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18 Cards in this Set

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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

Remnant kidney model

remove 5/6




ESRD in 4-6 months




rats are noted to have widespread FSGS

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

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

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

Maladaptations

inrease in urinary albumin


decrease in permeability


increase in segmental scarring

Pathogenesis of glomsclerosis

epithelial cell injury




hyaline accumulation and mesangial expansion




microaneurysm formation




endothelial cell dysfuncton

Epithelial cell injury

fusion of foot processes




loss of epitheilal cells




result in decreased local flow of water and salts, increased convective albumin flow

Effacemtn

loss of filtration slits, creating an area where nothing can get through or everything can get thru (denuded)

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

Hyaline accumulation

reduces the surface area for filtration

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

Endothelial cell dysfunction

loss of resistance to thrombosis

glomerulosclerosis

renal response to nephron loss shows similar pattern




proteinuriain patients following partial nephrectomy increases with decreasing amounts of remaining kidney

Pathogensis of vascular and tubular injury

calcium phosphate deposition




local ammonia accumulation




proteinuria causing direct injury

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

How to prevent secondary glom injury

dietary protein restriction




antihypertensive therapy (ace inhibitor)




hypolipidiemic threapy

Ang II

protective in that it lowers the GFR to prevent the GFR lowering due to injury