Hypertensive nephropathy pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
*Two pathophysiological mechanisms have been postulated for development of nephrosclerosis and [[chronic kidney disease]] in patients with [[hypertension]]. | *Two pathophysiological mechanisms have been postulated for development of nephrosclerosis and [[chronic kidney disease]] in patients with [[hypertension]]. | ||
*One mechanism suggests that glomerular [[ischemia]] results from [[Afferent arteriole|afferent arteriolar]] constriction, with a consequent reduction in [[glomerular filtration rate]]. | *One mechanism suggests that glomerular [[ischemia]] results from [[Afferent arteriole|afferent arteriolar]] constriction, with a consequent reduction in [[glomerular filtration rate]]. The afferent renal arteriole undergoes [[hyaline arteriosclerosis]]. | ||
*Another theory postulates that systemic [[hypertension]] causes injury to the nephrons. As a result, the remaining healthy nephrons undergo hyperfiltration and increase in intra-glomerular pressure from [[vasodilatation]] of afferent renal arterioles. This results in progressive glomerulosclerosis. | *Another theory postulates that systemic [[hypertension]] causes injury to the nephrons. As a result, the remaining healthy nephrons undergo hyperfiltration and increase in intra-glomerular pressure from [[vasodilatation]] of afferent renal arterioles. This results in progressive glomerulosclerosis. | ||
*In patients with primary [[hypertension]], intra-glomerular hemodynamic studies show a reduction in renal blood flow. | *In patients with primary [[hypertension]], intra-glomerular hemodynamic studies show a reduction in renal blood flow. | ||
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*The [[GFR]] is maintained from constriction of [[Efferent arterioles|efferent renal arterioles]] and [[systemic hypertension]]. Eventually, glomerular and tubular [[ischemia]] progresses and causes sclerosis. | *The [[GFR]] is maintained from constriction of [[Efferent arterioles|efferent renal arterioles]] and [[systemic hypertension]]. Eventually, glomerular and tubular [[ischemia]] progresses and causes sclerosis. | ||
*This suggests that hypertension accelerates the arteriolar changes and injury to the [[nephrons]]. | *This suggests that hypertension accelerates the arteriolar changes and injury to the [[nephrons]]. | ||
===Genetics=== | |||
Revision as of 02:52, 27 September 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
The kidneys may be damaged by or cause hypertension. Evidence from studies on renal transplant recipients and familial studies suggests a genetic component in occurrence of hypertensive nephropathy and nephrosclerosis.
Pathophysiology
- Two pathophysiological mechanisms have been postulated for development of nephrosclerosis and chronic kidney disease in patients with hypertension.
- One mechanism suggests that glomerular ischemia results from afferent arteriolar constriction, with a consequent reduction in glomerular filtration rate. The afferent renal arteriole undergoes hyaline arteriosclerosis.
- Another theory postulates that systemic hypertension causes injury to the nephrons. As a result, the remaining healthy nephrons undergo hyperfiltration and increase in intra-glomerular pressure from vasodilatation of afferent renal arterioles. This results in progressive glomerulosclerosis.
- In patients with primary hypertension, intra-glomerular hemodynamic studies show a reduction in renal blood flow.
- The reduction in glomerular pressure from afferent arteriolar constriction was thought to reduce ongoing damage to the nephrons. But, with time, sclerosis or scarring of afferent vessels slowly progresses, thereby further reducing the renal blood flow.
- The GFR is maintained from constriction of efferent renal arterioles and systemic hypertension. Eventually, glomerular and tubular ischemia progresses and causes sclerosis.
- This suggests that hypertension accelerates the arteriolar changes and injury to the nephrons.