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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]

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]

Background/Aims: In chronic kidney disease (CKD) patients blood pressure variability (BPV) is associated with poor outcome. Sleep disturbances alter BP profiles in hypertensives but their influence on BPV in CKD patients is unknown. We screened a cohort of CKD/ESRD patients to investigate whether sleep quality impacts on BPV. Methods: Consecutive CKD patients' sleep quality was assessed using validated questionnaires (Epworth Sleepiness Scale-ESS); International Restless legs scale-IRLS; Functional Outcomes of Sleep Questionnaire-FOSQ: Insomnia Severity Index-ISI; STOP-Bang). All patients underwent ambulatory blood pressure measurement. Results: 104 out of 143 enrolled patients (78.32% stage-3 CKD; 10.49% Stage-4; 11.19% Stage-5; 6.99% ESRD-under dialysis) completed all the questionnaires. 95.8% were hypertensives, 70% were non-dippers and 27.8% had resistant hypertension. STOPBang> 4 proved sleep disorders in 84.84% of patients. Patients with IRLS>10 had greater diastolic nocturnal standard deviation (DNSD) and a trend (p=0.05) for systolic nocturnal SD (SNSD). Patients with ISI>14 had greater SNSD and in 28.8% FOSQ showed severely impaired sleep quality. Their systolic nocturnal BPV was significantly greater. ISI was independently associated with SNSD. FOSQ and diastolic nocturnal BPV were negatively correlated at the bivariate analysis and FOSQ independently predicts systolic nocturnal BPV at multivariate regression analysis. Conclusions: In CKD patients impaired sleep quality increases BPV, might contribute to their disease progression and worsen prognosis. Searching for sleep problems in CKD patients could help planning their treatment of sleep problems contributing to CV risk reduction. Our data provide the rationale working hypothesis for the need of studies with larger number of patients aimed to demonstrate improved outcome of CKD progression and CV risk with the treatment also of sleep disorders. [ABSTRACT FROM AUTHOR]