Endothelin: A mediator of renal disease progression

Research output: Contribution to journalArticle

Abstract

Glomerulosclerosis and tubulointerstitial damage are characteristics of progressive renal diseases associated with chronic proteinuria. Since numerous studies have demonstrated a correlation between proteinuria and the degree of renal damage, a causal role for proteinuria in the development of progressive renal failure has been postulated. Some in vitro data suggest that endothelins (ET), a family of endogenous peptides, could be involved in the genesis and progression of glomerular damage. Moreover, evidence that tubular cells exposed to high molecular weight proteins are induced to release ET toward the basolateral compartment, together with the capability of these peptides to influence events occurring in the interstitium, suggest that ET could also participate in interstitial inflammation. Data are now available that ET actually plays a role in the progression of chronic renal disease in different experimental models including renal mass reduction, lupus nephritis and streptozotocin-induced diabetes.

Original languageEnglish
Pages (from-to)179-183
Number of pages5
JournalJournal of Nephrology
Volume10
Issue number4
Publication statusPublished - Jul 1997

Fingerprint

Endothelins
Disease Progression
Proteinuria
Kidney
Peptides
Lupus Nephritis
Experimental Diabetes Mellitus
Chronic Renal Insufficiency
Renal Insufficiency
Theoretical Models
Molecular Weight
Inflammation
Proteins

Keywords

  • Endothelin
  • Endothelin-receptor antagonists
  • Glomerulosclerosis
  • Progressive renal diseases
  • Tubulointerstitial damage

ASJC Scopus subject areas

  • Nephrology

Cite this

Endothelin : A mediator of renal disease progression. / Bruzzi, Isabella; Remuzzi, Giuseppe; Benigni, Ariela.

In: Journal of Nephrology, Vol. 10, No. 4, 07.1997, p. 179-183.

Research output: Contribution to journalArticle

@article{4e32fcc709334d61bfee84255f664dc8,
title = "Endothelin: A mediator of renal disease progression",
abstract = "Glomerulosclerosis and tubulointerstitial damage are characteristics of progressive renal diseases associated with chronic proteinuria. Since numerous studies have demonstrated a correlation between proteinuria and the degree of renal damage, a causal role for proteinuria in the development of progressive renal failure has been postulated. Some in vitro data suggest that endothelins (ET), a family of endogenous peptides, could be involved in the genesis and progression of glomerular damage. Moreover, evidence that tubular cells exposed to high molecular weight proteins are induced to release ET toward the basolateral compartment, together with the capability of these peptides to influence events occurring in the interstitium, suggest that ET could also participate in interstitial inflammation. Data are now available that ET actually plays a role in the progression of chronic renal disease in different experimental models including renal mass reduction, lupus nephritis and streptozotocin-induced diabetes.",
keywords = "Endothelin, Endothelin-receptor antagonists, Glomerulosclerosis, Progressive renal diseases, Tubulointerstitial damage",
author = "Isabella Bruzzi and Giuseppe Remuzzi and Ariela Benigni",
year = "1997",
month = "7",
language = "English",
volume = "10",
pages = "179--183",
journal = "Journal of Nephrology",
issn = "1121-8428",
publisher = "Springer International Publishing",
number = "4",

}

TY - JOUR

T1 - Endothelin

T2 - A mediator of renal disease progression

AU - Bruzzi, Isabella

AU - Remuzzi, Giuseppe

AU - Benigni, Ariela

PY - 1997/7

Y1 - 1997/7

N2 - Glomerulosclerosis and tubulointerstitial damage are characteristics of progressive renal diseases associated with chronic proteinuria. Since numerous studies have demonstrated a correlation between proteinuria and the degree of renal damage, a causal role for proteinuria in the development of progressive renal failure has been postulated. Some in vitro data suggest that endothelins (ET), a family of endogenous peptides, could be involved in the genesis and progression of glomerular damage. Moreover, evidence that tubular cells exposed to high molecular weight proteins are induced to release ET toward the basolateral compartment, together with the capability of these peptides to influence events occurring in the interstitium, suggest that ET could also participate in interstitial inflammation. Data are now available that ET actually plays a role in the progression of chronic renal disease in different experimental models including renal mass reduction, lupus nephritis and streptozotocin-induced diabetes.

AB - Glomerulosclerosis and tubulointerstitial damage are characteristics of progressive renal diseases associated with chronic proteinuria. Since numerous studies have demonstrated a correlation between proteinuria and the degree of renal damage, a causal role for proteinuria in the development of progressive renal failure has been postulated. Some in vitro data suggest that endothelins (ET), a family of endogenous peptides, could be involved in the genesis and progression of glomerular damage. Moreover, evidence that tubular cells exposed to high molecular weight proteins are induced to release ET toward the basolateral compartment, together with the capability of these peptides to influence events occurring in the interstitium, suggest that ET could also participate in interstitial inflammation. Data are now available that ET actually plays a role in the progression of chronic renal disease in different experimental models including renal mass reduction, lupus nephritis and streptozotocin-induced diabetes.

KW - Endothelin

KW - Endothelin-receptor antagonists

KW - Glomerulosclerosis

KW - Progressive renal diseases

KW - Tubulointerstitial damage

UR - http://www.scopus.com/inward/record.url?scp=0030762051&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030762051&partnerID=8YFLogxK

M3 - Article

C2 - 9377723

AN - SCOPUS:0030762051

VL - 10

SP - 179

EP - 183

JO - Journal of Nephrology

JF - Journal of Nephrology

SN - 1121-8428

IS - 4

ER -