Renal Volume

Front 1

Describe the distribution of water in the body

Back 1

-Total body water 60% of weight
-2/3 Intracellular
-1/3 Extracellular
-2/3 Interstitial
-1/3 Intravascular

Front 2

What is a good first approximation of salt content?

Back 2

Volume

Front 3

Describe congestive heart failure

Back 3

-ECF volume expanded
-NaCL (and H2O) retention
-Salt intake exceeds excretion

Front 4

Describe what happens if there is a sudden increase in salt in diet

Back 4

-Initially intake and output of salt are matched
-Weight is constant
-With step increase in Na intake, there is a slower increase in output
-Takes some time to reach steady state
-Weight increases
-The amount of salt increase is just a few grams, but must be properly diluted, so there are Kg of increased weight
-Return to normal salt intake has same lag in response

Front 5

Describe what happens if there is a sudden increase in pure water in diet

Back 5

You very suddenly start to put out water in urine

Front 6

Describe what happens with a change in dietary intake

Back 6

-Could be increased from diet or IV fluids
-Could be decreased through vomiting or diarrhea
-Change in Na content since initially U_Na is unchanged
-Change in Na content means change in extracellular volume
-Change in volume sensed (afferent limb)
-Change in U_Na via efferent limb re-establishes steady state

Front 7

Describe the response to a decrease in volume

Back 7

-Baroreceptors at juxtaglomerular apparatus (JGA) sense and increase renin
-Baroreceptors at the carotid/aortic arch sense and increase sympathetic outflow
-Baroreceptors at the atria sense and decrease atrial natriuretic peptide

Front 8

Describe the normal path of salt and water through the kidney

Back 8

-Blood flows into the afferent arteriole and out the efferent arteriole.
-The pressure gradient allows the extravasations of fluid into the urinary space.
-As that goes on that will be opposed by the proteins left behind.
-This fluid is the largely protein free ultrafiltrate.
-It enters the proximal tubule.
-The efferent arteriole then breaks into a peritubular capillary.
-The fluid goes through the loop of Henle into the thick ascending limb and then into the urinary tract.
-The total amount of salt filtered per day is 28000 mEq normallhy. Diet may be 100 mEq.
-In steady state, 27900 mEq are reabsorbed.
-This results in a constant weight.
-This is a process with a lot of filtration and a lot of reabsorption.

Front 9

Where in the renal tubule is the concentration of Na determined?

Back 9

From the thick ascending limb onward

Front 10

Describe the pressure relationship in the glomerular capillary and the peritubular capillary in the normal patient

Back 10

-No significant pressure or protein in the urinary space
-dP dominated by the pressure in the capillary and dPi dominated by the oncotic pressure in the capillary
-Difference between the two is the driving force for filtration and represents the GFR
-As you get to the end of the capillary you get the efferent arterile and that is a resistance vessel
-After the resistance is a pressure drop
-When there is pressure equilibrium is reachd there is no more filtration
-When dP drops below dPi, reabsorption occurs
-Glomerular capillary promotes filtration and peritubular capillary promotes reabsorption

Front 11

Describe the pressure relationship in the glomerular capillary and the peritubular capillary in the volume depleted patient

Back 11

-Renin is up, AII is up
-AII constricts efferent arteriole causing an increase in pressure and decrease in flow
-Pressure equilibrium reached much faster, but area under curve (GFR) unchanged
-With this constriction, high dPi carried over to the peritubular capillary
-There is constriction so presure falls even lower and there is an enormous gradient for reabsorption
-This is how vasoconstriction at the efferent arteriole modulates proximal reabsorption

Front 12

Describe the tubule flow and protein concentration in the normal glomerular and peritubular capillary

Back 12

-Renal plasma flow comes into the glomerular capillary and is fractionated between two bins
-One stays in the vessel of the efferent arteriole and the other becomes a protein-free ultrafiltrate
-The ultra filtrate portion is the GFR
-GFR is around 25% of glomerular capillary flow
-The fluid in the efferent arteriole has a high protein concentration

Front 13

Describe the tubule flow and protein concentration in the volume depleted glomerular and peritubular capillary

Back 13

-Less renal plasma flow comes into the glomerular capillary than in a normal individual
-This is fractionated between two bins: efferent arteriole and ultrafiltrate
-GFR/ultrafiltrate amount is same as in a normal individual
-GFR is now around 33% of glomerular capillay flow
-The fluid in the efferent arteriole now has a higher protein concentration than the efferent arteriole in the normal individual
-Filtration fraction went up as did peritubular capillary pressure
-The proximal tubule reabsorption of salt and water went up

Front 14

Describe what occurs in the peritubular capillary

Back 14

-There is a salt gradient from the proximal tubular capillary down through the cell, interstitium, and peritubular capillary
-In the proximal tubule this is a cotransporter
-Water travels with the Na down the gradient
-There is an Na:K ATPase in the cell that pumps out Na and with it goes water
-In the peritubular capillary the relationships aggressively favor fluid flow into the capillary
-If its not it will leak back in. if it leaks back in, it is like it never came through.

Front 15

Describe the formation and actions of angiotensin II

Back 15

-Angiotensinogen is coverted by renin to Angiotensin I
-Angiotensin I is coverted by ACE to angiotensin II
-Angiotensin II participates in:
-Vasoconstriction
-Aldosterone release
-Thirst
-Sympathetic tone
-Ion transport

Front 16

Describe how Angiotensin II conserves Na

Back 16

-Constricts the efferent arteriole
-Increased glomerular capillary hydrostatic pressure
-But flow decreasaes due to increased resistance. GFR unchanged
-Since RPF is decreased, the filtration fraction is increased
-Therefore increase in peritubular capillary oncotic pressure
-Proximal tubular Na reabsorption increases
-Increases proximal tubule Na transport directly
-Increased activity of NaH exchange
-Increased aldosterone

Front 17

Describe the consequences of sympathetic outflow on the kidney

Back 17

-Constrict efferent arteriole
-Descreases filtration through the entire system
-Patients with severe volume depletion have a decrease in GFR and can develop a prerenal state with elevation in creatinine
-Renin/Angiotensin II release
-Increases proximal tubule reabsorption
-If GFR is normal and proximal reabsorption is increased the BUN in the proximal tubule will be at higher concentration as more fluid is reabsorbed and this will drive BUN reabsorption
-BUN levels would then rise to a new steady state
-Direct effect on Na reabsorption

Front 18

How do you diagnose increased proximal tubular reabsorption?

Back 18

-Elevated BUN/creatinine ration
-It is a pre-renal state when the creatinine is normal
-If it is really severe and GFR has falled it is prerenal renal failure
-Creatinine rises means GFR fell and that is renal failure, but you can have a rise in BUN with normal creatinine. That is an indication that the patient is pre-renal but not in pre-renal renal failure

Front 19

Describe Atrial Netiuretic Peptide

Back 19

-Vasodilator
-Inhibits renin release
-Inhibits aldosterone release
-Decreases afferent arteriole tone
-Redistributes renal blood flow
-Decreases distal Na reabsorption
-Promotes Na excretion

Front 20

Describe autoregulation in the kidney if there is a jump in BP

Back 20

-If a patients BP jumps up, that high pressure is not going to cause them to excrete more Na.
-Autoregulation occurs because there is myogenic tone in the afferent arteriole.
-If the pressure gets jacked up you increase the pressure within a reasonable range, the renal blood flow changes by a relatively minor amount.
-The kidney has mechanisms to smooth out bounces in blood flow.
-As long as it doesn’t go outside the range you are fine

Front 21

Describe tubuloglomerular feedback

Back 21

-The relationship between what occurs at the glomerulus and what occurs at the tubule
-If you increase the rate of fluid that is perfusing the distal nephron then the more fluid you put through this thing the lower the single nephron GFR goes.
-It is like there is a sensor that knows if too much is being lost then we should clamp down on GFR to stop Na loses.

Front 22

Describe glomerular balance

Back 22

-Glomerulotubular balance says that when GFR goes up the amount that is reabsorbed proximally also goes up.
-That is the coupling in the pressure relationships between the glomerular capillary and the peritubular capillary that keep things in range.

Front 23

Describe what happens in the kidney when there is heart failure

Back 23

-Initial insult causes a drop in CO
-That drop is sensed
-There is increased sympathetic outflow and BP falls
-Falling BP causes increased pulse rate
-Drop in pressure sensed by JGA and renin activity is increased
-AII goes up causing aldosterone to go up

Front 24

What occurs when AII and aldosterone go up?

Back 24

-There is increased efferent arteriole tone, filtration fraction, and peritubular oncotic pressure
-There is increased proximal tubule reabsorption of salt and water
-Aldosterone goes up and there is a increase in distal reabsorption of salt
-If the increase is acute, Na secretion has dropped but intake remains constant

Front 25

What are the consequences of increased reabsorption of salt?

Back 25

-Plasma volume goes up
-Hematocrit goes down
-Weight goes up

Front 26

Describe starling curve shifts in CO decrrease in terms of salt

Back 26

-Heart failure can cause a downshift in the Starling curve
-CO falls and there are lots of mechanisms to retain Na
-As that extracellular fluid/intravascular volum expands, the LVEDP will increase.
-If you have salt intake and decreased salt output volume is going to expand and we are going to move up on the starling curve to a better position, thus increasing CO.
-This is at the expense of an increase in LVEDP which could leave the subject vulnerable to pulmonary edema.

Front 27

Describe the body's response to a decrease in CO

Back 27

-Increased baroreceptor
-Increased Renin/AII/Aldo
-Increased sympathetic outflow
-Decreased Na excretion
-Increased extracellular volume
-Interstitial (edema)
-Intravascular (LVEDV)
-Increased CO (starling curve)
-Decreased baroreceptors
-Na excretion increases to match intake
-New steady state

Front 28

Describe the new steady state reached after an insult that decreases CO

Back 28

-Renin is low, but slightly higher than old steady state
-Aldosterone is lower
-Urinary Na exretion is up
-Hct, plasma volume, and weight are all constant
-If you cure the proble with transplant, LV assist device, it is like releasing the constriction
-This really suppresses renin and aldosterone and sympathetics
-There is a spinke in salt excretion and weight goes back down

Front 29

Describe what occurs after a massive or multiple cardiac insults

Back 29

-Things can get so bad that no matter how much fluid you retain you can never get to a position on the starling curve where you can turn down the mechanisms.
-Seeing how your cardiac patient handles salt can tell you if they are compensated or decompensated.

Front 30

Describe Renal-Mediated Volume Disorders

Back 30

-Edematous states can arise from no GFR or excessive tubular reabsorption
-No GFR in renal failure
-Excessive tubular reabsorption in CHF, cirrhosis, nephrosis
-There are also ECF/Salt depleted states
-Hypoaldosteronism - not enough aldosterone to affect the last part of the distal nephron
-Osmotic diuresis (diabetes mellitus) - a lot of glucose and it draws water
-Diuretic abuse
-Not diarrhea - low volume state

Front 31

Describe how to interpret urine sodium

Back 31

-If urine sodium is low the salt retention mechanisms are activated
-You can look at the fractional excretion of sodium.
-You can also look at the BUN/creatinine ratio which gives you insight to whether proximal reabsorption is increased.

Front 32

Describe how to interpret urine sodium in a patient taking diuretics

Back 32

-If a patient is taking diuretics and the urine sodium is still low then you can interpret it, but if they are taking diuretics and the urine sodium is high then it doesn’t mean anything.

Front 33

Describe situations that cause abnormalities in the BUN/creatinine ratio

Back 33

-BUN/creatinine ratio can be artificially elevated if there is blood in the gut.
-BUN/creatinine can be lower than normal if your patient is starving because you need food in the system to mount a normal robust increase in BUN.