Nondiabetic kidney disease

Paolo Cravedi, Piero Ruggenenti, Giuseppe Remuzzi

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The burden of chronic kidney disease represents a major health problem. Experimental studies and evidence in humans suggest that renal damage progresses independently of the initial cause and follows pathogenic mechanisms that are common among different nephropathies. After an initial renal injury, the number of functioning nephrons declines and remaining ones undergo hypertrophy, with concomitant lowering of arteriolar resistance and increased glomerular plasma flow. This compensatory mechanism allows preservation of glomerular filtration rate but is ultimately detrimental. Indeed, high intraglomerular capillary pressure impairs the size selectivity of the membrane and allows passage of larger molecules, such as proteins. An excess of proteins in the tubular lumen exerts a nephritogenic effect that fuels progressive renal function loss. In animals with proteinuric renal disease, glomerular hypertension and sieving dysfunction are ameliorated by drugs that inhibit the activity of the renin-angiotensin system (RAS), such as angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. RAS inhibitor therapy is the key component of intervention strategies aimed at retarding or preventing progression of chronic renal disease, and available data indicate that effective inhibition of the RAS may even regress established renal injury in experimental animals and improve kidney function in patients otherwise expected to relentlessly progress to end-stage renal disease.

Original languageEnglish
Title of host publicationCardiorenal Syndrome: Mechanisms, Risk and Treatment
PublisherSpringer Milan
Pages341-356
Number of pages16
ISBN (Print)9788847014626
DOIs
Publication statusPublished - 2010

Fingerprint

Kidney Diseases
Kidney
Renin-Angiotensin System
Chronic Renal Insufficiency
Angiotensin Receptor Antagonists
Nephrons
Wounds and Injuries
Glomerular Filtration Rate
Angiotensin-Converting Enzyme Inhibitors
Hypertrophy
Chronic Kidney Failure
Proteins
Hypertension
Pressure
Membranes
Health
Pharmaceutical Preparations

Keywords

  • Angiotensin receptor blocker
  • Angiotensin-converting enzyme (ACE) inhibitor
  • Chronic kidney disease
  • Combined RAS inhibitor therapy
  • End-stage renal disease (ESRD)
  • Hypertension
  • Proteinuria
  • Regression
  • Remission
  • Renin-angiotensin system (RAS)

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Cravedi, P., Ruggenenti, P., & Remuzzi, G. (2010). Nondiabetic kidney disease. In Cardiorenal Syndrome: Mechanisms, Risk and Treatment (pp. 341-356). Springer Milan. https://doi.org/10.1007/978-88-470-1463-3_26

Nondiabetic kidney disease. / Cravedi, Paolo; Ruggenenti, Piero; Remuzzi, Giuseppe.

Cardiorenal Syndrome: Mechanisms, Risk and Treatment. Springer Milan, 2010. p. 341-356.

Research output: Chapter in Book/Report/Conference proceedingChapter

Cravedi, P, Ruggenenti, P & Remuzzi, G 2010, Nondiabetic kidney disease. in Cardiorenal Syndrome: Mechanisms, Risk and Treatment. Springer Milan, pp. 341-356. https://doi.org/10.1007/978-88-470-1463-3_26
Cravedi P, Ruggenenti P, Remuzzi G. Nondiabetic kidney disease. In Cardiorenal Syndrome: Mechanisms, Risk and Treatment. Springer Milan. 2010. p. 341-356 https://doi.org/10.1007/978-88-470-1463-3_26
Cravedi, Paolo ; Ruggenenti, Piero ; Remuzzi, Giuseppe. / Nondiabetic kidney disease. Cardiorenal Syndrome: Mechanisms, Risk and Treatment. Springer Milan, 2010. pp. 341-356
@inbook{c0bf3473ff4e420d9439951eb9645179,
title = "Nondiabetic kidney disease",
abstract = "The burden of chronic kidney disease represents a major health problem. Experimental studies and evidence in humans suggest that renal damage progresses independently of the initial cause and follows pathogenic mechanisms that are common among different nephropathies. After an initial renal injury, the number of functioning nephrons declines and remaining ones undergo hypertrophy, with concomitant lowering of arteriolar resistance and increased glomerular plasma flow. This compensatory mechanism allows preservation of glomerular filtration rate but is ultimately detrimental. Indeed, high intraglomerular capillary pressure impairs the size selectivity of the membrane and allows passage of larger molecules, such as proteins. An excess of proteins in the tubular lumen exerts a nephritogenic effect that fuels progressive renal function loss. In animals with proteinuric renal disease, glomerular hypertension and sieving dysfunction are ameliorated by drugs that inhibit the activity of the renin-angiotensin system (RAS), such as angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. RAS inhibitor therapy is the key component of intervention strategies aimed at retarding or preventing progression of chronic renal disease, and available data indicate that effective inhibition of the RAS may even regress established renal injury in experimental animals and improve kidney function in patients otherwise expected to relentlessly progress to end-stage renal disease.",
keywords = "Angiotensin receptor blocker, Angiotensin-converting enzyme (ACE) inhibitor, Chronic kidney disease, Combined RAS inhibitor therapy, End-stage renal disease (ESRD), Hypertension, Proteinuria, Regression, Remission, Renin-angiotensin system (RAS)",
author = "Paolo Cravedi and Piero Ruggenenti and Giuseppe Remuzzi",
year = "2010",
doi = "10.1007/978-88-470-1463-3_26",
language = "English",
isbn = "9788847014626",
pages = "341--356",
booktitle = "Cardiorenal Syndrome: Mechanisms, Risk and Treatment",
publisher = "Springer Milan",

}

TY - CHAP

T1 - Nondiabetic kidney disease

AU - Cravedi, Paolo

AU - Ruggenenti, Piero

AU - Remuzzi, Giuseppe

PY - 2010

Y1 - 2010

N2 - The burden of chronic kidney disease represents a major health problem. Experimental studies and evidence in humans suggest that renal damage progresses independently of the initial cause and follows pathogenic mechanisms that are common among different nephropathies. After an initial renal injury, the number of functioning nephrons declines and remaining ones undergo hypertrophy, with concomitant lowering of arteriolar resistance and increased glomerular plasma flow. This compensatory mechanism allows preservation of glomerular filtration rate but is ultimately detrimental. Indeed, high intraglomerular capillary pressure impairs the size selectivity of the membrane and allows passage of larger molecules, such as proteins. An excess of proteins in the tubular lumen exerts a nephritogenic effect that fuels progressive renal function loss. In animals with proteinuric renal disease, glomerular hypertension and sieving dysfunction are ameliorated by drugs that inhibit the activity of the renin-angiotensin system (RAS), such as angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. RAS inhibitor therapy is the key component of intervention strategies aimed at retarding or preventing progression of chronic renal disease, and available data indicate that effective inhibition of the RAS may even regress established renal injury in experimental animals and improve kidney function in patients otherwise expected to relentlessly progress to end-stage renal disease.

AB - The burden of chronic kidney disease represents a major health problem. Experimental studies and evidence in humans suggest that renal damage progresses independently of the initial cause and follows pathogenic mechanisms that are common among different nephropathies. After an initial renal injury, the number of functioning nephrons declines and remaining ones undergo hypertrophy, with concomitant lowering of arteriolar resistance and increased glomerular plasma flow. This compensatory mechanism allows preservation of glomerular filtration rate but is ultimately detrimental. Indeed, high intraglomerular capillary pressure impairs the size selectivity of the membrane and allows passage of larger molecules, such as proteins. An excess of proteins in the tubular lumen exerts a nephritogenic effect that fuels progressive renal function loss. In animals with proteinuric renal disease, glomerular hypertension and sieving dysfunction are ameliorated by drugs that inhibit the activity of the renin-angiotensin system (RAS), such as angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. RAS inhibitor therapy is the key component of intervention strategies aimed at retarding or preventing progression of chronic renal disease, and available data indicate that effective inhibition of the RAS may even regress established renal injury in experimental animals and improve kidney function in patients otherwise expected to relentlessly progress to end-stage renal disease.

KW - Angiotensin receptor blocker

KW - Angiotensin-converting enzyme (ACE) inhibitor

KW - Chronic kidney disease

KW - Combined RAS inhibitor therapy

KW - End-stage renal disease (ESRD)

KW - Hypertension

KW - Proteinuria

KW - Regression

KW - Remission

KW - Renin-angiotensin system (RAS)

UR - http://www.scopus.com/inward/record.url?scp=84892258667&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84892258667&partnerID=8YFLogxK

U2 - 10.1007/978-88-470-1463-3_26

DO - 10.1007/978-88-470-1463-3_26

M3 - Chapter

AN - SCOPUS:84892258667

SN - 9788847014626

SP - 341

EP - 356

BT - Cardiorenal Syndrome: Mechanisms, Risk and Treatment

PB - Springer Milan

ER -