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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