Renal parenchymal disease and hypertension

Richard A Preston, M. Epstein

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Renal parenchymal disease is the most common cause of secondary hypertension, accounting for 2.5% to 5.0% of all cases. Hypertension associated with renal parenchymal disease occurs as a complication of a wide variety of glomerular and interstitial renal diseases and may accelerate the decline in renal function if inadequately controlled. Renal parenchymal hypertension most probably represents the combined interactions of multiple independent mechanisms: potential factors include impaired sodium handling leading to volume expansion, perturbations of the renin-angiotensin system, alterations in endogenous vasodepressor compounds, and possibly increased activity of vasoactive substances. The past several years have witnessed newer insights into both the pathophysiology and the therapeutics of this disorder. The characterization of endothelin and the nitric oxide (NO)- arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. For example, methylated L-arginine derivatives that possess NO synthase inhibitor capabilities including N(G)-N- dimethylarginine and N-monomethyl-L-arginine are found in human plasma and in urine. Patients with chronic uremia have impaired elimination of these compounds, and circulating concentrations of these compounds may increase sufficiently to result in inhibition of NO production. Thus, accumulation of endogenous NO synthase inhibitors might contribute to the hypertension of advanced renal failure. Similarly, it has been proposed that increased endothelium-derived endothelin that results from hypertensive injury to vascular endothelium could lead to further vasoconstriction and worsening of hypertension. Additional insight into this fascinating problem must await further biochemical characterization of some of the mediators and a more precise delineation of their pathophysiological role.

Original languageEnglish
Pages (from-to)138-151
Number of pages14
JournalSeminars in Nephrology
Volume15
Issue number2
StatePublished - Jan 1 1995

Fingerprint

Hypertension
Kidney
Arginine
Renal Hypertension
Endothelins
Nitric Oxide Synthase
Nitric Oxide
Uremia
Vascular Endothelium
Renin-Angiotensin System
Vasoconstriction
Endothelium
Renal Insufficiency
Sodium
Medicine
Urine
Wounds and Injuries
Therapeutics
N,N-dimethylarginine

ASJC Scopus subject areas

  • Nephrology

Cite this

Renal parenchymal disease and hypertension. / Preston, Richard A; Epstein, M.

In: Seminars in Nephrology, Vol. 15, No. 2, 01.01.1995, p. 138-151.

Research output: Contribution to journalArticle

Preston, RA & Epstein, M 1995, 'Renal parenchymal disease and hypertension', Seminars in Nephrology, vol. 15, no. 2, pp. 138-151.
Preston, Richard A ; Epstein, M. / Renal parenchymal disease and hypertension. In: Seminars in Nephrology. 1995 ; Vol. 15, No. 2. pp. 138-151.
@article{c014d869d096460f97f61f0e53e51cf5,
title = "Renal parenchymal disease and hypertension",
abstract = "Renal parenchymal disease is the most common cause of secondary hypertension, accounting for 2.5{\%} to 5.0{\%} of all cases. Hypertension associated with renal parenchymal disease occurs as a complication of a wide variety of glomerular and interstitial renal diseases and may accelerate the decline in renal function if inadequately controlled. Renal parenchymal hypertension most probably represents the combined interactions of multiple independent mechanisms: potential factors include impaired sodium handling leading to volume expansion, perturbations of the renin-angiotensin system, alterations in endogenous vasodepressor compounds, and possibly increased activity of vasoactive substances. The past several years have witnessed newer insights into both the pathophysiology and the therapeutics of this disorder. The characterization of endothelin and the nitric oxide (NO)- arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. For example, methylated L-arginine derivatives that possess NO synthase inhibitor capabilities including N(G)-N- dimethylarginine and N-monomethyl-L-arginine are found in human plasma and in urine. Patients with chronic uremia have impaired elimination of these compounds, and circulating concentrations of these compounds may increase sufficiently to result in inhibition of NO production. Thus, accumulation of endogenous NO synthase inhibitors might contribute to the hypertension of advanced renal failure. Similarly, it has been proposed that increased endothelium-derived endothelin that results from hypertensive injury to vascular endothelium could lead to further vasoconstriction and worsening of hypertension. Additional insight into this fascinating problem must await further biochemical characterization of some of the mediators and a more precise delineation of their pathophysiological role.",
author = "Preston, {Richard A} and M. Epstein",
year = "1995",
month = "1",
day = "1",
language = "English",
volume = "15",
pages = "138--151",
journal = "Seminars in Nephrology",
issn = "0270-9295",
publisher = "W.B. Saunders Ltd",
number = "2",

}

TY - JOUR

T1 - Renal parenchymal disease and hypertension

AU - Preston, Richard A

AU - Epstein, M.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Renal parenchymal disease is the most common cause of secondary hypertension, accounting for 2.5% to 5.0% of all cases. Hypertension associated with renal parenchymal disease occurs as a complication of a wide variety of glomerular and interstitial renal diseases and may accelerate the decline in renal function if inadequately controlled. Renal parenchymal hypertension most probably represents the combined interactions of multiple independent mechanisms: potential factors include impaired sodium handling leading to volume expansion, perturbations of the renin-angiotensin system, alterations in endogenous vasodepressor compounds, and possibly increased activity of vasoactive substances. The past several years have witnessed newer insights into both the pathophysiology and the therapeutics of this disorder. The characterization of endothelin and the nitric oxide (NO)- arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. For example, methylated L-arginine derivatives that possess NO synthase inhibitor capabilities including N(G)-N- dimethylarginine and N-monomethyl-L-arginine are found in human plasma and in urine. Patients with chronic uremia have impaired elimination of these compounds, and circulating concentrations of these compounds may increase sufficiently to result in inhibition of NO production. Thus, accumulation of endogenous NO synthase inhibitors might contribute to the hypertension of advanced renal failure. Similarly, it has been proposed that increased endothelium-derived endothelin that results from hypertensive injury to vascular endothelium could lead to further vasoconstriction and worsening of hypertension. Additional insight into this fascinating problem must await further biochemical characterization of some of the mediators and a more precise delineation of their pathophysiological role.

AB - Renal parenchymal disease is the most common cause of secondary hypertension, accounting for 2.5% to 5.0% of all cases. Hypertension associated with renal parenchymal disease occurs as a complication of a wide variety of glomerular and interstitial renal diseases and may accelerate the decline in renal function if inadequately controlled. Renal parenchymal hypertension most probably represents the combined interactions of multiple independent mechanisms: potential factors include impaired sodium handling leading to volume expansion, perturbations of the renin-angiotensin system, alterations in endogenous vasodepressor compounds, and possibly increased activity of vasoactive substances. The past several years have witnessed newer insights into both the pathophysiology and the therapeutics of this disorder. The characterization of endothelin and the nitric oxide (NO)- arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. For example, methylated L-arginine derivatives that possess NO synthase inhibitor capabilities including N(G)-N- dimethylarginine and N-monomethyl-L-arginine are found in human plasma and in urine. Patients with chronic uremia have impaired elimination of these compounds, and circulating concentrations of these compounds may increase sufficiently to result in inhibition of NO production. Thus, accumulation of endogenous NO synthase inhibitors might contribute to the hypertension of advanced renal failure. Similarly, it has been proposed that increased endothelium-derived endothelin that results from hypertensive injury to vascular endothelium could lead to further vasoconstriction and worsening of hypertension. Additional insight into this fascinating problem must await further biochemical characterization of some of the mediators and a more precise delineation of their pathophysiological role.

UR - http://www.scopus.com/inward/record.url?scp=0028910694&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028910694&partnerID=8YFLogxK

M3 - Article

C2 - 7777724

AN - SCOPUS:0028910694

VL - 15

SP - 138

EP - 151

JO - Seminars in Nephrology

JF - Seminars in Nephrology

SN - 0270-9295

IS - 2

ER -