Background: Frailty is an aging-associated state of increased vulnerability, which raises the risk of adverse outcomes. Chronic kidney disease is associated with higher prevalence of frailty. Our aim was to estimate frailty prevalence in a hemodialysis population and its influence on shortterm outcomes. Design: Observational prospective longitudinal study of 277 prevalent hemodialysis patients. Frailty was estimated through the Edmonton Frail Scale (EFS). Demographic and clinical data, comorbidity index, and laboratory parameters were recorded. A 29-month follow-up was conducted on mortality, including hospitalization, and visits to hospital emergency services in the first 12 months of this period. Results: According to the EFS, 82 patients (29.6%) were frail, 53 (19.1%) were vulnerable, and 142 (51.3%) were non-frail. During follow-up, 58.5% frail patients, 30.2% vulnerable, and 16.2% non-frail ones died (p < .005). In the analysis of survival using an adjusted Cox model, a higher hazard of mortality was observed in frail than in non-frail patients (HR 2.34; 95% CI 1.39-3.95; p ¼ .001). During follow-up the hospitalization rate was 852 episodes/1000 patient-years for frail patients, 784 episodes/1000 patient-years for vulnerable patients, and 417 episodes/1000 patientyears for non-frail patients (p ¼ .0005). The incidence ratio of visits to emergency services was 3216, 1735, and 1545 visits/1000 patient-years for each group (p < .001). Conclusions: Hemodialysis patients present high frailty prevalence. Frailty is associated with poor short-term outcomes and higher rates of mortality, visits to hospital emergency services, and hospitalization.

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There is no approved therapy for coronavirus disease 2019 [severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection], and the number of worldwide deaths on current standard therapy is staggering [1]. Current therapy is aimed at decreasing viral replication, supporting vital functions and addressing the most damaging consequences of the disease such as hyperinflammation (the so-called cytokine storm) and thrombosis. The latter two involve the use of anti-inflammatory therapies and heparin, respectively. We suggest that complement-blocking strategies such as eculizumab should be considered in severe cases not responding well to current therapy, including tocilizumab, in the context of clinical trials. Complement is thought to contribute to microangiopathies associated with infectious diseases [2].Recent histological data from COVID-19 patients are compatible with acute respiratory distress syndrome (ARDS) [3]. Additionally, vascular congestion and inflammatory cell infiltrates were present [4], as well as microvascular thrombi in multiple organs including kidneys in patients who died of COVID-19 and SARS [5,6]. Immunohistochemically, deposits of C5b-9, C4d and mannose-binding lectin-associated serine protease-2 have been found in the microvasculature of lungs and skin in patients with . Furthermore, COVID-19 shares some features with entities that are complement mediated, such as disseminated intravascular coagulation, thrombotic microangiopathy (TMA) and antiphospholipid antibody syndrome. These include increased lactate dehydrogenase (LDH) , platelet disease, hypertransaminasaemia, anaemia and extrapulmonary involvement, such as the

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