Hypertensive nephropathy pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
Line 3: Line 3:
{{CMG}} {{AE}} {{AN}}
{{CMG}} {{AE}} {{AN}}


==Overview==
==Pathophysiology==
The [[kidney]]s 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.
*Hypertension can involve any compartment of the kidney <ref name="SecciaCaroccia2017">{{cite journal|last1=Seccia|first1=Teresa M.|last2=Caroccia|first2=Brasilina|last3=Calò|first3=Lorenzo A.|title=Hypertensive nephropathy. Moving from classic to emerging pathogenetic mechanisms|journal=Journal of Hypertension|volume=35|issue=2|year=2017|pages=205–212|issn=0263-6352|doi=10.1097/HJH.0000000000001170}}</ref> :
**'''Vessels'''
*** Intimal thickening of small arterioles due to migration of myofibroblasts from media into intimal layer and secretion of collagen which leads to narrowing of the afferent arterioles.
*** thining of media layer and [[hyalinosis]] of the afferent arteriole due to loss of smooth muscle cells, which have been changed into myofibroblasts, leads to reduction in [[glomerular filtration rate]].
**'''Glomerules'''
***Constriction of intraglomerular capillaries due to [[hyalinosis]] causes glomerular ischemia and reduced filtration which induce accumulation of Extracellular Matrix [[(ECM)]].
***Hypertrophy of the remaining healthy glomerules maintains filtration but increases intra-glomerular pressure and developing microalbuminuria.
***Podocyte loss due to hyperfiltration and glomerulosclerosis, leads to destroying the filtration barrier and developing proteinuria.
**'''Tubulointerestitium'''
 
 


==Pathophysiology==
*Activation of [[renin]] - [[angiotensin]] - [[aldosterone]] system further contributes to .
*Two pathophysiological mechanisms have been postulated for the development of nephrosclerosis and [[chronic kidney disease]] in patients with [[hypertension]]:
*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]].
*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.
*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 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]].


===Gross Pathology===
===Gross Pathology===

Revision as of 09:47, 31 May 2020

Hypertensive nephropathy Microchapters

Home

Patient Information

Overview

Classification

Pathophysiology

Differentiating Hypertensive Nephropathy from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Abdominal X Ray

CT

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hypertensive nephropathy pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hypertensive nephropathy pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hypertensive nephropathy pathophysiology

CDC on Hypertensive nephropathy pathophysiology

Hypertensive nephropathy pathophysiology in the news

Blogs on Hypertensive nephropathy pathophysiology

Directions to Hospitals Treating Hypertensive nephropathy

Risk calculators and risk factors for Hypertensive nephropathy pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]

Pathophysiology

  • Hypertension can involve any compartment of the kidney [1] :
    • Vessels
      • Intimal thickening of small arterioles due to migration of myofibroblasts from media into intimal layer and secretion of collagen which leads to narrowing of the afferent arterioles.
      • thining of media layer and hyalinosis of the afferent arteriole due to loss of smooth muscle cells, which have been changed into myofibroblasts, leads to reduction in glomerular filtration rate.
    • Glomerules
      • Constriction of intraglomerular capillaries due to hyalinosis causes glomerular ischemia and reduced filtration which induce accumulation of Extracellular Matrix (ECM).
      • Hypertrophy of the remaining healthy glomerules maintains filtration but increases intra-glomerular pressure and developing microalbuminuria.
      • Podocyte loss due to hyperfiltration and glomerulosclerosis, leads to destroying the filtration barrier and developing proteinuria.
    • Tubulointerestitium


Gross Pathology

  • Benign nephrosclerosis:
  • Malignant nephrosclerosis:
    • Hemorrhages from surface capillaries gives the kidney a "flea-bitten" appearance.

Microscopic Pathology

References

  1. ↑ Seccia, Teresa M.; Caroccia, Brasilina; Calò, Lorenzo A. (2017). "Hypertensive nephropathy. Moving from classic to emerging pathogenetic mechanisms". Journal of Hypertension. 35 (2): 205–212. doi:10.1097/HJH.0000000000001170. ISSN 0263-6352.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Hypertensive_nephropathy_pathophysiology&oldid=1610051"