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Kidney injury has already been reported as a result of immune response to several vaccines in various studies. However, reports of post-vaccine acute kidney injury have become relevant due to the COVID-19 pandemic and mass vaccination, despite being a rare event. This condition may arise either from the reactivation of a previous kidney disease or as an initial presentation, which can include collapsing glomerulopathy or acute tubular necrosis. The aim of this study is to present a case series detailing kidney injuries following COVID-19 vaccination and to outline the clinical characteristics of the patients.
This case series studied kidney injury onset in patients vaccinated for COVID-19. Between 2021 and 2022, 14 patients from different Brazilian states were included. Data collected included demographic and clinical characteristics, creatinine, urea, proteinuria, C3, and C4 levels, biopsy findings, immunization information and period of symptom presentation. Excel spreadsheets and the IBM SPSS software were used for data analysis.
Data were collected from 14 patients, including eight women, with a mean age of 37.64 ± 20.10 years. Six of these patients had comorbidities, including hypertension (n = 4), chronic kidney disease (n = 3), and dyslipidemia (n = 2). Regarding vaccination, seven patients received AstraZeneca, five received Pfizer BioNTech, and two received CoronaVac. Symptom onset occurred after the first dose in eight participants, after the second dose in five, and after the third dose in one. Symptoms started on average 25.67 ± 25.78 days after immunization. Regarding clinical presentation, ten participants had nephrotic syndrome (three associated with acute kidney injury), two had nephritic syndrome, and two had rapidly progressive glomerulonephritis. Biopsy findings revealed collapsing glomerulopathy (with one case associated with thrombotic microangiopathy) and acute tubular necrosis in seven patients, pauci-immune crescentic glomerulonephritis (with one case associated with thrombotic microangiopathy and another with class IV lupus nephritis) in three, segmental and focal glomerulosclerosis in two, thrombotic microangiopathy in one, and IgA nephropathy in one patient. Most patients presented increased serum creatinine (of the 13 samples with information collected, median = 2.56 ± 4.67, IQR = 1.29–3.13), and proteinuria was at nephrotic levels in nine of the ten patients undergoing the test (median = 3,800 ± 7,437, IQR = 2,025–9,456). Of the nine patients tested for C3 and C4, two had increased levels, and three had hematuria. Only one patient was positive for antineutrophil cytoplasmic antibody and factor associated with N-SMase activation markers.
Mass immunizations against COVID-19 have raised concerns about a potential association between vaccination and the new onset or reactivation of kidney injury in some cases. Although the study did not establish a clear causal relationship, it noted a temporal connection between the clinical presentation of kidney disease and vaccination. Despite its rarity, kidney injury should be considered a potential adverse effect.