Reply from the authors

B Cell Suppression in Primary Glomerular Disease

Pathophysiology and Pathology of Acute Kidney Injury in Patients With COVID-19.

De Novo and Relapsing Glomerular Diseases After COVID-19 Vaccination: What Do We Know So Far?

Personalized prophylactic anticoagulation decision analysis in patients with membranous nephropathy

Focal segmental glomerulosclerosis (FSGS) is a leading cause of nephrotic syndrome and end-stage renal disease worldwide. Although the mechanisms underlying this important disease are poorly understood, the glomerular podocyte clearly plays a central role in disease pathogenesis. In the current work, we demonstrate that the homophilic adhesion molecule sidekick-1 (sdk-1) is up-regulated in podocytes in FSGS both in rodent models and in human kidney biopsy samples. Transgenic mice that have podocyte-specific overexpression of sdk-1 develop gradually progressive heavy proteinuria and severe FSGS. We also show that sdk-1 associates with the slit diaphragm linker protein MAGI-1, which is already known to interact with several critical podocyte proteins including synaptopodin, alpha-actinin-4, nephrin, JAM4, and beta-catenin. This interaction is mediated through a direct interaction between the carboxyl terminus of sdk-1 and specific PDZ domains of MAGI-1. In vitro expression of sdk-1 enables a dramatic recruitment of MAGI-1 to the cell membrane. Furthermore, a truncated version of sdk-1 that is unable to bind to MAGI-1 does not induce podocyte dysfunction when overexpressed. We conclude that the up-regulation of sdk-1 in podocytes is an important pathogenic factor in FSGS and that the mechanism involves disruption of the actin cytoskeleton possibly via alterations in MAGI-1 function.

Screening Strategies for Tuberculosis in Children With Kidney Disease: What Is Cost-Effective?

Obesity and CKD: How to Assess the Risk?

Treatment of primary focal segmental glomerulosclerosis

Authors' reply:

The Impact of APOL1 on Chronic Kidney Disease and Hypertension.

Light Chain Podocytopathy Mimicking Recurrent Focal Segmental Glomerulosclerosis.

First Identification of an Antigen in Autoimmune Idiopathic Membranous Nephropathy: Toward Targeted Therapy?

Podocytes regulate the glomerular basement membrane protein nephronectin by means of miR-378a-3p in glomerular diseases

Circulating Antipodocyte Antibodies in Membranous Nephropathy: Pathophysiologic and Clinical Relevance

Repository Corticotropin Injections Promote Clinical Remission and Regulatory T Cell Expansion in Membranous Nephropathy