Hypertensive nephropathy pathophysiology

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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]

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.

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