Glomerular Filtration Flashcards
Filtration barrier
Ednothelium (fenestrated)
BM (collagen, laminin fibronectin)
Epithelium (podocytes with foot processes connected by slit membranes)..associated with footprocesses along the basement membrane
Filtration slit
COnnector proteins
Linker proteins
Actin-cytoskeleton complex
Mutations in these associated with glomerular dysfunction
Mesangial cells
Structural support for capillaries Secrete ECM Phagocytic Secrete prostaglands and cytokines Possess contractile activitiy
Granular cells synthesize renin
These are found between glomerular capillary loops
Macular densa - part of wall of distal tubule that comes back and touches the affarent/efferent complex
Ultrafiltrate of plasma formation
<5000 MW freely filtered
Above 5000, filterability governed by size and charge
High glycoprotein content of BM generates a net negative charge on the filtration pathway
Nephrotoxic serum nephritis - charge selectivity lost
COmpared to affarent arteriolar blood, concentration of protein and sodium in efferent arteriolar blood is?
Protein - Higher because it cannot be flitered out
Sodium - the same…this is because sodium is completely filterable…plasma filtered with sodium left in it
Compromised glomerular structure/function and consequences
Proteinuria
A/V thrombosis, hyperlipidemia, infection, edema
Starling forces in golmerular capillaries
GFR=Kf(Pgc-Pbs)-PiGc)
Pgc - cap HS pressure
Pbs - bowman’s space HS pressure
PIGc - glomerular capillary oncotic pressure
Typically net GFR into Bowman’s space
HS pressure along the glomerular capillary
Pgc is relatively constant
In systemic, it progressibley falls
Constant in glomerular due to the resistance AFTER the glomerular capillaries…the efferent arteriole**
Other starling forces across glomerular capillaries
Pigc - increases along the capillary because as fluid is filtered out the concentration of the non-filterable proteins increase
Net filtration pressure = 0 when PiGC increases to the point that it equals Pgc-Pbs
Kf
NFP is similar in glomerular and systemic capillaries
BUT The volume of fluid filtered across glomerular capillaries is MUH greater than systemic because Kf is higher
Kf = Lp*A
Water permability (Lp) 100* higher than systemic A = capillary surface area
Effect of change of Kf
Increase Kf means increased rate of rise of PiGC so NFP=0 achieved at earlier point along the capillary
Decreased Kf means decreased rate of rise so NFP=0 may never be achieved
GFR regulation
by Pgc
Dec affarnet - Pgc, GFR, RPF all go up and FF same
Increased in affarnet - decreased Pgc, GFR, RPF, and same FF
Decreased efferent - idecreased Pgc, GFR, FF…RPF increased
Increased in efferent - INcreased Pgc, GFP, and FF…decreased RPF
Affarent arteriole changes in resistance
Renal sympathetic nerves (vasoconstrictor decreases GFR)
Angiotensin 2 (vasoconstrictor) - affects btoh affarent and efferent arteriole
Vasodilatory protaglandins
Hemorrhage
Renal vasodilatory - PGE2 and PGI2
Decrease BP, increase RSN and increase AII - increase vasoconstriction
Increased RSN and AII - means increased PGE2 and PGI2 syntehsis and as a consequence the degree of renal vasoconstriction due to increased RNA/AII is reduced
NSAIDs and hemorrhage
Involved in accident…incease RSN and increase AII SHOULD induce PGE2 and PGI2…but it won’t with NSAIDs so increased renal vaosconstriction is HUGE and pre-renal acute renal failure
