Pathology of the urinary system


GLOMERULITIS AND GLOMERULONEPHRITIS



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PATHOLOGY OF THE URINARY SYSTEM

GLOMERULITIS AND GLOMERULONEPHRITIS

 

 



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the glomerular filtration membrane consists of three layers: capillary endothelium, glomerular 

basement membrane (GBM), epithelial cells (podocytes); the GBM is produced continuously by the 

podocytes and endothelial cells. 

 

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the glomerular filtration membrane excludes particles from filtration on the basis of: 

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size:   the GBM prohibits passage of particles with radius greater than 8 nm; 

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charge:   negatively charged sialoglycoproteins and heparan sulfate in the GBM and the 

negatively charged cell coats of the endothelial cells and podocytes repel anionic (negatively 

charged) molecules such as albumin (which has a radius of only 6 nm). 

 

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the mesangium is the central region of the glomerulus; it includes: 

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a mesengial matrix, composed of basement membrane-like glycoprotein; 

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mesangial cells, which are phagocytic and contractile cells derived from vascular smooth 

muscle cells; these cells participate in the turnover of the GBM, can remove deposited 

macromolecules, and, through contraction and relaxation, can influence intraglomerular 

blood flow; they can also produce a variety of cytokines which, in turn, can modulate 

immune responses. 

 

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glomerular lesions can cause: 

- interference with glomerular blood flow → decreased formation of filtrate and impaired 

 

peritubular blood perfusion; 



- altered glomerular permeability → leakage of protein into the tubules; proteinuria occurs 


 

 

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when protein leakage exceeds tubular reabsorption; excessive and persistent traffic 



 

through the proximal tubular epithelial cells of protein lost through the glomeruli can 

 

up-regulate vasoactive and pro-inflammatory molecules normally produced by these 



 

cells and thus lead to progressive renal injury. 

 

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extensive protein loss causes 


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