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It is known, in fact, that SARS-CoV-2 causes ACE2 downregulation impairing the ACE2-mediated Ang II conversion into Ang 1-7 with the loss of its vasodilatory, anti-inflammatory, antioxidant, and anti-atherosclerotic proprieties and of their protective impact on COVID-19 morbidity and mortality [[5]]. In vivo human data that may address the beneficial role of RAS blockers in COVID-19 and its complications may be provided by patients with Gitelman's and Bartter's syndromes (GS/BS). Keywords: Bartter's syndrome; Angiotensin II; RAS blockers; COVID-19; Gitelman's syndrome EN Bartter's syndrome Angiotensin II RAS blockers COVID-19 Gitelman's syndrome 593 596 4 11/14/22 20221220 NES 221220 The renin-angiotensin system (RAS) during COVID-19 pandemic has captured the interest as the severe coronavirus 2 (SARS-CoV-2) causing COVID-19 uses angiotensin-converting enzyme type 2 (ACE2) as an entry point into the cell [[1]]. [Extracted from the article]

COVID-19 often leads to acute respiratory distress syndrome complicated by acute kidney injury (AKI). The indications for renal replacement therapy for these patients are those commonly accepted to treat AKI. We describe a continuous veno-venous haemodialysis (CVVHD) protocol for AKI, which aims to provide the best treatment according to the particular patient's and medical personnels' needs in biohazard settings with limited human and technological resources. We designed a CVVHD protocol with a high cut-off (HCO) filter in regional citrate anticoagulation (RCA). The HCO filter in diffusion determines the enhanced cytokines clearance with less filter clotting due to a lower filtration fraction. In our hospital, at the beginning of the pandemic outbreak, we treated seven COVID-19 patients with AKI stage 2 and 3 and recorded the circuit lifespan and the number of interventions on monitors. CVVHD in RCA appears to be safe, effective and easy to be performed in a biohazard scenario using lower blood flows and less bag changes with fluid savings, a biohazard reduction and sparing of resources. Although the data come from a very small cohort, our protocol seems related to a low mortality. [ABSTRACT FROM AUTHOR]

The process of SARS-CoV-2 infection, responsible for the COVID-19 pandemic, is carried out through different steps, with the interaction between ACE2 and Spike protein (S) being crucial. Besides of that, the acidic environment of endosomes seems to play a relevant role in the virus uptake into cells and its intracellular replication. Patients affected by two rare genetic tubulopathies, Gitelman's and Bartter's Syndromes, and a rare genetic metabolic disease, Fabry Disease, have shown intrinsic protection from SARS-CoV-2 infection and COVID-19 on account of specific intrinsic features that interfere with the virus uptake into cells and its intracellular replication, which will be reported and discussed in this paper, providing interesting insights for present and future research. [ABSTRACT FROM AUTHOR]

Background: Gitelman's and Bartter's syndromes (GS/BS) are rare genetic tubulopathies characterized by electrolyte imbalance and activation of the renin-angiotensin-aldosterone system (RAAS). These syndromes have intriguing biochemical and hormonal abnormalities that lead them to be protected from hypertension and cardiovascular and renal remodeling. Summary: In this review, we explore the biochemical/molecular mechanisms induced by the activation of the RAAS and its counterregulatory arm which is particularly activated in GS/BS patients, in the context of blood pressure regulation. In addition, we report our findings in the context of the COVID-19 pandemic where we observed GS/BS subjects being protected from infection. Key Messages: The intracellular pathways induced by Ang II, starting from induction of oxidative stress and vasoconstriction, are crucial for the progression toward cardiovascular-renal remodeling and might be useful targets in order to reduce/halt the progression of Ang II/oxidative stress-induced cardiovascular-renal morbidity in several diseases. [ABSTRACT FROM AUTHOR]