Antibody Response after 3-Dose Booster against SARS-CoV-2 mRNA Vaccine in Kidney Transplant Recipients

Author:

Tripodi Domenico12ORCID,Dominici Roberto1ORCID,Sacco Davide34,Santorelli Gennaro5,Rivera Rodolfo5,Acquaviva Sandro6,Marchisio Marino6,Brambilla Paolo12,Battini Graziana5,Leoni Valerio12ORCID

Affiliation:

1. Laboratory of Clinical Pathology and Toxicology, Hospital Pio Xi of Desio, Azienda Socio Sanitaria Territoriale della Brianza (ASST-Brianza), 20832 Desio, Italy

2. Department of Medicine and Surgery, University of Milano-Bicocca, 20126 Monza, Italy

3. Department of Brain and Behavioral Sciences, University of Pavia, 27100 Pavia, Italy

4. Department of Molecular Genetics and Cytogenetics, Centro Diagnostico Italiano, 20147 Milan, Italy

5. Clinical Unit of Nephrology and Dialysis, Hospital Pio Xi of Desio, Azienda Socio Sanitaria Territoriale della Brianza (ASST-Brianza), 20832 Desio, Italy

6. Diagnostics Bioprobes s.r.l. DIA.PRO, Via G. Carducci, 27, Sesto San Giovanni, 20099 Milan, Italy

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with a high rate of mortality in kidney transplant recipients (KTRs). Current vaccine strategies for KTRs seem to be unable to provide effective protection against coronavirus disease 2019 (COVID-19), and the occurrence of severe disease in some vaccinated KTRs suggested a lack of immunity. We initially analyzed the antibody response in a group of 32 kidney transplant recipients (KTRs) followed at the nephrology and dialysis unit of the Hospital Pio XI of Desio, ASST-Brianza, Italy. Thus, we studied the differences in antibody levels between subjects who contracted SARS-CoV-2 after the booster (8 individuals) and those who did not contract it (24 individuals). Furthermore, we verified if the antibody response was in any way associated with creatinine and eGFR levels. We observed a significant increase in the antibody response pre-booster compared to post-booster using both a Roche assay and DIAPRO assay. In the latter, through immunotyping, we highlight that the major contribution to this increase is specifically due to IgG S1 IgM S2. We observed a significant increase in IgA S1 and IgA NCP (p = 0.045, 0.02) in the subjects who contracted SARS-CoV-2. We did not find significant associations for the p-value corrected for false discovery rate (FDR) between the antibody response to all assays and creatinine levels. This observation allows us to confirm that patients require additional vaccine boosters due to their immunocompromised status and therapy in order to protect them from infections related to viral variants. This is in line with the data reported in the literature, and it could be worthwhile to deeply explore these phenomena to better understand the role of IgA S1 and IgA NCP antibodies in SARS-CoV-2 infection.

Publisher

MDPI AG

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