Background There is scarce evidence on fourth doses of SARS-CoV-2 vaccines in chronic kidney disease (CKD) patients. We have evaluated the humoral response and effectivity of the fourth dose in the CKD spectrum: non-dialysis CKD (ND-CKD), hemodialysis (HD), peritoneal dialysis (PD) and kidney transplant (KT) recipients. Methods This is a prespecified analysis of the prospective, observational, multicentric SENCOVAC study. In patients with CKD who had received a complete initial vaccination and one or two boosters and had anti-Spike antibody determinations 6 and 12 months after the initial vaccination, we analyzed factors associated to persistent negative humoral response and to higher anti-Spike antibody titers as well as the efficacy of vaccination on COVID-19 severity. Results Of 2186 patients (18% KT, 8% PD, 69% HD and 5% ND-CKD), 30% had received a fourth dose. The fourth dose increased anti-Spike antibody titers in HD (P = 0.001) and ND-CKD (P = 0.014) patients and seroconverted 72% of previously negative patients. Higher anti-Spike antibody titers at 12 months were independently associated to repeated exposure to antigen (fourth dose, previous breakthrough infections), previous anti-Spike antibody titers and not being a KT. Breakthrough COVID-19 was registered in 137 (6%) patients, of whom 5% required admission. Admitted patients had prior titers below 620 UI/ml and median values were lower (P = 0.020) than in non-admitted patients. Conclusions A fourth vaccine dose increased anti-Spike antibody titers or seroconverted many CKD patients, but those with the highest need for a vaccine booster (i.e. those with lower pre-booster antibody titers or KT recipients) derived the least benefit in terms of antibody titers. Admission for breakthrough COVID-19 was associated with low anti-Spike antibody titers.

Introduction Patients on hemodialysis are at high-risk for complications derived from coronavirus disease-19 (COVID-19). The present analysis evaluated the impact of a booster vaccine dose and breakthrough severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections on humoral immunity three months after the booster dose. Methods This is a multicentric and prospective study assessing IgG anti-Spike antibodies 6 and 9 months after initial SARS-CoV-2 vaccination in patients on hemodialysis that had also received a booster dose before the 6-month assessment (early booster) or between the 6- and 9-month assessments (late booster). The impact of breakthrough infections, type of vaccine, time from the booster and clinical variables were assessed. Results A total of 711 patients (67% male, 67 [20-89] years) were included. Of which, 545 (77%) received an early booster and the rest a late booster. At 6 months, 64 (9%) patients had negative anti-Spike antibody titers (3% of early booster and 29% of late booster patients, p = 0.001). At 9 months, 91% of patients with 6-month negative response had seroconverted and there were no differences in residual prevalence of negative humoral response between early and late booster patients (0.9% vs 0.6%, p = 0.693). During follow-up, 35 patients (5%) developed breakthrough SARS-CoV-2 infection. Antibody titers at 9 months were independently associated to mRNA-1273 booster (p = 0.001), lower time from booster (p = 0.043) and past breakthrough SARS-CoV-2 infection (p<0.001). Conclusions In hemodialysis patients, higher titers of anti-Spike antibodies at 9 months were associated to mRNA-1273 booster, lower time from booster and past breakthrough SARS-CoV-2 infection.

No abstract

No abstract

Background Acute kidney injury (AKI) is associated with short- and long-term complications but the consequences of the AKI-to-CKD transition are still poorly understood. We aimed to evaluate the association between the AKI-to-CKD transition and the long-term risk of infection. Methods This retrospective study included patients admitted in a tertiary hospital with community-acquired AKI in 2013 and 2014 that had estimated glomerular filtration rate (eGFR) assessed at 3 months (±2 weeks) after serum creatinine peaked in the AKI episode. Key exclusion criteria were baseline CKD or confounding factors (active neoplasia, primary immunodeficiency, HIV, immunosuppressive drugs). The association between the AKI-to-CKD transition (defined as having eGFR < 60 ml/min/1.73 m2 at 3 months) and long-term infections (defined using clinical features, blood/urine analysis, cultures and image) was assessed during a follow-up of 9 (2–56) months. Results Among the 1731 patients admitted with AKI, 367 (21%) were included in the present analysis (64% male, 71 ± 15 years). Three months after AKI, 159 (43%) developed AKI-to-CKD transition. Baseline and post-AKI eGFR were independent predictors of AKI-to-CKD transition (HR 0.97, p = 0.044 and HR 0.96, p < 0.001, respectively). During follow-up, 153 (42%) patients developed an infection. Factors associated to infection were older age, cognitive impairment, lower post-AKI eGFR, eGFR loss from baseline to 3 months and AKI-to-CKD transition. Adjusted Cox regression showed that baseline eGFR, 3-month eGFR, eGFR loss and AKI-to-CKD transition were independent predictors of the long-term risk of infection. Conclusions The AKI-to-CKD transition independently predicts the long-term risk of infection following an episode of AKI.

No abstract

No abstract

No abstract