Targeting the Endothelin A Receptor in IgA Nephropathy

Donald E. Kohan; Jonathan Barratt; Hiddo J.L. Heerspink; Kirk N. Campbell; Mariannne Camargo; Ike Ogbaa; Ruth Haile-Meskale; Dana V. Rizk; Andrew King

doi:10.1016/j.ekir.2023.07.023

Targeting the Endothelin A Receptor in IgA Nephropathy

Donald E. Kohan
, Jonathan Barratt
, Hiddo J.L. Heerspink
, Kirk N. Campbell
, Mariannne Camargo
, Ike Ogbaa
, Ruth Haile-Meskale
, Dana V. Rizk
, Andrew King

Research output: Contribution to journal › Review article › peer-review

33 Scopus citations

Abstract

Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and carries a substantial risk of kidney failure. New agency-approved therapies, either specifically for IgAN or for chronic kidney disease (CKD) in general, hold out hope for mitigating renal deterioration in patients with IgAN. The latest addition to this therapeutic armamentarium targets the endothelin-A receptor (ET_AR). Activation of ET_AR on multiple renal cell types elicits a host of pathophysiological effects, including vasoconstriction, cell proliferation, inflammation, apoptosis, and fibrosis. Blockade of ET_AR is renoprotective in experimental models of IgAN and reduces proteinuria in patients with IgAN. This review discusses the evidence supporting the use of ET_AR blockade in IgAN as well as addressing the potential role for this class of agents among the current and emerging therapies for treating this disorder.

Original language	English
Pages (from-to)	2198-2210
Number of pages	13
Journal	Kidney International Reports
Volume	8
Issue number	11
DOIs	https://doi.org/10.1016/j.ekir.2023.07.023
State	Published - Nov 2023

Keywords

IgA nephropathy
antagonist
endothelin
kidney
proteinuria
receptor

Access to Document

10.1016/j.ekir.2023.07.023

Cite this

@article{b981e68681fb4084a0c55c4dbc3863ee,

title = "Targeting the Endothelin A Receptor in IgA Nephropathy",

abstract = "Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and carries a substantial risk of kidney failure. New agency-approved therapies, either specifically for IgAN or for chronic kidney disease (CKD) in general, hold out hope for mitigating renal deterioration in patients with IgAN. The latest addition to this therapeutic armamentarium targets the endothelin-A receptor (ETAR). Activation of ETAR on multiple renal cell types elicits a host of pathophysiological effects, including vasoconstriction, cell proliferation, inflammation, apoptosis, and fibrosis. Blockade of ETAR is renoprotective in experimental models of IgAN and reduces proteinuria in patients with IgAN. This review discusses the evidence supporting the use of ETAR blockade in IgAN as well as addressing the potential role for this class of agents among the current and emerging therapies for treating this disorder.",

keywords = "IgA nephropathy, antagonist, endothelin, kidney, proteinuria, receptor",

author = "Kohan, \{Donald E.\} and Jonathan Barratt and Heerspink, \{Hiddo J.L.\} and Campbell, \{Kirk N.\} and Mariannne Camargo and Ike Ogbaa and Ruth Haile-Meskale and Rizk, \{Dana V.\} and Andrew King",

note = "Publisher Copyright: {\textcopyright} 2023 International Society of Nephrology",

year = "2023",

month = nov,

doi = "10.1016/j.ekir.2023.07.023",

language = "English",

volume = "8",

pages = "2198--2210",

journal = "Kidney International Reports",

issn = "2468-0249",

publisher = "Elsevier Inc.",

number = "11",

}

TY - JOUR

T1 - Targeting the Endothelin A Receptor in IgA Nephropathy

AU - Kohan, Donald E.

AU - Barratt, Jonathan

AU - Heerspink, Hiddo J.L.

AU - Campbell, Kirk N.

AU - Camargo, Mariannne

AU - Ogbaa, Ike

AU - Haile-Meskale, Ruth

AU - Rizk, Dana V.

AU - King, Andrew

PY - 2023/11

Y1 - 2023/11

N2 - Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and carries a substantial risk of kidney failure. New agency-approved therapies, either specifically for IgAN or for chronic kidney disease (CKD) in general, hold out hope for mitigating renal deterioration in patients with IgAN. The latest addition to this therapeutic armamentarium targets the endothelin-A receptor (ETAR). Activation of ETAR on multiple renal cell types elicits a host of pathophysiological effects, including vasoconstriction, cell proliferation, inflammation, apoptosis, and fibrosis. Blockade of ETAR is renoprotective in experimental models of IgAN and reduces proteinuria in patients with IgAN. This review discusses the evidence supporting the use of ETAR blockade in IgAN as well as addressing the potential role for this class of agents among the current and emerging therapies for treating this disorder.

AB - Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and carries a substantial risk of kidney failure. New agency-approved therapies, either specifically for IgAN or for chronic kidney disease (CKD) in general, hold out hope for mitigating renal deterioration in patients with IgAN. The latest addition to this therapeutic armamentarium targets the endothelin-A receptor (ETAR). Activation of ETAR on multiple renal cell types elicits a host of pathophysiological effects, including vasoconstriction, cell proliferation, inflammation, apoptosis, and fibrosis. Blockade of ETAR is renoprotective in experimental models of IgAN and reduces proteinuria in patients with IgAN. This review discusses the evidence supporting the use of ETAR blockade in IgAN as well as addressing the potential role for this class of agents among the current and emerging therapies for treating this disorder.

KW - IgA nephropathy

KW - antagonist

KW - endothelin

KW - kidney

KW - proteinuria

KW - receptor

UR - https://www.scopus.com/pages/publications/85168825674

U2 - 10.1016/j.ekir.2023.07.023

DO - 10.1016/j.ekir.2023.07.023

M3 - Review article

AN - SCOPUS:85168825674

SN - 2468-0249

VL - 8

SP - 2198

EP - 2210

JO - Kidney International Reports

JF - Kidney International Reports

IS - 11

ER -

Targeting the Endothelin A Receptor in IgA Nephropathy

Abstract

Keywords

Access to Document

Fingerprint

Cite this