Glomerular Disease in Temporal Association with SARS-CoV-2 Vaccination: A Series of 29 Cases : Kidney360

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Original Investigation: Glomerular and Tubulointerstitial Diseases

Glomerular Disease in Temporal Association with SARS-CoV-2 Vaccination: A Series of 29 Cases

Caza, Tiffany N.1; Cassol, Clarissa A.1; Messias, Nidia1; Hannoudi, Andrew2; Haun, Randy S.1; Walker, Patrick D.1; May, Rebecca M.1; Seipp, Regan M.3; Betchick, Elizabeth J.4; Amin, Hassan5; Ziadie, Mandolin S.6; Haderlie, Michael7; Eduwu-okwuwa, Joy8; Vancea, Irina9; Seek, Melvin10; Elashi, Essam B.11; Shenoy, Ganesh12; Khalillullah, Sayeed13; Flaxenburg, Jesse A.14; Brandt, John15; Diamond, Matthew J.16; Frome, Adam17; Kim, Eugene H.18; Schlessinger, Gregory19; Ulozas, Erlandas20; Weatherspoon, Janice L.21; Hoerschgen, Ethan Thomas22; Fabian, Steven L.23; Bae, Sung Yong24; Iqbal, Bilal25; Chouhan, Kanwalijit K.26; Karam, Zeina27; Henry, James T.28; Larsen, Christopher P.1

Author Information
Kidney360 2(11):p 1770-1780, November 2021. | DOI: 10.34067/KID.0005372021
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination is considered safe in patients with kidney disease and is prioritized in this population due to increased mortality from coronavirus disease 2019 (COVID-19) (1). However, given the ability to activate the immune system, immunizations carry a risk of exacerbating disease or inducing flares in patients with glomerulonephritides. Prior to the onset of SARS-CoV-2 vaccinations, there were rare reports of immunizations temporally associated with glomerular disease. The incidence of these adverse events is unknown, although is likely exceedingly rare and is primarily described in single patient reports. Minimal change disease (MCD) has been reported in temporal association with influenza, hepatitis B, and tetanus-diphteria-poliomyelitis vaccinations. Additionally, crescentic glomerulonephritis (GN) has been triggered by influenza and pneumococcal immunizations (2).

The mechanism for which vaccines could elicit an autoimmune response resulting in GN is unknown, but it potentially could result from molecular mimicry of an antigen with host proteins in individuals with underlying genetic susceptibility or particular HLA haplotypes. Molecular mimicry has been described to induce autoimmune reactions in conjunction with influenza, hepatitis B, and human papillomavirus immunizations (3).

Currently, more individuals are being vaccinated than in any other time period before, and vaccinations include different vectors (nanoparticles or adenoviral-based replication-deficient virions). This worldwide vaccination program for SARS-CoV-2 during the COVID-19 pandemic provides an opportunity to investigate vaccine-related glomerular diseases. Here, we describe 29 cases of glomerular disease temporally associated with SARS-CoV-2 vaccination reviewed at a single center.

Materials and Methods

Patient Selection

Kidney biopsies from patients who developed AKI, nephritic syndrome, or nephrotic syndrome within 1 month of either the first or second dose of SARS-CoV-2 vaccination were included in the study, following approval by the Solutions Institutional Review Board. The guidelines of the Declaration of Helsinki for the protection of human subjects were followed. Native and allograft biopsies, as well as new-onset and recurrent kidney disease, were investigated. All kidney biopsies of patients with SARS-CoV-2 vaccine with close temporal association (within 1 month) to development of kidney disease were included to avoid selection bias. No patients in this study had known prior COVID-19. Kidney biopsies were reviewed at a single center, and clinical information was provided from nephrologists for clinicopathologic correlation.

Clinical Assessment and Follow-Up

Biopsies were reviewed at a single center, and clinical information was obtained (demographics, vaccine type, temporality to symptom onset, laboratory parameters, medical comorbidities, treatments, and follow-up). Clinical parameters included demographics, vaccine type, temporality of vaccine to onset of symptoms, laboratory parameters, medical history, treatments, and clinical follow-up. Patient demographics included age, race/ethnicity (which was physician-ascribed race), and sex. SARS-CoV-2 immunization types were recorded (Pfizer-BioNTech BNT162b2 mRNA, Moderna mRNA-1273, AstraZeneca adenoviral ChAdOx1 nCoV-19, or Johnson & Johnson/Janssen adenoviral JNJ-78436735). Documented medical comorbidities included preexisting chronic kidney disease (CKD; GFR <60 ml/min prior to disease onset), autoimmune disease, hypertension, diabetes, smoking, chronic obstructive pulmonary disease, and obesity. The number of weeks elapsed between the first and second vaccine doses to the time of biopsy and the number of days from vaccination to onset of symptoms were noted. Laboratory values included serum creatinine, proteinuria, hematuria, serologies (antinuclear antibodies, ANCA, hepatitis B, hepatitis C, and HIV), and serum albumin (grams per deciliter). Clinical follow-up parameters included the time interval between biopsy and last follow-up, treatment(s) provided prior to and after biopsy, requirement of kidney replacement therapy (KRT)/dialysis, clinical response, serum creatinine, and proteinuria.

Biopsy Database Comparisons

The frequencies of glomerular diseases during the period of mass vaccination (January 1, 2021–July 1, 2021) were compared with 2 years of biopsies evaluated by our laboratory prior to the pandemic (January 1, 2018–December 31, 2019) through searching a PowerPath kidney biopsy database by natural language searches and/or ICD10 codes. Within our database, the racial distribution includes 48.3% Whites, 15.4% Blacks, 4.7% Hispanics, 2.8% Asians, 1.9% Native Americans, and 27.0% patients of unknown descent (4). This is representative of the kidney biopsy database, although the demographics of each individual clinical practice submitting these biopsies are unknown.

Pathologic Assessment

Histopathologic review included evaluation of light, immunofluorescence, and electron microscopy processed by standard techniques. Light microscopy parameters included mesangial expansion, mesangial hypercellularity, endocapillary hypercellularity, fibrinoid necrosis, crescent formation, segmental sclerosis (including type according to the Columbia classification), and presence/absence of microangiopathic changes within glomeruli. Tubulointerstitial changes evaluated included acute tubular injury, interstitial edema, interstitial inflammation, lymphocytic tubulitis, interstitial fibrosis, and tubular atrophy. Vascular assessment included degree of arteriosclerosis and arteriolar hyalinosis. Immunofluorescence included IgA, IgG, IgM, C3, C1q, albumin, fibrinogen, and κ- and λ-light chain staining for all cases and was graded on a 0–3+ scale. Ultrastructural features recorded included the presence/absence of subepithelial, subendothelial, and mesangial electron dense deposits, as well as the degree of podocyte foot process effacement.

For biopsies with membranous nephropathy (MN), immunostaining for antigenic targets was performed using antibodies against phospholipase A2 receptor (PLA2R; Sigma-Aldrich; catalog no. HPA012657), neural epidermal growth factor like-1 (NELL1; Novus Biologicals; catalog no. H00004745), thrombospondin type 1 domain containing 7A (THSD7A; Atlas Antibodies; catalog no. AMA91234), and exostosin 1 (EXT1; Invitrogen; catalog no. PA5–27958). For all antigens, presence of granular capillary loop staining (1+ or greater) was considered a positive result.

APOL1 Genotyping

Genotyping for APOL1 G1 and G2 risk alleles was performed in patients with collapsing glomerulopathy (CG). Briefly, APOL1 genotyping was performed by nested multiplex PCR to amplify the regions of the APOL1 gene carrying the G1 single nucleotide polymorphism (rs73885319) and the G2 six–base pair insertion/deletion (rs71785313). A ViiA 7 real-time PCR system was used to perform TaqMan PCR. Data were evaluated on ViiA7 sequence detection software. Allelic discrimination plots were used to determine the call results.

Statistical Analyses

Means±SDs were used to compare patients’ ages. Other continuous variables were assessed by median±interquartile range (IQR). Frequency data were compared using chi-squared testing with GraphPad Prism software with a cutoff of P=0.01 for significance.

Literature Review

All patient reports and series describing glomerular disease in temporal association with SARS-CoV-2 vaccination were included in a review of the literature. PubMed and Google Scholar were used to identify articles, and only those written in the English language were included.


Twenty-nine patients with kidney disease within 1 month of SARS-CoV-2 vaccination were identified; all had glomerular disease. Twenty-eight patients had native kidney biopsy (all of which were de novo GN), and there was one case of recurrent disease in a transplant recipient identified on allograft biopsy. Of the 29 patients, 27 received mRNA vaccines (11 Moderna, 12 Pfizer-BioNTech, and four unknown), and two received adenoviral vaccines (one Johnson & Johnson/Jensen and one AstraZeneca). Patients with an unknown vaccine type were vaccinated during a time period where only the Moderna and Pfizer-BioNTech vaccines were available under the Food and Drug Administration's emergency release authorization. Twenty-three patients who had mRNA vaccines received two vaccine doses. There were 12 men and 17 women, with a mean age of 55.2±19.3 years. Twenty patients were White, two were Black, three were Asian, one was Indian, and three were of Hispanic descent. Twenty-two patients had at least one comorbidity, including hypertension (n=16), diabetes mellitus (n=7), obesity (n=9), smoking (n=2), chronic obstructive pulmonary disease (n=4), autoimmune disease(s) (n=8), and CKD (n=7).

The most common presentation was AKI with concurrent nephritic or nephrotic syndrome (n=15), followed by nephritic syndrome (n=11) and nephrotic syndrome with preserved kidney function (n=3) (Table 1). A majority of patients had an elevated serum creatinine (median, 2.17±3.455 IQR, 1.195; 4.65), 28 had proteinuria (nephrotic range in 12 patients), 25 had hematuria, and 23 had hypoalbuminemia (of 27 with available data; median, 2.75±1.1 IQR, 2.3; 3.4). Five patients had hypocomplementemia (of 24 with available data). Twelve patients had antinuclear antibodies, and ten had a positive ANCA serology (Table 1). One patient had a positive hepatitis C serology (of 22 patients with data available), and one patient was HIV positive (of 18 patients with available data). There were no patients who were positive for hepatitis B sAg (n=22).

Table 1. - Clinical and laboratory features of patients with severe acute respiratory syndrome coronavirus 2 vaccine–associated glomerular disease
Patient Number Age, yr Sex Race Vaccine Type 1st/2nd Dose a Time Indication Diagnosis Creatinine Proteinuria Albumin Hematuria Antinuclear Antibodies ANCA Treatment before Biopsy Treatment after Biopsy Follow-Up Recovery Follow-Up Creatinine Follow-Up Proteinuria
1 67 F B Moderna 7 wk/3 wk <1 wk AKI, n.s. CG 6.7 12 2.7 Pos Neg Neg D D; IS 1 12 wk Partial 1.8 2.5
2 26 F B Moderna 5 wk/1 wk <1 wk AKI, n.s. CG, MN 7.7 6 2.4 Pos Pos Neg D; IS 1+IS 2 D; IS 3 1 wk No D* D*
3 70 F W Pfizer 7 wk/3 wk <1 wk AKI, n.s. MCD 2.2 19.2 1.5 Neg Neg ND Diur IS 1 4 wk Yes 1 Neg
4 43 F Indian Pfizer 11 wk/7 wk 2 wk n.s. MCD Unk 10 1.9 Neg Neg Neg None IS 1 4 wk Yes <1 Neg
5 79 M Asian mRNA a 2 wk <2 wk AKI, n.s. MCD 2.1 4+ Low Pos Pos Neg IS 1; Diur IS 1 4 wk No 2.5 UA 3+
6 72 M W Moderna 9 wk/5 wk 1 wk n.s. MCD 0.7 16.1 2.7 Pos Pos Neg Diur; ARB IS 1, ACEI 2 wk Yes 0.9 UA Pos
7 47 F W Pfizer 5 wk/1 wk <2 wk AKI, n.s. MCD 6.1 >600 mg/dl 1.9 Neg Neg Neg D D; IS 1; ACEI 4 wk No 4.3; D* UA Pos; D*
8 23 M W AstraZeneca 2 wk 2 wk AKI, n.s. MCD 2.9 14 1.7 Pos Pos Neg None IS 1; Diur 3 wk Yes 1.0 0.07
9 45 F W Moderna <2 wk <2 wk n.s. MCD 0.86 6 2.8 Pos Neg Neg Diur IS 1 NA NA NA NA
10 33 F W Pfizer 4 wk/<1 wk 2 d Nephritic IgA N 1.1 0.6 4.0 Pos Neg Neg None None None a Unk WNL Unk
11 52 F W mRNA a 5 wk/2 wk 1 d, both Hem IgA N 1.7 0 ND Pos Neg Neg None None 6 wk Yes <1 Neg
12 37 F W mRNA a 5 wk/<2 wk 12 d Nephritic IgA N 1.4 3.5 3.1 Pos Neg Neg None IS 1; ACEI 7 wk No Unk UA Pos
13 35 M W Pfizer 6 wk/3 wk 1 d Nephritic IgA N 1.4 >300 mg/dl 4.2 Pos Neg Neg ARB IS 1; ARB 2 wk No Unk Unk
14 72 F Hisp Pfizer 10 wk/7 wk 2 d AKI, nephritic IgA N 4.9 0.6 ND Pos Neg Pos IS 1 IS 1; IS 5 2 wk No 4 UA Pos
15 57 M W Moderna 4 wk/ 3d 1 d AKI, CKD, nephritic IgA N 6.2 3+ 2.5 Pos Neg Neg Diur IS 1; IS 5 4 wk No 8; D* Pos; D*
16 30 M W Pfizer 4 wk/<1 wk 1 d Nephritic IgA N 1.1 2 4.2 Pos Neg Neg None None 2 wk Yes 1.1 UA Pos
17 40 F W Moderna 4 mo/3 mo <1 wk Nephritic IgA N 1.3 30 mg/dl 3.4 Pos Pos Pos None ARB 2 wk No Unk Unk
18 73 M W Pfizer 3 mo/2 mo 2 wk AKI, nephritic IgA N, AIN 3.4 0.5 1.9 Pos Pos Neg None IS 1 2.5 wk Partial 1 2.4
19 66 M Hisp mRNA a 6 wk/3 wk 3 d AKI, nephritic IgA N, DN 9.77 3.3 2.4 Pos Neg Neg D D 4 mo No D* D*
20 76 M W Pfizer 7 wk/<3 wk 11 d AKI, nephritic Cres GN 8.6 2+ 2.3 Pos Pos Pos D D, IS 1, IS 4 3 wk No 5.8 Unk
21 81 F W Pfizer 6 wk/3 wk 2 d AKI, nephritic Cres GN 3.1 1.8 3.4 Pos Pos Pos None IS 4, ARB 3 wk No 2.2 2.3
22 76 F W Moderna <1 wk 5 d AKI, nephritic Cres GN 3.0 2 3.1 Pos Pos Pos IS 1 IS 1, IS 4 5 wk Partial 1.1 2+
23 71 F W Moderna 4 mo/3 mo 2 wk Nephritic Cres GN 1.3 2.1 3.3 Pos Pos Pos IS 1 IS 1, IS 4 1 wk No NA NA
24 65 F W Pfizer 4 mo/3 mo 2 wk AKI, nephritic Cres GN 3.29 2.07 2.2 Pos Neg Pos None IS 1, IS 5 2 wk No 4.83 2.9
25 79 F W Moderna 8 wk/5 wk 3 wk Nephritic Cres GN (recur) 1.12 20 mg/dl 4.0 Pos Neg Pos IS 1, IS 3, IS 6 IS 4 4 mo Yes 0.82 None
26 54 M Asian Moderna 12 wk/9 wk 1 d Nephritic MN 1.3 3+ 3.4 Pos Pos Pos None IS 1, IS 4 8 wk No 0.86 3.5
27 68 M W J+J 4 wk < 4 wk AKI, CKD, nephritic MN 3.3 0.6 3.2 Neg ND Neg Diur Diur 3 wk Partial 2.74 0.38
28 47 M Asian Moderna 8 wk/5 wk 6 d Nephritic MN 0.7 2.7 2.3 Pos ND Neg None None 2 wk Partial 0.7 2.7
29 16 F Hisp Pfizer 4 wk 2 d Nephritic Diffuse LN 0.7 0.8 3 Pos Pos Pos None IS 1 2 wk Yes 0.48 0.53
F, woman; B, Black; n.s., nephrotic syndrome; CG, collapsing glomerulopathy; Pos, positive; Neg, negative; D, dialysis; I.S. 1, immunosuppression 1: steroid therapy (methylprednisolone or high-dose prednisone); MN, membranous nephropathy; I.S. 2, immunosuppression 2: plasmapheresis; I.S. 3, immunosuppression 3: mycophenolate mofetil; D*, measurement unknown or inaccurate due to patient on dialysis (creatinine and/or proteinuria value unreliable); W, White; MCD, minimal change disease; ND, not done; Diur, diuretics; Unk, unknown; M, man; UA, urinalysis; ARB, angiotensin receptor blocker; ACEI, angiotensin-converting enzyme inhibitor; NA, not applicable; IgA N, IgA nephropathy; WNL, within normal limits; Hem, hematuria; Hisp, Hispanic; I.S. 5, immunosuppression 5 (cyclophosphamide); AIN, acute interstitial nephritis; DN, diabetic nephropathy; Cres GN, crescentic GN; I.S. 4, immunosuppression 4 (rituximab); I.S. 6, immunosuppression 6 (calcineurin inhibitor); J+J, Johnson & Johnson; LN, lupus nephritis.
aPatient 10 had no impairment of kidney function, where clinical follow-up would not be required for months.

Prior to biopsy, six patients received immunosuppression, six had diuretic therapy, and five required dialysis. Three patients had oliguria. At follow-up (median, 20 days±IQR 43, 13; 56; n=27 patients), 22 patients received immunosuppression (most commonly corticosteroids). Eight patients had full recovery of kidney function, with return to baseline creatinine, proteinuria, and albumin levels and absence of blood and protein on urinalysis. Five patients showed partial recovery, with a reduction in serum creatinine but with persistent hematuria and/or proteinuria. Fourteen patients had no improvement in kidney function, and five required dialysis (Table 1).

Biopsy diagnoses included IgA nephropathy (IgAN; n=10), MCD (n=7), CG (n=2), crescentic GN (n=6), MN (n=3), and diffuse lupus nephritis (n=1). One of the patients with CG had concurrent exostosin-positive MN. One patient with MN was positive for PLA2R. The remaining MN cases were negative for PLA2R, THSD7A, NELL1, and EXT. All patients with crescentic GN had a positive ANCA serology (Table 1). Additionally, two patients with IgAN had a positive ANCA, and one of which had crescentic disease. Both patients with CG were of Black descent and were homozygous for APOL1 high-risk alleles (G1/G1 and G1/G2). Histopathologic features are shown in Table 2.

Table 2. - Histopathology of severe acute respiratory syndrome coronavirus 2 vaccine–related glomerular disease biopsies
Patient Number Diagnosis Global Glomerulosclerosis Mesangial Matrix Expansion Mesangial Hyper cellularity Endocapillary Hyper cellularity Necrosis Crescents Segmental Sclerosis Acute Tubular Injury Interstitial Fibrosis/ Tubular Atrophy Arterio sclerosis Arteriolar Hyalinosis Immunofluorescence Mesangial Deposits Subend othelial Deposits Subepi thelial Deposits Foot Process Effacement
1 CG 0/24 No No No No No Yes Yes Mild No No No staining No No No Severe
2 CG, MN 0/45 No No No No No Yes Yes Mild Mild No 3+IgG and C3, gr cap loop Yes No Yes Severe
3 MCD 1/31 No No No No No No Yes None No No No staining No No No Severe
4 MCD 0/35 No No No No No No Yes Mild Mod Mild No staining No No No Severe
5 MCD 3/33 Yes No No No No No Yes Mild Mod No No staining No No No Severe
6 MCD 0/20 Yes Yes No No No No No No No No No staining No No No Severe
7 MCD 6/30 No No No No No No Yes No Mod Mild No staining No No No Severe
8 MCD 0/40 No No No No No No Yes No No No No staining No No No Severe
9 MCD 0/60 No No No No No No No No No No No staining No No No Severe
10 IgA N 1/29 Yes Yes Yes No No Yes No No No No 3+IgA and C3 gr mes Yes Yes No None
11 IgA N 3/27 No No No No No No No No No No 3+IgA gr mes Yes No No Mild.
12 IgA N 1/16 Yes Yes Yes No No No Yes No Mild Mild 3+IgA+C3, 1+IgG gr mes Yes No Yes Mod
13 IgA N 0/86 Yes Yes No No Yes No Yes No No No 3+IgA gr mes Yes No No Mod
14 IgA N 10/40 Yes Yes No Yes Yes Yes Yes Mod Mod Mild 2+IgA+IgM, 3+C3, trace IgG gr mes No No No Mild
15 IgA N 23/52 Yes Yes Yes Yes Yes Yes Yes Yes Severe Mod 2+IgA, 1+C3 gr mes Yes No No Mod
16 IgA N 2/50 Yes Yes No No No Yes Yes Mild Mod No 3+IgA, 2+IgG, 3+C3 gr mes Yes Yes Yes Mild
17 IgA N 6/19 Yes No No No No No Yes Mild Mod No 3+IgA, trace IgG, 2+C3 gr mes Yes No No Mod
18 IgA N, AIN 1/13 Yes No No No No No Yes No N/A Mild 3+IgA, 1+IgG, 2+IgM, trace C3 gr mes Yes No No Mod
19 IgA N, DN 35/46 Yes Yes No No No Yes No Severe Severe Severe 1+IgA, 1+IgG, 1+IgM gr mes No No No Mod
20 Cres GN 1/24 No No No Yes Yes No No Mild Severe No 2+IgA, 1+C3 gr mes No No No Severe
21 Cres GN 4/13 Yes No No No Yes Yes Yes Mild Severe Mild 1+IgM, trace C3 gr mes No No No Mild
22 Cres GN 9/36 No No No Yes Yes No Yes Mild Severe Mod 3+C3 gr mes Yes No No Severe
23 Cres GN 20/29 No No No No No No Yes Mod Severe No 3+IgM, 1+C3 gr mes Yes No No Mod
24 Cres GN 5/30 No No No Yes Yes No Yes Mod N/A No 1+IgG, 1+C3 gr cap loop N/A N/A N/A N/A
25 Cres GN 13/51 No No No Yes Yes Yes Yes Mild No No No staining No No No None
26 MN 3/15 No No No No Yes Yes Yes No No Mod 3+IgG, 2+C3 gr cap loop Yes No Yes Severe
27 MN 20/29 No No No No No Yes Yes Mild Severe No 2+IgG, 2+IgM gr cap loop No No Yes Severe
28 MN 1/39 No No No No No No No Mild No No 3+IgG, 2+C3 gr cap loop No No Yes Severe
29 Diffuse LN 0/55 Yes Yes Yes No No No No No No No 3+IgA, 3+IgG, 3+IgM, 3+C3, 3+C1q gr mes +gr cap loop Yes No Yes Mod
CG, collapsing glomerulopathy; MN, membranous nephropathy; gr cap loop, granular capillary loop; MCD, minimal change disease; Mod, moderate; IgA N, IgA nephropathy; gr mes, granular mesangial; AIN, acute interstitial nephritis; N/A, not applicable; DN, diabetic nephropathy; Cres GN, crescentic GN; LN, lupus nephritis.

In three patients, confounding factors were present that could represent additional or alternative antigenic triggers. These included long-term nonsteroidal anti-inflammatory drug use in a patient with MCD, although there was no recent increase or change in nonsteroidal anti-inflammatory drug use prior to vaccination. There was one patient with crescentic GN who had prior hydralazine use, although use was discontinued prior to the time of biopsy. One patient with IgAN had concurrent HIV infection, although IgAN is an unlikely cause of HIV-associated immune complex disease of the kidney.

There was no significant increase in kidney biopsy diagnoses of glomerular diseases during this period of mass vaccination. Although not an epidemiologic study, the frequency of diagnoses during this period (1/1/2021–7/1/2021; n=11,192 cases) was compared with each diagnosis 2 years prior to the COVID-19 pandemic and SARS-CoV-2 vaccination (1/1/2018–12/31/2019) through searching a biopsy database (n=36,389 cases). The overall frequencies of these glomerular diseases were not increased during this period of mass vaccination compared with prior to the pandemic for MCD (1.8% versus 2.2%; P=0.007), IgAN (7.0% versus 7.2%; P=0.70), pauci-immune crescentic GN (4.4% versus 4.4%; P>0.99), CG (2.6% versus 2.3%; P=0.06), and MN (5.6% versus 5.4%; P=0.41). The slight, nonsignificant increase in CG during this time period may be related to COVID-19–associated nephropathy cases (5). The true incidence of glomerular disease is unknown, as this is from a single center, and not all patients with glomerular disease (particularly those with recurrence) would undergo kidney biopsy.


In the recent literature, multiple cases of kidney disease temporally related to SARS-CoV-2 vaccination have been reported (n=52 patients), including IgAN (n=20) (6789101112131415–16), MCD (n=17) (17181920212223242526272829–30), ANCA-associated pauci-immune crescentic GN (n=5) (313233–34), antiglomerular basement membrane antibody disease (n=2) (6,35), MN (n=3; of which one was PLA2R positive and one was THSD7A positive) (3637–38), membranous lupus nephritis (n=1) (39), IgG4-related kidney disease (n=1) (40), granulomatous interstitial nephritis (n=1) (41), thrombotic microangiopathy with sclerodermal renal crisis (n=1) (42), and T cell–mediated allograft rejection (n=1) (43) (Table 3). These reports included 27 cases of new-onset glomerular disease, with the remainder being relapses of patients with prior biopsy-proven GN (Table 3). Although we identified many of the same pathologic findings, unique to our series are cases of CG and proliferative lupus nephritis. Of note, there were no patients of African descent reported with vaccine-related glomerular disease in the literature, although race was not mentioned for all patients; only 12 of 52 patients had race mentioned, of which ten were White and two were of Asian descent. Although allograft rejection was reported in association with SARS-CoV-2 vaccination, we did not identify any cases of rejection at our institution.

Table 3. - Severe acute respiratory syndrome coronavirus 2 vaccine–associated glomerular disease cases reported in the literature
Patient Number N Diagnosis Age, yr Sex Type 1st/2nd Time Indication Serum Creatinine Proteinuria Hematuria Serum Albumin Antinuclear Antibodies ANCA Treatment Follow-Up Recovery Follow-Up Creatinine
6 (new) 2 IgAN; anti-GBM 41; 60 F; F Pfi; Toz 2nd 1 d Nephritic; AKI+n.s. 1.73; 6.12 2.03; 7.58 Yes; Yes Unk Pos; Neg Unk I.S. 1+I.S. 5; I.S. 1+I.S. 2 NA NA NA
7 (new) 2 IgAN; Cres GN 39; 81 M; M Mod 1st Unk Nephritic; AKI Inc; Inc Pos; Pos Yes Unk Unk Unk; Pos I.S. 1+I.S. 5; I.S. 1+I.S. 2+I.S. 5 NA No; Yes Unk
8 (recur) 3 IgAN 22; 41; 27 M; F; F Mod; Pfi; Pfi 1st; 2nd; 2nd 2 d Nephritic Unk 0.34; 0.47; 1.9 Yes Unk Unk Unk I.S. 1+RAASi; I.S. 1+I.S. 3+I.S. 6; I.S. 1+I.S. 3+I.S. 6 Unk Yes; Yes; Yes Unk
9 (new) 2 IgAN 50; 19 F; M Mod 2nd 2 d Nephritic 1.7; 2.1 2.0; None Yes Unk Neg; Unk Neg; Unk None 5 d; 2 d Yes; Yes Unk
10 (1 new, 1 recur) 2 IgAN 13; 17 M; M Pfi 2nd 1 d AKI+ nephritic 1.31; 1.78 1.1; 1.8 Yes; Yes 3.4; 3.8 Unk Unk ACEI; I.S. 1 1 wk; Unk Yes; No Unk
11 (recur) 2 IgAN 38 F; F Mod 2nd 1 d Nephritic Unk 0.82; 0.59 Yes; Yes Unk Unk Unk None 21 d Yes Unk
12 (recur) 1 IgAN 52 F Pfi 2nd 1 d Nephritic Unk 2.4 Yes Unk Unk Unk Unk 1 wk Partial Unk
13 (recur) 4 IgAN 22; 39; 50; 67 F; F; M; M Mod; Mod; Mod; Mod 2nd 2 d; 2 d; 1 d; 4 wk Nephritic Unk; Unk; Unk; Unk 0.4; 0.9; 3.56; 2.10 Yes; Yes; Yes; Yes Unk Unk Unk None; None; RAASi; I.S. 1 4 wk; 4 wk; 4 wk; 4 wk Yes; Yes; Yes; Yes Unk; Unk; Unk; Unk
14 (new) 1 IgAN 30 M Pfi 2nd 1 d Nephritic 1.02 4+ Yes Unk Neg Neg RAASi 6 wk Partial 1.03
15 (recur) 1 IgAN 78 F Mod 1st 7 d Nephritic 1.18 Unk Yes Unk Neg Neg I.S. 1 Unk Yes Unk
16 (recur) 2 IgAN Unk Unk Pfi 2nd 5 d AKI+nephritic 3.53; 1.16 4.97;0.61 Yes Unk Unk Unk I.S. 1 2 mo Yes Unk
17 (new) 1 MCD 77 M Pfi 1st 7 d n.s. 2.33 4+ Unk 3.0 Unk Unk I.S. 1 21 d No 3.74
18 (new) 1 MCD 50 M Pfi 1st 4 d AKI+n.s. 2.31 6.9 Unk 1.93 Neg Neg I.S. 1 17 d Yes 0.97
19 (recur) 1 MCD 34 F Pfi 1st 10 d n.s. Unk 2.4 Unk Unk Unk Unk I.S. 1 Unk Partial Unk
20 (recur) 2 MCD 30; 40 M; F AZ 1st 2 d; 1 d Nephritic; n.s. 0.931.19 0.21; 3+ Unk 4.7; Unk Unk Unk I.S. 1; I.S. 1+I.S. 6 10 d; 14 d Yes; Yes Unk
21 (new) 1 MCD 63 F Pfi 1st 7 d n.s. 1.48 3+ Yes 0.7 Unk Unk ARB; I.S. 1 Unk Unk Unk
22 (new) 1 MCD 80s M Pfi 1st 7 d n.s. 1.43 15.3 Unk 1.0 Unk Unk I.S. 1 10 d Yes Unk
23 (recur) 1 MCD 60s M Pfi 1st 8 d n.s. 0.99 11.5 Unk 2.8 Unk Unk I.S. 1+I.S. 6 14 d Yes Unk
24 (recur) 1 MCD 22 M Pfi 1st 3 d n.s. 0.8 3+ Unk 2.3 Unk Unk I.S. 1+I.S. 6 17 d Yes Unk
25 (recur) 1 MCD 39 M Pfi 1st 3 d AKI+n.s. 1.8 8 Unk 2.7 Unk Unk I.S. 1 4 wk Yes Unk
26 (new) 1 MCD 61 F Pfi 1st 8 d n.s. 1.47 12 Unk 2.1 Neg Neg D; I.S. 1 21 d Partial Unk
27 (1 new, 2 recur) 3 MCD 33;41; 34 F; F; F Mod; Pfi; Pfi 2nd 3 wk; 5 d; 4 wk n.s.; n.s.; n.s. Unk; Unk; Unk 6.4;14.4;12.9 Unk; Yes; Unk 2.3;2.6;2.8 Unk; Unk; Unk Unk; Unk; Unk Unk Unk Unk Unk
28 (new) 1 MCD 51 M J+J 1st 28 d n.s. 1.54 8.6 Yes 1.6 Neg Neg I.S. 1 2 wk Yes 0.95
29 (new) 1 MCD 71 M AZ 1st 13 d AKI+n.s. 10.6 20.5 Yes 2.6 Neg Neg I.S. 1; D 38 d Yes 1.4
30 (new) 1 MCD 19 F AZ 1st 8 d n.s. 1.09 3.18 Unk 2.15 Unk Unk I.S. 1 Unk Yes Unk
31 (new) 1 Cres GN, ANCA 29 F Pfi 2nd 7 wk Nephritic; AKI 1.91 0.633 Yes 4.4 Unk Pos I.S. 1; I.S. 4; I.S. 5 10 wk Yes 1.01
32 (new) 1 Cres GN, ANCA 52 M Mod 2nd 14 d Nephritic; AKI 8.41 1+ Yes Unk Unk Pos D; I.S. 5 Unk No Unk; D
33 (new) 1 Cres GN, ANCA 78 F Pfi 2nd 8 d Nephritic; AKI 3.54 2.05 3+ Unk Unk Pos, MPO I.S. 1; I.S. 4 1 mo Partial 1.71
34 (new) 1 Cres GN, ANCA 63 M AZ 1st 2 d Nephritic; AKI 2.91 2+ Yes Unk Unk Pos I.S. 1; I.S. 5 6 wk Partial 2.09
35 (new) 1 Cres GN, anti-GBM NA F Mod 2nd 14 d AKI 7.8 1.9 Yes Unk Neg Neg D; I.S. 1+I.S. 2+I.S. 5 Unk No Unk
36 (new) 1 MN 66 F Sino 1st 14 d n.s. 2.78 9.42 Unk 2.6 Unk Unk Unk NA NA NA
37 (recur) 1 MN. THSD7A Pos 70 M Pfi 2nd 1 d n.s. 1.29 4.4 Yes 1.7 Unk Unk ARB; diuretics 2 mo No Unk
38 (new) 1 MN, PLA2R Pos (no biopsy) 76 M Pfi; Mod (2nd) 1st 4 d n.s. 0.86 6.5 Yes 1.6 Unk Unk I.S. 4 2 mo Partial 1.15
39 (recur) 1 MLN 42 F Pfi 1st 1 wk n.s. wnl 8.4 Neg Low Pos Unk I.S. 1; I.S. 3 3 wk Partial Unk
40 (recur) 1 IgG4 KD 66 M Pfi 2nd 14 d AKI 2.38 Unk Unk Unk Neg Unk I.S. 1+I.S. 4 Unk Yes 0.57
41 (new) 1 Gran TIN 77 M AZ 1st 4 wk AKI 2.78 Neg Neg Unk Neg Neg I.S. 1 4 wk Yes Unk
42 (new) 1 TMA/SRC 34 F Pfi 1st <1 wk AKI 2.07 0.8 Neg Unk Neg Unk ACEi 1 wk Yes Unk
43 (new) 1 TCMR 23 F Pfi 2nd 8 d AKI 4.07 Unk Unk Unk Pos Unk I.S. 1+I.S. 3+I.S. 6 10 d Partial 2.6
The designations of (new) or (recur) represent de novo glomerular disease or recurrent glomerular disease for each report. IgAN, IgA nephropathy; GBM, glomerular basement membrane antibody disease; F, woman; Pfi, Pfizer-BioNTec BNT162b vaccine; Toz, BioNTech Tozinameran mRNA vaccine; n.s., nephrotic syndrome; Unk, unknown; Pos, positive; Neg, negative; I.S. 1, immunosuppression 1: steroid therapy (methylprednisolone or high-dose prednisone); I.S. 5, immunosuppression 5 (cyclophosphamide); I.S. 2, immunosuppression 2: plasmapheresis; NA, not applicable (lack of follow-up data); Cres GN, crescentic GN; M, man; Mod, Moderna mRNA-1273 vaccine; Inc, XXX; RAASi; renin-angiotensin-aldosterone system inhibitor; I.S. 3, immunosuppression 3: mycophenolate mofetil; I.S. 6, immunosuppression 6 (calcineurin inhibitor); ACEI, angiotensin-converting enzyme inhibitor; MCD, minimal change disease; AZ, AstraZeneca AZD1222/ChAdOx1-nCoV-19 vaccine; D, dialysis; J+J, Johnson & Johnson; I.S. 4, immunosuppression 4 (rituximab); MPO, myeloperoxidase; MN, membranous nephropathy; Sino, Sinovac-Coronovac vaccine; THSD7A, thrombospondin type 1 domain containing 7A; ARB, angiotensin receptor blocker; PLA2R, phospholipase A2 receptor; MLN, membranous lupus nephritis; wnl, within normal limits; IgG4 KD, IgG4-related kidney disease; Gran TIN, granulomatous tubulointerstitial nephritis; TMA, thrombotic microangiopathy; SRC, scleroderma renal crisis; ACEi, angiotensin converting enzyme inhibitor; TCMR, acute T cell-mediated rejection.

Both mRNA and adenoviral vaccines have been associated with induction of glomerular disease in patients vaccinated against SARS-CoV-2. Although the vector varies (lipid nanoparticles versus replication-deficient adenovirus), the antigenic target is common between these—the SARS-CoV-2 spike protein. The mechanism for this phenomenon is unknown but potentially, could result from molecular mimicry of the spike protein with host peptides.

The most common disease manifestation in our series and in the literature is IgAN (44). An IgA immune response against SARS-CoV-2 spike protein (45) could trigger IgAN in patients who produce galactose-deficient IgA antibodies, as previously reported with influenza vaccine (46). In a study of 89 patients with IgAN who received at least one dose of SARS-CoV-2 vaccine, no patients had gross hematuria or impaired kidney function at follow-up (47). In 29 patients examined in a shorter time interval (mean=11 days), two patients had a mild increase in serum creatinine with mild hematuria and proteinuria. This suggests that although IgA flare is possible, the incidence is <10% of individuals who had self-resolved in this series (47).

CG, although a common cause of AKI in COVID-19, has not been previously described in the setting of vaccination. CG is well described in association with COVID-19 infection, in which the pathogenesis is thought to be related the inflammatory response against the virus acting as a “second hit” to APOL1 risk alleles (48) rather than resulting from direct viral infection of the renal parenchyma. Likewise, the immune response to the SARS-CoV-2 spike protein from immunization may induce a similar “second hit” in susceptible individuals. Similarly, in patients with lupus, the immune response to COVID-19 disease or vaccination could be a trigger for disease flares (49).


Given that there is only a temporal relationship between the onset of symptoms and vaccination, causality is unclear. It is possible that immunization did not trigger the onset of glomerular disease within all of these patients. The study was restricted to patients developing glomerular disease within 1 month of SARS-CoV-2 vaccination and did not compare with other time frames. This 1-month cutoff, although arbitrary, is similar to that of cases reported in the literature (Table 2).

Although there was no overall increase in glomerular disease diagnosed on biopsies during the time of mass SARS-CoV-2 vaccinations in our practice, there was no control group for comparison for a patient-control design, and we did not conduct an epidemiologic study. We are thus unable to determine the frequency of glomerular injury after vaccination. Further data are required to determine the true risk of induction or flare of glomerular disease in response to SARS-CoV-2 vaccination.


The current mass vaccination against the SARS-CoV-2 virus provides the ability to observe the association of glomerular disease with vaccination. Although there are cases of glomerular disease in temporal association with vaccination, we do not know the true incidence or prevalence of disease. Within clinical trials, patients who were immunosuppressed (including those with glomerular disease) were excluded. This results in a lack of safety and efficacy data for SARS-CoV-2 vaccines within this population (50). As patients with kidney disease have an increased risk of morbidity and mortality from COVID-19, it is a priority to immunize these individuals against SARS-CoV-2. Additionally, as poorer immune responses are generated in response to vaccination, more potent vaccines (i.e., mRNA) and booster doses are recommended (1). Further data are required to determine the incidence of glomerular disease induction or recurrence in response to vaccination, response to therapy, and long-term clinical outcomes. To examine this, a registry has been created at the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases to examine these outcomes (International Registry of COVID infection in Glomerulonephritis-2). We suggest that new-onset or recurrent glomerular disease should be monitored as a potential adverse event.


J.T. Henry reports ownership interest in Fort Smith Regional Dialysis. G. Schlessinger reports consultancy agreements with Medtronic and ownership interest in US Renal Care. Z. Karam reports honoraria from Spherix. R.M. Seipp reports honoraria from M3 Global Research and Spherix Global Insights. P.D. Walker reports consultancy agreements with Apellis and Travere and honoraria from Apellis and Travere. All remaining authors have nothing to disclose.




A portion of this work was accepted as an abstract at the 2021 American Society of Nephrology annual meeting held virtually on November 4, 2021.

Author Contributions

T.N. Caza, C.P. Larsen, N. Messias, and P.D. Walker conceptualized the study; H. Amin, S.Y. Bae, E.J. Betchick, J. Brandt, C.A. Cassol, T.N. Caza, K.K. Chouhan, M.J. Diamond, J. Edwu-okwuwa, E.B. Elashi, S.L. Fabian, J.A. Flaxenburg, A. Frome, M. Haderlie, A. Hannoudi, R.S. Haun, J.T. Henry, E.T. Hoerschgen, B. Iqbal, Z. Karam, S. Khalillullah, E.H. Kim, C.P. Larsen, R.M. May, N. Messias, G. Schlessinger, M. Seek, R.M. Seipp, G. Shenoy, E. Ulozas, I. Vancea, P.D. Walker, J.L. Weatherspoon, and M.S. Ziadie were responsible for data curation; T.N. Caza, A. Hannoudi, R.S. Haun, and C.P. Larsen were responsible for investigation; T.N. Caza, A. Hannoudi, R.S. Haun, C.P. Larsen, and R.M. May were responsible for formal analysis; T.N. Caza and R.S. Haun were responsible for methodology; C.P. Larsen was responsible for project administration; C.P. Larsen was responsible for resources; T.N. Caza, C.P. Larsen, and N. Messias were responsible for visualization; C.P. Larsen provided supervision; T.N. Caza and A. Hannoudi wrote the original draft; and C.A. Cassol, T.N. Caza, C.P. Larsen, and R.M. May reviewed and edited the manuscript.


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glomerular and tubulointerstitial diseases; ANCA; APOL1; collapsing glomerulopathy; COVID-19; crescentic glomerulonephritis; IgA nephropathy; lupus nephritis; membranous nephropathy; minimal change disease; SARS-CoV-2 vaccine

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