Chronic renal failure pathophysiology: Difference between revisions
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{{CMG}} {{AE}} {{AN}} | {{CMG}} {{AE}} {{AN}} | ||
==Overview== | |||
Each [[kidney]] is made of approximately one million [[nephrons]]. In the event of an injury to the [[nephrons]], the remaining healthy [[nephron]]s compensate for the decrease in [[GFR]] by hypertrophy and hyperfiltration. This innate ability of nephrons allows for continued removal of waste products from the body. | |||
==Pathophysiology== | ==Pathophysiology== | ||
* | *The pathophysiology of [[chronic renal failure]] involves two broad mechanisms: | ||
**the initiating mechanism responsible for the injury to [[nephron]]s and compromising its filtration function eg: [[diabetes]], [[hypertension]], [[immune complex]] deposition, toxin exposure, [[inflammation]], chronic infections, genetically determined abnormality in development of [[nephron]]s. | |||
* | **a set of mechanisms, involving [[hypertrophy]] and hyperfiltration of the remaining healthy [[nephron]]s, that are a consequence of long term reduction of renal mass, irrespective of the underlying etiology. | ||
*This response of the healthy [[nephron]]s, is mediated by various [[growth factor]]s, vasoactive hormones, angiogenic factors and [[cytokines]]. | |||
* | *As the disease process progresses, this adaptive response becomes maladaptive, and increased filtration pressure in the healthy [[nephron]]s leads to distortion of its structural architecture, causing [[sclerosis]] and eventual dropout of these [[nephron]]s. | ||
*The [[renin]]-[[angiotensin]] axis is thought to contribute to the adaptive [[hypertrophy]] and [[sclerosis]], the latter, in part, from the action of [[transforming growth factor β]] (TGF-β). | |||
* | *This explains how a long standing disease process affecting the [[kidney]]s can eventually lead to decreased renal mass and function over a period of many years. | ||
* | ===Pathophysiology of cardiovascular complications=== | ||
*The excess cardiovascular risk and mortality is demonstrable in early renal disease and in patients with [[chronic renal failure]], with highest relative risk mortality in younger patients. | |||
* | *This high risk for cardiovascular mortality results from hemodynamic as well as pressure overload, causing [[left ventricular hypertrophy]] and [[cardiomyopathy]]. Accelerated [[atherosclerosis]] and [[arteriosclerosis]] also contributes. | ||
*Damage to the large vessels and [[atherosclerosis]] is a major contributing factor for high incidence of [[congestive cardiac failure]], [[ischemic heart disease]], [[left ventricular hypertrophy]], [[cerebrovascular accidents]], [[peripheral artery disease]] and [[sudden death]].<ref name="pmid12641870">{{cite journal |author=London GM |title=Cardiovascular disease in chronic renal failure: pathophysiologic aspects |journal=Semin Dial |volume=16 |issue=2 |pages=85–94 |year=2003 |pmid=12641870 |doi= |url=http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0894-0959&date=2003&volume=16&issue=2&spage=85}}</ref> | |||
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==References== | ==References== | ||
Revision as of 14:59, 25 July 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Each kidney is made of approximately one million nephrons. In the event of an injury to the nephrons, the remaining healthy nephrons compensate for the decrease in GFR by hypertrophy and hyperfiltration. This innate ability of nephrons allows for continued removal of waste products from the body.
Pathophysiology
- The pathophysiology of chronic renal failure involves two broad mechanisms:
- the initiating mechanism responsible for the injury to nephrons and compromising its filtration function eg: diabetes, hypertension, immune complex deposition, toxin exposure, inflammation, chronic infections, genetically determined abnormality in development of nephrons.
- a set of mechanisms, involving hypertrophy and hyperfiltration of the remaining healthy nephrons, that are a consequence of long term reduction of renal mass, irrespective of the underlying etiology.
- This response of the healthy nephrons, is mediated by various growth factors, vasoactive hormones, angiogenic factors and cytokines.
- As the disease process progresses, this adaptive response becomes maladaptive, and increased filtration pressure in the healthy nephrons leads to distortion of its structural architecture, causing sclerosis and eventual dropout of these nephrons.
- The renin-angiotensin axis is thought to contribute to the adaptive hypertrophy and sclerosis, the latter, in part, from the action of transforming growth factor β (TGF-β).
- This explains how a long standing disease process affecting the kidneys can eventually lead to decreased renal mass and function over a period of many years.
Pathophysiology of cardiovascular complications
- The excess cardiovascular risk and mortality is demonstrable in early renal disease and in patients with chronic renal failure, with highest relative risk mortality in younger patients.
- This high risk for cardiovascular mortality results from hemodynamic as well as pressure overload, causing left ventricular hypertrophy and cardiomyopathy. Accelerated atherosclerosis and arteriosclerosis also contributes.
- Damage to the large vessels and atherosclerosis is a major contributing factor for high incidence of congestive cardiac failure, ischemic heart disease, left ventricular hypertrophy, cerebrovascular accidents, peripheral artery disease and sudden death.[1]
References
- ↑ London GM (2003). "Cardiovascular disease in chronic renal failure: pathophysiologic aspects". Semin Dial. 16 (2): 85–94. PMID 12641870.