Hypertensive nephropathy pathophysiology: Difference between revisions
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*Two pathophysiological mechanisms have been postulated for the development of nephrosclerosis and [[chronic kidney disease]] in patients with [[hypertension]]: | *Two pathophysiological mechanisms have been postulated for the 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]]. The afferent renal arteriole undergoes [[Arteriosclerosis|hyaline arteriosclerosis]]. | *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 [[Arteriosclerosis|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. | ||
*Activation of [[renin]] - [[angiotensin]] - [[aldosterone]] system further contributes to the acceleration and perpetuation of glomerular and tubular injury | *Activation of [[renin]] - [[angiotensin]] - [[aldosterone]] system further contributes to the acceleration and perpetuation of glomerular and tubular injury. | ||
*In patients with primary [[hypertension]], intra-glomerular hemodynamic studies show a reduction in renal blood flow. This leads to increased permeability of glomerular capillaries to [[plasma]] components like [[plasma proteins]] especially [[fibrin]], initiating the [[clotting]] cascade and subsequently [[microangiopathic hemolytic anemia]], thus perpetuating the vascular pathology | *In patients with primary [[hypertension]], intra-glomerular hemodynamic studies show a reduction in renal blood flow. This leads to increased permeability of glomerular capillaries to [[plasma]] components like [[plasma proteins]] especially [[fibrin]], initiating the [[clotting]] cascade and subsequently [[microangiopathic hemolytic anemia]], thus perpetuating the vascular pathology. | ||
*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 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 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]]. | ||
===Gross Pathology=== | ===Gross Pathology=== | ||
*Benign nephrosclerosis: | *Benign nephrosclerosis: | ||
** The size of the [[kidney]]s is reduced or shrunken with loss of [[Renal cortex|cortical mass]] and fine granularity | ** The size of the [[kidney]]s is reduced or shrunken with loss of [[Renal cortex|cortical mass]] and fine granularity. | ||
*Malignant nephrosclerosis: | *Malignant nephrosclerosis: | ||
** [[Hemorrhage]]s from surface capillaries gives the kidney a "flea-bitten" appearance | ** [[Hemorrhage]]s from surface capillaries gives the kidney a "flea-bitten" appearance. | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
Revision as of 19:36, 12 March 2013
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Hypertensive nephropathy Microchapters |
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Differentiating Hypertensive Nephropathy from other Diseases |
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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 the 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.
- Activation of renin - angiotensin - aldosterone system further contributes to the acceleration and perpetuation of glomerular and tubular injury.
- In patients with primary hypertension, intra-glomerular hemodynamic studies show a reduction in renal blood flow. This leads to increased permeability of glomerular capillaries to plasma components like plasma proteins especially fibrin, initiating the clotting cascade and subsequently microangiopathic hemolytic anemia, thus perpetuating the vascular pathology.
- 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.
Gross Pathology
- Benign nephrosclerosis:
- The size of the kidneys is reduced or shrunken with loss of cortical mass and fine granularity.
- Malignant nephrosclerosis:
- Hemorrhages from surface capillaries gives the kidney a "flea-bitten" appearance.
Microscopic Pathology
- Benign nephrosclerosis:
- Afferent arterioles have eosinophilic fibrin deposits in the wall, causing hyaline arteriosclerosis
- Malignant nephrosclerosis:
- Fibrinoid necrosis in afferent arteriole
- Hyperplastic arteriosclerosis in inter-lobar arterioles
- Sclerosis in glomeruli and renal tubules