Hypertensive nephropathy pathophysiology
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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] Nasrin Nikravangolsefid, MD-MPH [3]
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 a reduction in glomerular filtration rate (GFR).
- 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
- Dilatation, flattening and loss of epithelial tubular cells
- overexpression of fibrogenic and angiogenic factors such as transforming growth factor b1 (TGF-b1), Endothelin 1 (ET-1), and vascular endothelial growth factor (VEGF) results in disruption of tubular cells junction, transition of epithelial into mesenchymal cells, production of metalloproteinases, cell migration, production of collagen by myofibroblasts in the interstitial and subsequent tubulointerstitial fibrosis.
- Activation of Renin - Angiotensin - Aldosterone system further contributes to vasoconstriction, cell proliferation, reactive oxygen species production,inducing inflammation and ECM production.
- Angiotensin II induces differentiation of fibroblasts into myofibroblasts, which synthesize collagen in the periglomerular and peritubular regions.
- Dilatation, flattening and loss of epithelial tubular cells
- Vessels
- 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.
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
References
- ↑ 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.