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Maria Jose Soler Romeo

The year 2020 brought a pandemic that prompted the kidney community to modify daily clinical practice to avoid severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in our patients with advanced chronic kidney disease (CKD). Advanced CKD and solid organ transplantation have been identified as risk factors for mortality in patients with coronavirus infectious disease 2019 (COVID-19) (1). Moreover, patients with end-stage kidney disease (ESKD) were also identified to be at high risk of mortality compared to the general population (2).

Amid the pandemic, how do we communicate with our high-risk patients? How do we take care

Maria Jose Soler and Natalia Ramos

During the last decade, several therapeutics targeting the complement cascade have begun to enter the nephrology scene (Figure 1). Examples include the following diseases:

Atypical hemolytic uremic syndrome (aHUS)

C3 glomerulopathy

Lupus nephritis

Anti-neutrophil cytoplasmic antibody (ANCA) vasculitis

Immunoglobulin A (IgA) nephropathy

Summary of the drugs that target the complement cascade in glomerular disease

IgAN, IgA nephropathy; C3GN, C3 glomerulonephritis; HUS, hemolytic uremic syndrome; SLE, systemic lupus erythematosus; AAV, anti-neutrophil cytoplasmic autoantibodies; MBL, mannose-binding lectin; MASP, mannose-binding lectin-associated serine protease; CR1, complement receptor type 1; CR2, complement receptor type 2; DAF, decay-accelerating factor; ALP2, alkaline protease
Nestor Toapanta and María José Soler

Chronic kidney disease is one of the risk factors that has been associated with higher risk of infection and mortality from SARS-CoV-2 (1, 2). The increased rate of SARS-CoV-2 infection has been related to the transportation and greater hospital exposure of patients (3, 4). In addition, the higher mortality rate has been, in part, ascribed to alterations in the immune system.

Vaccination against SARS-CoV-2 infection has raised hopes for the pandemic to end. Recent studies reported that the BNT162b2 (Pfizer-BioNTech) vaccine against SARS-CoV-2 is effective for symptomatic COVID-19 in the general population,

Marina Lopez-Martinez and María José Soler

Endothelin-1 (ET-1) plays a role in chronic kidney disease (CKD) progression (1). In the kidney, ET-1 binding of the endothelin A (ETA) receptor drives afferent arteriole vasoconstriction, cell proliferation, podocyte and glycocalyx damage, matrix accumulation, and proinflammatory effects, whereas binding of the endothelin B (ETB) receptor produces vasodilation, antifibrotic effects, and decreased sodium reabsorption and natriuresis (1, 2). Although renin-angiotensin-aldosterone system (RAAS) inhibition has proven a reduction of albuminuria and a proportional effect on kidney protection (3, 4), residual albuminuria still implies a significant risk of CKD progression (5