Search

The COVID-19 pandemic has resulted in major disruption to the delivery of both routine and urgent healthcare needs in many institutions across the globe. Vascular access (VA) for haemodalysis (HD) is considered the patient's lifeline and its maintenance is essential for the continuation of a life saving treatment. Prior to the COVID-19 pandemic, the provision of VA for dialysis was already constrained. Throughout the pandemic, inevitably, many patients with chronic kidney disease (CKD) have not received timely intervention for VA care. This could have a detrimental impact on dialysis patient outcomes in the near future and needs to be addressed urgently. Many societies have issued prioritisation to allow rationing based on clinical risk, mainly according to estimated urgency and need for treatment. The recommendations recently proposed by the European and American Vascular Societies in the COVID-19 pandemic era regarding the triage of various vascular operations into urgent, emergent and elective are debatable. VA creation and interventions maintain the lifeline of complex HD patients, and the indication for surgery and other interventions warrants patient-specific clinical judgement and pathways. Keeping the use of central venous catheters at a minimum, with the goal of creating the right access, in the right patient, at the right time, and for the right reasons, is mandatory. These strategies may require local modifications. Risk assessments may need specific "renal pathways" to be developed rather than applying standard surgical risk stratification. In conclusion, in order to recover from the second wave of COVID-19 and prepare for further phases, the provision of the best dialysis access, including peritoneal dialysis, will require working closely with the multidisciplinary team involved in the assessment, creation, cannulation, surveillance, maintenance, and salvage of definitive access.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality among patients with end-stage renal disease (ESRD). Clustering of traditional atherosclerotic and non-traditional risk factors drive the excess rates of coronary and non-coronary CVD in this population. The incidence, severity and mortality of coronary artery disease (CAD) as well as the number of complications of its therapy is higher in dialysis patients than in non-chronic kidney disease patients. Given the lack of randomized clinical trial evidence in this population, current practice is informed by observational data with a significant potential for bias. Furthermore, guidelines lack any recommendation for these patients or extrapolate them from trials performed in non-dialysis patients. Patients with ESRD are more likely to be asymptomatic, posing a challenge to the correct identification of CAD, which is essential for appropriate risk stratification and management. This may lead to "therapeutic nihilism", which has been associated with worse outcomes. Here, the ERA-EDTA EUDIAL Working Group reviews the diagnostic work-up and therapy of chronic coronary syndromes, unstable angina/non-ST elevation and ST-elevation myocardial infarction in dialysis patients, outlining unclear issues and controversies, discussing recent evidence, and proposing management strategies. Indications of antiplatelet and anticoagulant therapies, percutaneous coronary intervention and coronary artery bypass grafting are discussed. The issue of the interaction between dialysis session and myocardial damage is also addressed.

Background: IgA nephropathy (IgAN) is a common form of primary glomerulonephritis characterized by diffuse glomerular mesangial IgA1 deposition that leads to mesangial proliferation and chronic glomerular inflammation. Analyses of serum IgA1 from IgAN patients revealed an abnormal galactosylation of the O-linked carbohydrate moieties of IgA that may be a result of altered activity of core 1 beta1,3-galactosyltransferase (C1GalT1). To evaluate the association between C1GalT1 single nucleotide polymorphisms (SNPs) and IgAN, we performed a case control study on cohorts from the Italian population., Methods: We sequenced C1GalT1 coding and promoter regions in 284 IgAN patients and 210 healthy controls. The functional role of 3' untranslated region (3'UTR) SNPs was studied using electrophoretic mobility shift assays and real-time quantitative PCR., Results: We analyzed 8 SNPs in the C1GalT1 gene: 5 SNPs were in the promoter region and 3 SNPs in the 3'UTR. The allele 1365G in the 3'UTR was significantly more frequent in IgAN patients than in healthy controls., Conclusion: The 1365G allele and 1365G/G genotype seem to confer susceptibility to IgAN.