New Ways of Understanding Membranous Nephropathy.
Adult
Autoantibodies
/ immunology
Calcium-Binding Proteins
/ immunology
Complement System Proteins
/ immunology
Glomerulonephritis, Membranous
/ immunology
Humans
Kidney Function Tests
N-Acetylglucosaminyltransferases
/ immunology
Receptors, Phospholipase A2
/ immunology
Thrombospondins
/ immunology
Autoimmune diseases
Glomerulonephritis
Membranous nephropathy
Nephrotic syndrome
Phospholipase A2 receptor
Journal
Nephron
ISSN: 2235-3186
Titre abrégé: Nephron
Pays: Switzerland
ID NLM: 0331777
Informations de publication
Date de publication:
2020
2020
Historique:
received:
04
12
2019
accepted:
29
02
2020
pubmed:
2
4
2020
medline:
8
7
2021
entrez:
2
4
2020
Statut:
ppublish
Résumé
In the last decade, great advances have been made in the field of membranous nephropathy (MN). The autoimmune nature of the disease has been confirmed with the description of diverse antigens, and few but very important prospective trials regarding treatment alternatives have been published, changing profoundly the way we understand this entity. Nowadays, an individualized therapeutic scheme based on clinical and serologic data appears to be the most appropriate method to manage patients with MN. Although there is still a long way to go, it is expected that future scientific progress will enable a patient-centered medicine based on concept-driven therapies. MN is the most common cause of nephrotic syndrome (NS) in white adults. Approximately one-third of patients achieve spontaneous remission, one-third remain stable, and one-third have an aggressive course with persistent NS and deterioration of renal function. About 80% of patients have circulating autoantibodies to phospholipase A2 receptor 1. Numerous therapies have been described including alkylating agents, rituximab, and calcineurin inhibitors, but new drugs are currently being explored. Here, we review the most important aspects regarding MN with an emphasis on results of the most recent clinical trials and pathophysiologic advances. Key Messages: 1. Evolving pathophysiologic concepts and recently published clinical trials have deeply changed our view of MN. 2. Most patients with MN present autoantibodies against diverse glomerular antigens. 3. Currently, an individual patient-centered management based on clinical and serologic markers is the most adequate approach to treat patients with MN.
Sections du résumé
BACKGROUND
In the last decade, great advances have been made in the field of membranous nephropathy (MN). The autoimmune nature of the disease has been confirmed with the description of diverse antigens, and few but very important prospective trials regarding treatment alternatives have been published, changing profoundly the way we understand this entity. Nowadays, an individualized therapeutic scheme based on clinical and serologic data appears to be the most appropriate method to manage patients with MN. Although there is still a long way to go, it is expected that future scientific progress will enable a patient-centered medicine based on concept-driven therapies.
SUMMARY
MN is the most common cause of nephrotic syndrome (NS) in white adults. Approximately one-third of patients achieve spontaneous remission, one-third remain stable, and one-third have an aggressive course with persistent NS and deterioration of renal function. About 80% of patients have circulating autoantibodies to phospholipase A2 receptor 1. Numerous therapies have been described including alkylating agents, rituximab, and calcineurin inhibitors, but new drugs are currently being explored. Here, we review the most important aspects regarding MN with an emphasis on results of the most recent clinical trials and pathophysiologic advances. Key Messages: 1. Evolving pathophysiologic concepts and recently published clinical trials have deeply changed our view of MN. 2. Most patients with MN present autoantibodies against diverse glomerular antigens. 3. Currently, an individual patient-centered management based on clinical and serologic markers is the most adequate approach to treat patients with MN.
Identifiants
pubmed: 32229730
pii: 000506948
doi: 10.1159/000506948
doi:
Substances chimiques
Autoantibodies
0
Calcium-Binding Proteins
0
NELL1 protein, human
0
PLA2R1 protein, human
0
Receptors, Phospholipase A2
0
THSD7A protein, human
0
Thrombospondins
0
Complement System Proteins
9007-36-7
N-Acetylglucosaminyltransferases
EC 2.4.1.-
exostosin-1
EC 2.4.1.224
exostosin-2
EC 2.4.1.224
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
261-271Informations de copyright
© 2020 S. Karger AG, Basel.