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18 Cards in this Set

  • Front
  • Back

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


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


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


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