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18 Cards in this Set
- Front
- Back
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CKD intro |
progression of CKD continues not due to the initial disease but due to the reduction in functional nephrons indepednent changes in glom vasculature and tubulointerstium |
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Remnant kidney model |
remove 5/6 ESRD in 4-6 months rats are noted to have widespread FSGS |
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Loss of nephrons |
due to vesicoureteral reflux leads to chronic nephritis causing destruction of tubules and intersitium loss of the neophrons triggers proliferation in other nephrons to maintain GFR overworked nephrons develop the segmental collapse of glomberular capillareis even wiht relief ESRD occur |
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Adaptations to 5/6 nephrectomy |
increase in SNGFR increase in glom pressure increase in renal plasma flow increase in glomerular proliferation cant see hyperplasia of epithelial cells, therefore the number of epithelial cells per glom decreasesa |
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Reduction of SNGFR |
due to decreae in afferent arteriolar resistnce and leads to high intraglomerular pressure and an increase in plasma flow functional changes cause an increased volume of the glom tuft and decreased density of epithelial cells |
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Maladaptations |
inrease in urinary albumin decrease in permeability increase in segmental scarring |
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Pathogenesis of glomsclerosis |
epithelial cell injury hyaline accumulation and mesangial expansion microaneurysm formation endothelial cell dysfuncton |
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Epithelial cell injury |
fusion of foot processes loss of epitheilal cells result in decreased local flow of water and salts, increased convective albumin flow |
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Effacemtn |
loss of filtration slits, creating an area where nothing can get through or everything can get thru (denuded) |
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Hyaline accumulation and mesangial expansion |
large proteins accumulate in the subendothelial space too large to pass through the glom BM form hyaline material leading to narrowing of the capillary lumen |
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Hyaline accumulation |
reduces the surface area for filtration |
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Microanerurysm formation |
enlargement of the tuft and increase in pressure of the tuft results in mesangial cells pulling off of the GMB which can then thrombose |
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Endothelial cell dysfunction |
loss of resistance to thrombosis |
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glomerulosclerosis |
renal response to nephron loss shows similar pattern proteinuriain patients following partial nephrectomy increases with decreasing amounts of remaining kidney |
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Pathogensis of vascular and tubular injury |
calcium phosphate deposition local ammonia accumulation proteinuria causing direct injury |
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Glomerular damage |
causes increasing amount of protein uptake into the cell triggers the Nf-Kb pathway that causes the tubules to increase prpduction of cytokines and increase converison to intersitial fibrosis |
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How to prevent secondary glom injury |
dietary protein restriction antihypertensive therapy (ace inhibitor) hypolipidiemic threapy |
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Ang II |
protective in that it lowers the GFR to prevent the GFR lowering due to injury |
