Chronic renal failure pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* | *[[Chronic kidney disease]] (CKD) is the progressive loss of renal function caused by a heterogeneous group of diseases but involving a common final pathophysiological process. [[CKD]] results from irreversible loss of glomeruli by glomerulosclerosis, a process consisting mainly of glomerular scarring. | ||
* | *Age related [[glomerulosclerosis]] and progressive decrease in renal function is a manifestation of normal aging. In fact, the [[GFR]] normally decreases by 1 ml/min/year after the age of 40. However, accelerated scarring of [[glomeruli]] and their premature irreversible loss occurs in pathological contexts where kidneys undergo glomerulosclerosis secondary to insults. | ||
*Some insults on the kidneys lead to the initiation of progressive kidney injury that becomes self perpetuating. These initiating factors are commonly related to systemic vascular diseases, like [[diabetes]], [[hypertension]] or [[atherosclerosis]]. Kidneys are well-vascularized organs consisting of millions of [[glomerulus|glomeruli]], which makes the kidney function highly dependent on the systemic vascular status and susceptible to systemic vascular diseases. Other diseases that contribute to CKD include toxin exposure, immune complex deposition and [[autoimmune diseases]]. | |||
*Regardless of the type of the primary cause, the pathological sequence of events involved in CKD is almost the same. The initiating factor causes decrease in the number of nephrons leading to structural and functional changes in the remaining surviving nephrons to compensate for the nephrons loss. Hence, adaptive mechanisms initially occur to increase the blood flow to the non sclerosed glomeruli and hence maintain a normal [[GFR]]. This is called hyperfiltration and it is mediated by vasoactive mediators, RAAS, cytokines, [[transforming growth factor β]] (TGF-β) as well as by other growth factors. | |||
* | *This adaptive mechanism leads to increase in the pressure in the remaining glomeruli and cause their accelerated sclerosis leading to further loss of the nephrons number. Further adaptation by hyperfiltration overwhelm the remaining normal nephron that will be at further risk of sclerosis. Hence, chronic kidney disease progresses in a self perpetuating way. | ||
*As the number of nephrons decreases more and more, the GFR further decrease and renal shrinkage occurs. When GFR dramatically decreases, symptoms of uremia start and the patient would be having end stage renal disease. | |||
*This | |||
===Pathophysiology of | ===Pathophysiology of Cardiovascular Complications=== | ||
*Cardiovascular risk and mortality is connected with the early stages of renal disease and in patients with [[chronic renal failure]], with its highest relative risk mortality in younger patients. | *Cardiovascular risk and mortality is connected with the early stages of renal disease and in patients with [[chronic renal failure]], with its highest relative risk mortality in younger patients. | ||
*This high risk for cardiovascular mortality results from hemodynamic and pressure overload, causing [[left ventricular hypertrophy]] and [[cardiomyopathy]]. Accelerated [[atherosclerosis]] and [[arteriosclerosis]] also contribute to the cardiovascular mortality risk. | *This high risk for cardiovascular mortality results from hemodynamic and pressure overload, causing [[left ventricular hypertrophy]] and [[cardiomyopathy]]. Accelerated [[atherosclerosis]] and [[arteriosclerosis]] also contribute to the cardiovascular mortality risk. | ||
Revision as of 09:12, 3 February 2013
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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 hypertrophying and hyperfiltrating. This innate ability of nephrons allows for continued removal of waste products from the body. Over time, this compensation mechanism becomes maladaptive, and the increased filtration pressure in the healthy nephrons leads to distortion of its structural architecture, causing sclerosis and eventual dropout of these nephrons.
Pathophysiology
- Chronic kidney disease (CKD) is the progressive loss of renal function caused by a heterogeneous group of diseases but involving a common final pathophysiological process. CKD results from irreversible loss of glomeruli by glomerulosclerosis, a process consisting mainly of glomerular scarring.
- Age related glomerulosclerosis and progressive decrease in renal function is a manifestation of normal aging. In fact, the GFR normally decreases by 1 ml/min/year after the age of 40. However, accelerated scarring of glomeruli and their premature irreversible loss occurs in pathological contexts where kidneys undergo glomerulosclerosis secondary to insults.
- Some insults on the kidneys lead to the initiation of progressive kidney injury that becomes self perpetuating. These initiating factors are commonly related to systemic vascular diseases, like diabetes, hypertension or atherosclerosis. Kidneys are well-vascularized organs consisting of millions of glomeruli, which makes the kidney function highly dependent on the systemic vascular status and susceptible to systemic vascular diseases. Other diseases that contribute to CKD include toxin exposure, immune complex deposition and autoimmune diseases.
- Regardless of the type of the primary cause, the pathological sequence of events involved in CKD is almost the same. The initiating factor causes decrease in the number of nephrons leading to structural and functional changes in the remaining surviving nephrons to compensate for the nephrons loss. Hence, adaptive mechanisms initially occur to increase the blood flow to the non sclerosed glomeruli and hence maintain a normal GFR. This is called hyperfiltration and it is mediated by vasoactive mediators, RAAS, cytokines, transforming growth factor β (TGF-β) as well as by other growth factors.
- This adaptive mechanism leads to increase in the pressure in the remaining glomeruli and cause their accelerated sclerosis leading to further loss of the nephrons number. Further adaptation by hyperfiltration overwhelm the remaining normal nephron that will be at further risk of sclerosis. Hence, chronic kidney disease progresses in a self perpetuating way.
- As the number of nephrons decreases more and more, the GFR further decrease and renal shrinkage occurs. When GFR dramatically decreases, symptoms of uremia start and the patient would be having end stage renal disease.
Pathophysiology of Cardiovascular Complications
- Cardiovascular risk and mortality is connected with the early stages of renal disease and in patients with chronic renal failure, with its highest relative risk mortality in younger patients.
- This high risk for cardiovascular mortality results from hemodynamic and pressure overload, causing left ventricular hypertrophy and cardiomyopathy. Accelerated atherosclerosis and arteriosclerosis also contribute to the cardiovascular mortality risk.
- Damage to and narrowing from atherosclerosis of the large vessels are major contributing factors for the 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.