Flashcards in Unit 7 - Filtration and Clearance Deck (29)
what is glomerular filtration? its components? what causes it?
process by which plasma is filtered across glomerular capillaries to form a protein-free ultrafiltrate in Bowman's space
-Starling forces across capillaries drive net efflux of ultrafiltrate from plasma
-with exception of plasma protein, organic and inorganic anionic and cationic solutes are freely filtered across glomerular capillaries and exist in same concentration in plasma and ultrafiltrate
what is the daily GFR? how does this compare to other capillaries? to ECF?
125 ml/min = 180 L/day
-only 3-4 L of plasma are filtered daily to form interstitial fluid
-ECF is only 14 L, meaning the entire ECF is filtered every 2 hours
--maintains ECF volume and solute composition within narrow limits
how does hydrostatic pressure inside the glomerular capillary decrease by only a small amount (45-50 --> 41-57) from beginning to end?
post capillary efferent arteriole constriction uniquely specific to glomerular (not systemic) capillaries
-happens despite decrease of plasma volume
how does Kf of glomerular capillaries compare to systemic? what does it account for?
filtration coefficient is more than 200x greater, accounting for large disparity in plasma filtration
why does oncotic pressure increase from beginning to end (25 --> 35) of glomerular capillary? why does Bowman's space oncotic pressure increase significantly in nephrotic syndrome?
plasma filtration and concentration of plasma protein
-increased Bowman's space oncotic pressure causes edema due to increased filtration of plasma PRO
what are the 3 components of the glomerular barrier to filtration? how do they help filter?
1. endothelial cells of glomerular capillaries restrict passage of cellular elements into Bowman's space
-fenestrations are ~70 nm
2. capillary basement membrane restricts filtration of solutes > 1 kDa
-has anionic charge (due to proteoglycans), to favor filtration of cations and restrict filtration of anionic PRO
3. podocytes of visceral epithelial layer of Bowman's capsule have foot processes covering outer glomerular capillaries
-contiguous foot processes are separated by filtration slits connected by thin slit diaphragm with pores 4-14 nm
-glycoPRO with negative charge cover podocytes, filtration slits, and slit diaphragms favoring filtration of small cationic solutes
what size solutes are freely filtered?
those below 4 nm (most effective are s only reabsorbed
equation of filterability
solute concentration in Bowman's space / solute concentration in plasma
-a solute freely filtered exists at same concentration in plasma and filtrate (ratio of 1)
how is solute filtration dependent on solute charge? what happens if this "barrier" is gone?
negative charge on basement membrane and foot processes impedes passage of negatively charged solutes (PRO) while allowing neutral and positively charged solutes
-removing the negative charge from the barrier will increase passage of anions
--serum nerphritis has increased filtration of plasma PRO
what are the renal hemodynamics and how do they relate to each other?
cardiac output = HR x SV = 5-6 L/min = 7200-8640 L/day
renal blood flow (RBF) = 1-1.2 L/min = 1440-1728 L/day
renal plasma flow (RPF) = 600-720 mL/min = 860-1040 L/day (55% of RBF)
GFR = 125 mL/min = 180 L/day (20% of RPF)
what is the filtration fraction? what is it usually?
GFR/RPF = fraction of RPF filtered at the glomeruli
-125 mL/min / 600 mL/min = 0.2
how is urine flow affected if chronic/acute renal failure reduces blood flow to zero? how should drugs be changed?
there is no urine output
-drugs should be reduced to allow less toxicity
what happens to RPF and GFR if...
1. afferent arteriolar constriction
2. efferent arteriolar constriction
3. both afferent and efferent arteriolar constriction
4. increased plasma PRO
5. decreased plasma PRO
6. ureter obstruction
1. decreased glomerular hydrostatic pressure causes decreased RPF and GFR
2. increased glomerular hydrostatic pressure causes decreased RPF and increased GFR
3. no change in glomerular hydrostatic pressure causes very low RPF, but no change in GFR (since starling force are constant)
4. increased glomerular oncotic pressure causes no change in RPF, but decreased GFR
5. decreased glomerular oncotic pressure causes no change in RPF, but increased GFR
6. increased Bowman's hydrostatic pressure causes no change in RPF, but decreased GFR
what do Starling forces do in post-glomerular peritubular capillaries?
drive fluid reabsorption from interstitial space
-oncotic pressure difference > hydrostatic pressure difference
what is the direction of filtration from tubular fluid in lumen to peritubular capillary?
tubular fluid in lumen --> tubular cell --> interstitial fluid --> peritubular capillary
when does renal failure begin?
when GFR decreases to below 20 mL/min (loss of founction of 85% of nephrons)
when can the renal clearance of a solute be used to measure GFR?
if renal handling of the solute is:
-freely filtered at the glomerulus (100%)
-not reabsorbed in any segment of the nephron (0%)
-not secreted in any segment of the nephron (0%)
-not synthesized by the kidney (0%)
-not metabolized (or otherwise chemically changed) by the kidney (0%)
if the above properties are matched, the amount of solute filtered should equal the amount excreted
what are solutes used to measure GFR? why?
exogenous inulin (fructose polymer)
-IV infusion to maintain constant plasma concentration
-measured very accurately in plasma and urine even if low concentration
endogenous creatinine (from creatine phosphate metabolism in skeletal muscle)
-if no strenous exercise or disease, there should be a constant amount of creatinine/time diffusion from skeletal muscle to plasma
these 2 are used because both are filtered 100% from glomeruli
if creatinine production is constant, what does increased plasma creatinine concentration indicate?
decreased clearance of creatinine from plasma
-indicates decreased GFR due to decreased number of functional nephrons
if kidneys are recovering from acute renal disease, what should happen to plasma creatinine levels?
they should decrease, indicating an increase in creatinine clearance and increased GFR
what is the equation for clearance of a solute?
Cs = Us x V / Ps
how does "renal handling" of a solute differ within nephron?
may be only reabsorption, only secretion, or both, in same or different segments of a nephron
-if both occur, the difference in solute reabsorption and secretion determines either net solute reabsorption (Cs/Cin < 1) or net solute secretion (Cs/Cin > 1)
fractional excretion of water
FEwater = V / GFR
fraction of glomerular filtrate not reabsorbed from tubular fluid along nephron, and thus appears as urine
-ratio of urine flow rate to GFR
how is FE of water measured?
draw blood and collect urine specimen to measure plasma and urine [creatinine] without having to time flow
fractional excretion of solute
FEs = Cs/Ccreatinine
-estimated as ratio of Cs to GFR
what is fractional reabsorption?
fraction of filtered water or solute that is reabsorbed thus not in urine
-usually quantified as 1 - FE
when water and Na are in balance, how much of filtered water and Na appears in urine? in negative water balance (dehydration)? in positive water balance? what about fractional reabsorption?
usually, FEwater = FEsodium = 1%, so fractional reabsorption is 99%
-negative balance: FEwater < 1%
-positive balance: FEwater > 5%
FEsodium constant at 1%
what is autoregulation of RBF due to?
-myogenic response of renal vasculature to pressure changes
-tubuloglomerular feedback at macula densa cells, sensing an increase/decrease in GFR to cause increased/decreased resistance (constriction) of afferent arteriole to return GFR to normal