included podocytopathies, most commonly MCD; immune-complex glomerulonephritis, including Henoch-Schönlein purpura-associated nephritis, lupus nephritis, and membranous nephropathy; and rapidly progressive glomerulonephritis, including pauci-immune vasculitis-associated glomerulonephritis and leukocytoclastic vasculitis. Additional mechanisms involved tubulointerstitial and vascular renal disorders, such as acute tubulointerstitial nephritis, atypical haemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and milk-alkali syndrome, as well as systemic causes, including rhabdomyolysis, hemophagocytic lymphohistiocytosis, and systemic capillary leak syndrome. Neurological immune disorders, including Guillain-Barré syndrome, were also reported with secondary renal involvement.

Treatment most commonly consisted of systemic corticosteroids, with adjunctive therapies including cyclophosphamide, rituximab, azathioprine, mycophenolate mofetil, intravenous immunoglobulin, and plasma exchange, depending on disease subtype and severity. Recovery duration ranged from 7 days to 13 months, with prolonged recovery observed in severe crescentic and immune-mediated disease. Renal replacement therapy was needed in 11 cases, most often in pauci-immune glomerulonephritis, immune-complex glomerulonephritis, thrombotic microangiopathy, systemic inflammatory syndromes, and transplant-related rejection. Two patients progressed to chronic dialysis, while three patients were reported to recover renal function and discontinue dialysis. Mortality was low, with two deaths reported: One due to pneumonia following treatment for pauci-immune vasculitis–associated glomerulonephritis, and one due to bronchopneumonia after treatment for polyarteritis causing glomerulonephritis.

Ten observational studies evaluated the association between seasonal inactivated influenza vaccination and kidney injury, focusing on populations with kidney transplantation, nephrotic syndrome, pauci-immune vasculitis-associated glomerulonephritis, and thrombotic thrombocytopenic purpura with AKI. Three observational studies reported no evidence of adverse renal outcomes following influenza vaccination in kidney transplant recipients. One study reported a relative incidence of acute graft rejection of 0.91 (95%CI: 0.44-1.87) during the 30-day post-vaccination risk period[37]. Another study found no significant differences in estimated glomerular filtration rate, serum creatinine, or proteinuria rates between vaccinated and unvaccinated transplant recipients[55]. A prospective cohort study reported low incidence rates of acute graft rejection, at 0.22 per 1000 transplant-days for adjuvanted vaccines and 0.18 per 10000 transplant-days for non-adjuvanted vaccines, with a graft loss incidence of 0.18 per 1000 transplant-days in the non-adjuvanted group[35].

Five observational studies assessed the risk of nephrotic syndrome relapse following influenza vaccination and consistently reported no increased relapse risk. One study showed a significant reduction in relapse risk, with a risk ratio of 0.22 (95%CI: 0.14-0.35), and a post-vaccination relapse risk ratio of 0.31 (95%CI: 0.17-0.56)[40]. Similar findings were reported observed a significant reduction in relapse rates among vaccinated children (P-value < 0.001)[41]. Other studies reported no significant differences in relapse incidence between vaccinated and unvaccinated groups[32,54].

One observational study reported no serious adverse events over a six-month follow-up period following influenza vaccination in patients with pauci-immune vasculitis-associated glomerulonephritis. No significant changes were seen in C-reactive protein, Birmingham Vasculitis Activity Score, serum creatinine, or autoantibody profiles. Two isolated findings were reported: One patient with microscopic polyangiitis experienced disease relapse six months after vaccination, and one healthy individual developed transient ANCA positivity without clinical manifestations[49]. A large VAERS pharmacovigilance analysis identified 934 reports of influenza vaccine-associated thrombotic thrombocytopenic purpura, but no safety signal was detected, with a reported odds ratio of 0.82 (95%CI: 0.77-0.88) and an IC of -0.28 (IC025: -0.39), indicating lower-than-expected reporting relative to other vaccines[68].

Inactivated H1N1 influenza vaccine: A total of nine case reports, comprising nine patients, described renal adverse events temporally associated with inactivated H1N1 pandemic influenza vaccination. The interval between vaccination and symptom onset ranged from a few hours to 20 days, with the majority of cases presenting within the first two weeks. Common presenting features included haematuria, proteinuria, oedema, and myalgia, and all patients demonstrated elevated serum creatinine, consistent with AKI. Reported renal manifestations encompassed podocytopathies (including relapse of nephrotic syndrome), immune complex-mediated glomerulonephritis (including Henoch-Schönlein purpura nephritis and membranous glomerulonephritis), and systemic inflammatory or multiorgan conditions, such as rhabdomyolysis, multiorgan failure, drug reaction with eosinophilia and systemic symptoms (DRESS), and serum sickness. Systemic corticosteroids were the primary treatment in most cases, commonly initiated as oral prednisolone or intravenous methylprednisolone and subsequently tapered as clinical and biochemical parameters improved. Additional supportive or disease-specific therapies were reported, including aggressive intravenous fluid resuscitation for rhabdomyolysis and supportive intensive care for multiorgan failure. Most patients demonstrated recovery of renal function within one week to 2.5 months, although three patients required temporary haemodialysis.

Two observational studies evaluated the association between inactivated H1N1 influenza vaccination and renal allograft function or transplant rejection. In a cohort study of 78 kidney transplant recipients, Moghaddasi et al[34] reported no significant differences in serum creatinine, creatinine clearance, or 24-hour urinary protein excretion before vaccination and one month after vaccination. No episodes of acute rejection were observed during a 2.5-year follow-up period. Similarly, a self-controlled case series by Cohet et al[36] reported a relative incidence of transplant rejection of 0.85 (95%CI: 0.38-1.90) within 30 days after vaccination and 0.68 (95%CI: 0.33-1.40) within 60 days after vaccination, indicating no increased risk of rejection following vaccination.

DISCUSSION
Summary of results

Overall, population-level evidence indicates that both COVID-19 and influenza vaccines are associated with a low absolute risk of adverse renal outcomes, with most observational studies showing no statistically significant increase in AKI or glomerular disease relapse following vaccination. In several cohorts, vaccination was associated with a reduction in AKI-related events, particularly among high-risk populations. In contrast, pharmacovigilance analyses and a substantial number of case reports and case series describe rare instances of de novo or relapsing glomerular disease, including MCD, IgA nephropathy, membranous nephropathy, and pauci-immune glomerulonephritis, typically occurring within days to weeks of vaccination. The majority of reported cases improved with supportive or disease-specific therapy.

Proposed mechanisms of kidney injury

Figure 2 summarises the hypothesised biological pathways through which renal injury has been reported in temporal association with influenza and COVID-19 vaccination. The proposed mechanisms are derived from established principles of immunology and renal pathophysiology and are supported by evidence from observational studies, pharmacovigilance analyses, and case reports cited in this study. These mechanisms largely centre on loss of immune tolerance[83], molecular mimicry[84,85], complement activation[86], hypersensitivity reactions[87] and excess cytokine release[88]. Renal manifestations are categorised according to dominant patterns of injury, including podocytopathies, immune complex glomerulonephritis[89], pauci-immune[90] and anti–glomerular basement membrane disease[91], vascular and thrombotic disorders, tubulointerstitial injury, and systemic or multiorgan inflammatory syndromes. These pathways are presented to illustrate biological plausibility and do not imply a causal relationship between vaccination and kidney injury.

Figure 2
Figure 2 Proposed immunopathological mechanisms of influenza and coronavirus disease 2019 vaccine-associated kidney injury. This figure illustrates the potential mechanisms by which influenza and coronavirus disease 2019 vaccinations may be associated with kidney injury. The mechanisms are categorized into different pathways leading to acute kidney injury (AKI). The green pathway represents various proposed mechanisms underlying different forms of glomerulonephritis, including antineutrophil cytoplasmic antibody-associated vasculitis and pauci-immune glomerulonephritis, anti-glomerular basement membrane disease, and immune complex glomerulonephritis. The red pathway describes the proposed mechanisms for vascular-related causes of AKI, such as atypical haemolytic uremic syndrome, renal vein thrombosis, and renal thrombotic microangiopathy. The blue pathway describes the proposed mechanisms of podocytopathies, such as minimal change disease. The purple pathway describes the systemic causes related to AKI, such as rhabdomyolysis and pre-renal causes of AKI. This figure provides a comprehensive overview of how immune responses triggered by vaccinations may lead to kidney injury through both direct renal effects and systemic processes. AKI: Acute kidney injury; ANCA: Antineutrophil cytoplasmic antibody; Anti-GBM: Anti-glomerular basement membrane; DRESS: Drug reaction with eosinophilia and systemic symptoms; GBS: Guillain-Barré syndrome; IL-13: Interleukin-13; iTTP: Immune-mediated thrombotic thrombocytopenic purpura; MIS: Multisystem inflammatory syndrome; MOI: Multiorgan inflammation; TAFRO: Thrombocytopenia, anasarca, fever, reticulin myelofibrosis, renal dysfunction, and organomegaly; HLH: Haemophagocytic lymphohistiocytosis; COVID-19: Coronavirus disease 2019.
Salient points for each vaccine

COVID-19 vaccine: Across all COVID-19 vaccine platforms, both observational and pharmacovigilance analyses describe a varied and heterogeneous spectrum of renal outcomes and reported incidences. While some observational, cohort, and pharmacovigilance studies report a notable number of post-vaccination renal adverse events, there are population-level studies that do not demonstrate a statistically significant increase in adverse renal outcomes attributable to COVID-19 vaccination. Generally, observational and cohort studies report a low incidence of adverse renal effects after COVID-19 vaccination[19,70]. Tsai et al[30] further demonstrated a modestly increased hazard of AKI (HR = 1.20) and dialysis initiation (HR = 1.84) compared with unvaccinated controls, suggesting a temporal association between COVID-19 vaccination and adverse renal outcomes. However, there are studies that report otherwise, showing there is no statistically significant association between COVID-19 and AKI[15,76] or incidence in MCD, membranous nephropathy, pauci-immune glomerulonephritis or IgA nephropathy[20]. The discrepancies between observational studies likely reflect differences in study design, outcome definitions, comparator populations, background renal risk, and residual confounding, highlighting the inherent limitations of non-randomised data in establishing causality.

The presence of an association is further supported by consistent pharmacovigilance signals across all COVID-19 vaccine platforms, with reports of adverse renal outcomes, including renal failure, described by Nurminen et al[72]. However, the contrast between strong disproportionality signals and low absolute incidence in population-based studies suggests that these reports may represent rare idiosyncratic immune-mediated events, reporting bias due to increased surveillance, or unmasking of pre-existing subclinical kidney disease, rather than a widespread vaccine-related nephrotoxic effect. Collectively, these findings suggest that while AKI has been temporally associated with vaccination, a consistent population-level increase in risk has not been established. Nonetheless, when considered alongside the substantial number of case reports identified in this review, continued clinical vigilance remains warranted. Notably, data from patients with pre-existing CKD were reassuring. Vaccinated individuals with CKD demonstrated lower risks of major adverse kidney events and mortality in some cohorts, consistent with the protective effect of vaccination against severe COVID-19 infection, a well-established cause of AKI[31]. These findings support current recommendations advocating vaccination in CKD populations.

With respect to disease relapse, available evidence suggests small but measurable increases in relapse risk were observed for MCD, FSGS, IgAN, membranous nephropathy, and ANCA-associated glomerulonephritis following second or third vaccine doses in some cohorts, typically in the range of 1%-5% absolute risk increase[16,18,21,24,25]. In contrast, evidence regarding lupus nephritis and other forms of glomerulonephritis remains mixed, with some studies reporting an increased risk of flare[21] while others demonstrate low or no association[16,23,77]. Clinicians should therefore remain vigilant in patients with pre-existing glomerular disease, counsel regarding potential relapse, and actively monitor for early symptoms of renal deterioration following vaccination.

Evidence linking COVID-19 vaccination to tubulointerstitial nephritis, renal vasculitis, thrombotic microangiopathy, or thrombotic thrombocytopenic syndromes remains limited and largely confined to rare case reports and pharmacovigilance signals[68,77]. While disproportionality analyses identified signals for glomerulonephritis and tubulointerstitial nephritis, absolute incidence rates were extremely low[61]. The mRNA vaccines accounted for the majority of reported renal adverse events, reflecting their widespread global use rather than necessarily higher intrinsic risk. Despite numerous case reports describing diverse renal phenotypes and elevated reporting signals[60-63,79], large population-based[13,56-59] and 1 cohort study[14] consistently demonstrated low incidence rates of AKI and no statistically significant excess risk. Furthermore, while observational studies observed the presence of adverse renal effects following vaccination[11], there are population analysis that highlight that there is no statistically significant increased risk[20], reinforcing the overall reassuring safety profile.

Vector-based vaccines were associated with fewer reported renal events overall[60], though pharmacovigilance data suggested signals for glomerulonephritis and thrombotic syndromes[63,68]. While these signals warrant attention, the absence of consistent findings in large population-based studies limits causal inference. As with mRNA vaccines, these observations likely represent rare, event-specific risks rather than a generalized increase in renal injury. Inactivated vaccines were associated with limited renal safety data, with available studies suggesting low AKI incidence and no increased relapse risk in membranous nephropathy[13,27]. However, the small number of studies and limited follow-up mean that rare adverse renal events cannot be definitively excluded, and conclusions should be interpreted cautiously. Evidence for recombinant protein nanoparticle vaccines remains extremely sparse, precluding meaningful conclusions[69]. The absence of reported signals should not be interpreted as evidence of safety but rather as a consequence of limited exposure and under-representation in current datasets.

Influenza vaccine: The quantity and methodological quality of observational evidence examining renal adverse outcomes following inactivated seasonal influenza vaccination varied across different disease entities. The observational studies[40,41,54] assessing nephrotic syndrome consistently demonstrated no increased risk of disease onset or relapse in children, with one study[32] reporting a lower relapse risk among vaccinated children, providing reassuring evidence for the renal safety of influenza vaccination in this population. In contrast, evidence relating to pauci-immune vasculitis-associated glomerulonephritis remains limited, with multiple isolated case reports describing temporal associations with influenza vaccination, suggesting a potential signal that warrants further investigation. However, the currently available observational and interventional data[49] are underpowered due to small sample sizes and have not demonstrated statistically significant associations, precluding firm conclusions regarding causality.

Similarly, although the two observational studies[37,55] have reported no significant adverse effects of influenza vaccination on kidney allograft function or rejection risk, these findings were generally not statistically significant due to small sample sizes and the frequent absence of comparator groups. Together with isolated reports of post-vaccination renal events, this highlights the need for larger, well-designed observational studies with appropriate comparators to more definitively establish vaccine safety in kidney transplant and dialysis populations. Finally, while population-level pharmacovigilance analyses did not identify a safety signal for thrombotic thrombocytopenic purpura following influenza vaccination[68], thrombotic thrombocytopenic purpura remains a recognised cause of AKI when it occurs, and clinical vigilance for renal involvement is warranted in the rare event of vaccine-associated thrombotic thrombocytopenic purpura.

With respect to the impact of the pandemic H1N1 influenza vaccine on renal allograft function, the available evidence remains limited. Existing studies[34,36] are characterised by small sample sizes, low event rates, and wide confidence intervals, which restrict the precision of effect estimates. Consequently, while no clear signal of adverse allograft outcomes has been identified, the current data are insufficient to draw definitive conclusions regarding the absence of an effect. Larger, well-designed observational studies with adequate follow-up and appropriate comparators are therefore required to more robustly evaluate the relationship between influenza vaccination and renal allograft function.

Comparison with other vaccines

The presence of adverse renal effects is documented in other vaccines as well. As the hypothesis of the mechanism and pathogenesis of vaccine-related AKI is broadly applicable to most vaccine platforms, the presence of adverse renal effects in other vaccines is not uncommon. For example, a VAERS study found 26 cases of glomerulonephritis reported after administration of hepatitis B vaccines[92]. While such reports may signal a possible association, the available evidence remains limited and insufficient to establish causality, echoing our findings for the influenza vaccination. A similar heterogeneity in the evidence seen with COVID-19 vaccines is observed with other vaccines as well. For instance, for the meningococcal vaccine, 2 population-based studies found that there was no increased risk of nephrotic syndrome relapse following the vaccine[93,94]. In contrast, a cohort study found there was a significant increase in the relapse rate of nephrotic syndrome after administration of the meningococcal vaccine[95]. While large population-based studies suggest no clear increase in relapse risk, smaller clinically detailed cohorts raise the possibility of an association. This underscores the need for cautious interpretation of vaccine safety data in patients with underlying glomerular disease and supports ongoing post-marketing surveillance and targeted studies in high-risk populations.

Strengths of our paper

A key strength of this systematic review is the integration of multiple levels of evidence, including case reports, case series, observational cohort studies, and pharmacovigilance analyses, to examine AKI temporally associated with influenza and COVID-19 vaccination. By synthesising individual case reports and case series, this review provides a detailed characterisation of clinical manifestations, timing of onset, management strategies, and recovery trajectories, which may support clinicians in recognising and managing these rare and heterogeneous presentations in clinical practice.

In parallel, the inclusion of observational and pharmacovigilance studies offers a population-level perspective on the incidence and relative risk of vaccine-associated kidney injury, helping to contextualise individual case observations and mitigate the inherent limitations of case-based evidence. This dual approach allows for a more nuanced interpretation of the available data, balancing detailed clinical insights with broader epidemiological trends. By integrating individual-level and population-level evidence, this review provides a comprehensive and balanced synthesis of the current literature on vaccine-associated kidney disease, reflecting the scope and quality of evidence available to date.

Limitations of our paper

However, our paper is limited by the nature of the studies we have included. The case reports and series reported are isolated cases of temporally associated acute kidney disease and the vaccinations. They are rare and do not represent the true population hazard that vaccinations pose to the kidneys. They also do not prove the causality of AKI from vaccinations. The observational studies included are studies with a small cohort group, with many studies lacking an adequate comparator group. These studies hence produce results that are not statistically significant. This limits our study in providing a definite picture of the relationship between influenza and COVID-19 vaccines and AKI. Secondly, the literature search was limited to PubMed and EMBASE, which may have resulted in the omission of relevant studies indexed exclusively in other databases such as Web of Science or Scopus, as well as non-English literature, which may limit the completeness of data extraction and evidence synthesis. Future studies using broader database coverage and inclusion of grey literature may further strengthen the understanding of rare renal outcomes following vaccination.

Research gaps and future directions

We wish to emphasise that although reported renal adverse events following vaccination are rare, individual cases may present with clinically significant disease. To date, observational studies have not consistently demonstrated a causal relationship between vaccination and AKI; rather, findings remain heterogeneous, with some studies reporting low incidence, others suggesting modestly increased risk, and several demonstrating no significant association. Although available observational evidence does not clearly establish a causal relationship between vaccination and AKI, the presence of biologically plausible mechanisms and consistent temporal patterns in rare case reports supports the need for continued surveillance. These show that there is a positive signal to further investigate the relationship between renal effects and vaccinations. The current literature is limited by small sample sizes, heterogeneity in outcome definitions, and residual confounding, particularly in studies lacking appropriate comparator groups. Future research should prioritise large, well-designed population-based studies with appropriate unvaccinated or self-controlled comparators to better define absolute and relative renal risks following vaccination. Focused studies in patients with pre-existing glomerular disease may help identify susceptible subgroups and inform monitoring strategies. Importantly, given the shared immunological mechanisms across vaccine platforms, similar approaches may be applied to the evaluation of renal outcomes following other routine vaccinations.

In this systematic review, we synthesised evidence from case reports, observational cohorts, and pharmacovigilance databases to evaluate AKI and other renal complications temporally associated with COVID-19 and influenza vaccination. Across both vaccine types and platforms, population-level studies consistently demonstrate a low absolute risk of adverse renal outcomes, with no clear evidence of a sustained increase in AKI or glomerular disease attributable to vaccination. Despite this reassuring population-level safety profile, pharmacovigilance signals and numerous case reports describe rare instances of de novo or relapsing glomerular disease, including MCD, IgA nephropathy, membranous nephropathy, and ANCA-associated glomerulonephritis, often occurring shortly after vaccination. Most reported cases responded favourably to supportive or disease-specific therapy, and irreversible renal outcomes were uncommon. These findings likely reflect rare idiosyncratic immune-mediated events, heightened reporting, or unmasking of subclinical disease, rather than a widespread nephrotoxic effect of vaccines. Importantly, available evidence in patients with CKD, kidney transplantation, and nephrotic syndrome is largely reassuring, with several studies demonstrating reduced risks of AKI, disease progression, or mortality among vaccinated individuals, reinforcing the protective benefits of vaccination against severe viral infection.

CONCLUSION

Overall, the benefits of COVID-19 and influenza vaccination substantially outweigh the potential renal risks. While clinicians should remain vigilant for renal symptoms following vaccination, particularly in patients with pre-existing glomerular disease, these rare events should not deter vaccination. Ongoing post-marketing surveillance and well-designed population-based studies remain essential to further refine risk estimates and identify susceptible subgroups.

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Footnotes

Peer review: Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Urology and nephrology

Country of origin: Singapore

Peer-review report’s classification

Scientific quality: Grade B

Novelty: Grade B

Creativity or innovation: Grade B

Scientific significance: Grade B

P-Reviewer: Martínez-Sánchez FD, MD, Professor, Mexico S-Editor: Bai SR L-Editor: A P-Editor: Xu ZH

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