Background We determined circulating anti-S SARS-CoV-2 IgG antibody titres in a vaccinated healthcare workers (HCWs) cohort from Northern Israel in the 11 months following primary vaccination according to age, ethnicity and previous infection status. Methods All consenting HCWs were invited to have their IgG levels measured before vaccination and at 6 subsequent timepoints using a quantitative S1/S2 IgG assay. All HCWs with suspected COVID-19 were PCR tested. We described trends in circulating IgG geometric mean concentration (GMC) by age, ethnicity, timing of boosting and previous infection status and compared strata using Kruskall-Wallis tests. Results Among 985 vaccinated HCWs, IgG titres between 1 month post 2 nd dose to pre-boosting gradually decreased in all age groups. Younger or previously infected individuals had higher initial post-vaccination IgG levels (p<0.001 in both cases); differences substantially decreased or disappeared at 7-9 months, before boosting. The proportion of individuals infected prior to initiating vaccination and re-infected after dose 1 was comparable to the proportion of breakthrough infection post-dose 2 in those not previously infected (4.2 vs 4.7%). Pre-infection IgG levels in the 40 participants with breakthrough infection after dose 2 were similar to levels measured at the same timepoint in vaccinated HCWs who remained uninfected (p>0.3). Post-dose3 IgG levels were more than 10-fold those 1month post-dose 2. Conclusions Immunity waned in all age groups and previously infected individuals, reversed by boosting. IgG titres decrease and reinfections in individuals with hybrid immunity (infection+vaccination) suggests they may also require further doses. Our study also highlights the difficulty in determining protective IgG levels.

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BackgroundHemodialysis (HD) triggers recurrent and cumulative ischemic insults to the brain and the heart. Cooled dialysate may have a protective effect on major organs and improve hemodynamic tolerability of dialysis. The aim of the study was to compare HD with cooled dialysate with routine dialysis in terms of hemodynamic stability and levels of high‐sensitivity Troponin I (hs‐TnI) and N‐terminal pro b‐type natriuretic peptide (NTproBNP) pre and postdialysis.MethodsThe 45 patients were randomized into two groups. The first group received a 35.5°C dialysate first (hypothermic dialysis) and the second group a 36.5°C dialysate first (routine dialysis). Then groups crossed over, so each group received the alternate dialysate (self‐controls) For each patient, the first sample was collected at the beginning of dialysis, and a second sample was taken at the end of dialysis.Results and conclusionhs‐TnI and NTproBNP increased after routine HD by 10.7 ng\ml (p < 0.001) and (12.0 pg/μl) (p < 0.001), respectively, and by −3.1 ng\ml (p = 0.25) and (4.3 pg/μl) (p < 0.001), respectively after hypothermic HD. Our study results showed a tendency towards less rise in hsTnI and NTproBNP during hypothermic HD (35.5°C) as compared to routine HD (36.5°C). Neither arm experienced statistically significant changes in blood pressure. Further studies in larger cohorts and long follow up are warranted in order to confirm that lower rise in (hs‐TnI) and NTproBNP actually translate into lower clinical risk for cardiovascular events.

BACKGROUND AND AIMS Genetic etiologies are estimated to affect ∼10% of adults with advanced CKD. However, significant population disparities in genetic kidney disease exist and population-based screening are lacking especially among minority groups. The Druze population is a middle-eastern minority with high rates of end-stage renal disease (ESRD) and consanguinity, which suggests high rates of population-specific monogenic CKD etiologies. We therefore hypothesized that by exome sequencing we will identify a unique distribution of monogenic ESRD causes as compared with prior studies and that important ramifications for clinical practice may ensue. METHOD We initiated a national multicenter study of all Israeli dialysis units in order to provide comprehensive evidence for ESRD's genetic basis (Israeli ESRD Genetic Consortium Cohort). Specifically, during 2020, we recruited 97% (n = 94) of Israeli Druze individuals on dialysis from 12 different hospitals and community-based units. We conducted exome sequencing and diagnostic analysis for all patients. We assessed the diagnostic yield of genetic analysis and its relation to baseline clinical phenotypes. RESULTS Overall, the cohort consists of 94 individuals from 91 different families with first-degree consanguinity rate of 28%. Participants mean age was 62 years (ranging from 18 to 88 years). Most common primary clinical diagnoses were diabetic kidney disease, nephropathy of unknown origin, glomerular or cystic kidney disease, together encompassing 90% of all cases. None had previous molecular diagnosis. Using exome sequencing, we identified a genetic etiology in 27 out of 94 (28.7%) participants. We identified WDR19 (NPHP13) homozygous mutation c.878G &gt; A (p.C293Y) as the most common genetic diagnosis (5.3%). Follow-up clinical characterization revealed that all affected individuals exhibited non-syndromic adulthood-onset ESRD, supporting a profound mutation-dependent phenotypic heterogeneity and weak pre-exome phenotypic specificity. Other prevalent genetic diagnoses included type IV collagen, PKD1, PKD2 and UMOD mutations as well as monogenic forms of diabetes and hyperlipidemia. Molecular diagnosis corresponded to the pre-exome clinical diagnosis in only one-third of the participants. CONCLUSION Exome sequencing in Druze with ESRD yields a genetic diagnosis in just &lt;30% of cases with WDR19 mutation being the most prevalent single-gene etiology. These results, which remarkably inform clinical management, emphasize the importance of revealing population-specific mutations given the underutilization of genetic testing, particularly among adult minorities.