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Renal Module > Normal Renal Str and Func 2- Wall > Flashcards

Normal Renal Str and Func 2- Wall Flashcards

1
Q

What is the definition of renal clearance? Units?

A

The volume of plasma cleared of a particular substance by elimination into the urine per unit time (Units: mL/min)

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2
Q

What is excretion rate? Units?

A

It is the quantity of a substance in the urine per unit time (Units: mg/min). It is not the same thing as renal clearance

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3
Q

How is the renal clearance of a particular substance calculated/determined?

A

Clearance=Excretion Rate/Plasma Concentration
Cl(X)=UV/P= (U[X] x UFR)/P[X]
where U[X] is urine concentration of X, V=urine flow rate, P[X]=plasma concentration of X

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4
Q

What is approximately equal to GFR? Why?

A

Creatinine Clearance (CrCl) is approximately equal to GFR bc creatinine only enters the urine thru glomerular filtration and is not reabsorbed or secreted or metabolized to any great degree.

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5
Q

What does CrCl and therefore GFR tell you about kidney function? Why is CrCl not a perfect estimate of GFR?

A

CrCl is ~equal to GFR, which gives you an overall picture of kidney function.
There is ~10% creatinine secretion, so creatinine clearance slightly overestimates the true GFR.

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6
Q

How does the Clearance ration work? How is it calculated? What does it give you an indication of?

A

CR compares the clearance of a particular substance to the GFR;
CR=Cx/GFR, where Cx= clearance of substance X.
CR gives you an indication of how the kidney handles the particular substance.

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7
Q

What does a CR= 1.0 for a substance mean?

A

It means that the solute is handled like inulin or creatinine and its elimination (excretion rate) is equal to the GFR

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8
Q

CR<1? Example? Why for is this important for this example?

A

This means that the solute is filtered and then REABSORBED; Na→the filtered load of sodium is enormous (over 25000meq/day), and if all of this Na were eliminated, you would die in minutes; therefore, it must be reabsorbed and conserved

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9
Q

CR>1? Example?

A

This means that the solute is filtered and ACTIVELY SECRETED from the peritubular capillaries to the tubular fluid; Potassium or H+

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10
Q

CR=0? Examples?

A

This means that either the solute is too large to be filtered (protein), bound to plasma proteins, or it is filtered and 100% reabsorbed (Glc and AA’s should not be excreted to avoid wasting fuel).

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11
Q

Are there any endogenous markers for RPF (ml/min)? What is used as a marker of RPF?

A

Unfortunately, there is no endogenous substance that can be used to estimate RPF; however, para-aminohippurate (PAH) can be used exogenously as a marker for RPF

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12
Q

How is PAH used to measure RPF? Why is it a good marker for RPF?

A

It is administered IV to maintain a constant serum level. It is easily filtered and extremely avidly secreted, so that in one pass thru the kidney, almost all plasma is cleared of PAH.

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13
Q

How do you measure RPF? How is RPF calculated?

A

Clearance of PAH is used to estimate RPF;

Cpah=(Upah x V)/Ppah

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14
Q

What does the Filtration Fraction (FF) represent?

A

FF represents the percentage of renal plasma that became glomerular filtrate

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15
Q

How is FF calculated? What is normal GFR, RPF and FF?

A

FF=GFR/RPF;
Normal GFR= ~120 ml/min (10-20% lower in females)
Normal RPF= ~600 ml/min
Normal FF= ~120/600=0.2 or ~20%

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16
Q

What percentage of RPF usually becomes glomerular filtrate?

A

~20% (usually kept constant)

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17
Q

When can FF change?

A

It can change with a perturbation of volume state

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18
Q

How does the kidney respond if there is volume depletion (for instance in hypovolemia due to bleeding)?

A

Reduced CO→slight decrease in renal arterial perfusion pressure→Activation of RAAS

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19
Q

In volume depletion, how will the kidney alter the FF? How does this affect GFR?

A

In order to keep the GFR constant, the kidney will increase FF (autoregulation) by:

  1. Vasodilation of afferent arteriole
  2. Vasonconstriction of efferent arteriole
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20
Q

How does autoregulation vasodilate the afferent arteriole in volume depletion? Why does ANG-II not cause vasoconstriction of the afferent arteriole?

A

ANG-II produces vasodilatory prostaglandins (PGs) → Myogenic response of the vessel will cause dilation for more blood flow (less resistance)
Aff arteriole has minimal ANG-II receptors

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21
Q

How does autoregulation in volume depletion vasoconstrict the efferent arteriole?

A

Caused by local ANG-II, as the eff arteriole has abundant ANG-II receptors.
Since more plasma became filtrate at the glomerulus (dilation of aff arteriole), the hydrostatic pressure of the efferent arteriole (and thus peritub cap’s) is now much lower than normal.
Also, since no protein was filtered at the glomerulus, the same amount of protein reaches the efferent arteriole in a smaller volume, so therefore, the oncotic pressure in the peritubular capillaries is higher than normal. These starling forces enhance peritubular capillary reabsorption

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22
Q

Why is there enhanced peritubular capillary reabsorption in volume depletion? (2)

A

A. Since more plasma became filtrate at the glomerulus (dilation of aff arteriole), the hydrostatic pressure of the efferent arteriole (and thus peritub cap’s) is now much lower than normal.
B. Also, since no protein was filtered at the glomerulus, the same amount of protein reaches the efferent arteriole in a smaller volume, so therefore, the oncotic pressure in the peritubular capillaries is higher than normal.
Net: These starling forces enhance peritubular capillary reabsorption

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23
Q

What are the net effects of these autoregulation mechanisms in volume depletion?

A

a) maintain relatively constant RBF
b) GFR is maintained bc glomerular capillary pressure remains constant despite a decreased in perfusion pressure
c) Augmented reabsorption in the peritubular capillaries in the cortex, where most bulk reabsorption takes place
d) Thus delivery to the distal nephron is limited and the kidney gets better conservation of water and solutes

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24
Q

What two things can disturb the efficiency of the autoregulatory response in a hypovolemic state?

A
  1. Preventing local production of ANG-II (ACE inhibitors, ARBs, or direct renin inhibitors)
  2. Preventing the production of vasodilatory prostaglandins (NSAIDs)
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25
Q

What happens to the renal perfusion pressure in volume expansion?

A

Increased CO→Increased RPF→ Increased perfusion pressure

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26
Q

How does autoregulation alter the FF in response to hypervolemia causing increased renal perfusion pressure?

A

Autoregulation decreases FF (opposite effects as described above for hypovolemia):

a) kidney will shut off renin and ANG-II production
b) Net effect is to augment delivery to the distal nephron; therefore, it is easier to excrete solute and water

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27
Q

What happens in the proximal nephron?

A

bulk reabsorption occurs in the proximal nephron

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28
Q

What happens in the distal nephron?

A

Fine-tuning of solute and water reabsorption occurs at the distal nephron

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29
Q

What is the most important factor to control overall reabsorption and maintain homeostasis?

A

Controlling delivery to the distal nephron

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30
Q

What is the main filtered solute? Why is it important?

A

Na+→huge filtered load and its reabsorption is linked to the reabsorption of many solutes and water

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31
Q

What is the key cell type in reabsorption?

A

Renal epithelial cell (tubular cell)

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32
Q

What two features of these renal epithelial cells enhances their reabsorptive capacities?

A
  1. They are polarized cells (different transporters in apical vs basolateral membranes)
  2. PT epithelial cells have enormous surface area due to villi and microvilli
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33
Q

Why are the different segments of the nephron able to do different functions?

A

Different transporters are located in different segments of the nephron

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34
Q

How are adjacent epithelial cells attached to each other? What other purpose do these attachments serve?

A

Tight Junctions (think of them as gates); they separate the luminal/apical transporters from the basolateral transporters, which causes polarization of renal epithelial cells and separation of the unique apical transporters from the basolateral side and transporters

35
Q

What is abundant on the basolateral side of the renal epithelial cells?

A

Na/K ATPase

36
Q

What is the purpose of the abundant basolateral NaKATPase? Are there any apical NKA’s? Why?

A

The cell is reabsorbing a huge amount of Na+, which then must be removed from the cell and returned to the circulation; No, there are no apical NKA’s bc that would be counterproductive

37
Q

What allows huge amounts of reabsorption?

A

Specific transport proteins, ion channels, water channels, and transporters linking Na transport to solute transport which are specifically in the apical vs basolateral membrane

38
Q

What are the two ways that a solute can be reabsorbed?

A
  1. Transcellularly

2. Paracellularly (thru tight junctions)

39
Q

How are the proximal portions of the nephron, particularly the PCT characterized? What is the use of this?

A

as high capacity and low resistance;
So, there is bulk reabsorption without the creation of steep gradients (reabsorb a large amt, but the osmolality of the fluid remains the same with the constituents changed)

40
Q

How is the distal tubule characterized? What is this used for?

A

as low capacity and high resistance;

Not for bulk reabsorption, but for creation/maintenance of steep gradients between the urine and plasma

41
Q

How does paracellular reabsorption across tight junctions relate to the segment of the nephron they are in?

A

Paracellular reabs across TJ’s follows the transcellular patterns for each nephron segment

42
Q

What are the TJ’s composed of? What do these influence

A

claudin proteins that influence the properties of paracellular reabsorption

43
Q

What are the mechanisms of reabsorption? (6)

A
  1. Simple diffusion
  2. Facilitated or carrier-mediated diffusion
  3. Active transporters
  4. Coupled Transport
  5. Countertransport
  6. Channles
44
Q

What substances are reabsorbed by simple diffusion?

A

lipid soluble substance, urea, CO2

45
Q

What is an example of a facilitated diffusion transporter?

A

glucose transporter

46
Q

What are the active transporters in the nephron? Which is the main O2 and energy requiring thing in the kidney?

A
  1. Na/K-ATPase→main O2/energy requiring factor in the kidney
  2. H+ATPase→acid excretion
  3. Ca2+ATPase→calcium homeostasis
47
Q

How does cotransport (coupled transport) work? Why? Examples?

A

it links the transport of Na+ to the transport of other substances to avoid using energy in more than one step.
(Cl-, glc, AA’s, phosphate, urate, organic anions such as lactate and ketoanions,

48
Q

How does countertransport work?

A

one solute into the cell, another solute out of the cell (Na-H antiporter, Cl-HCO3 exchanger)

49
Q

What is the purpose of the channels in renal epithelial cells? Specific examples?

A

They are structures capable of reabsorbing enormous quantities

a. Aquaporins (AQP’s)
b. Ion specific channels
c. Urea channels

50
Q

What are aquaporins?

A

channels to transport H2O when simple diffusion isn’t enough; constitutively expressed in the proximal tubule and thin descending limb

51
Q

What are some examples of ion specific channels? Where are they located?

A

for Na+, K+, Cl-; can be apical or basolateral

52
Q

What is the major difference between carriers and channels?

A

Channels are not saturable. As long is there is an electrochemical gradient for the ion or water, it WILL move across a channel.

53
Q

Are carriers or channels saturable? What does this mean? What happens when the transport capacity is exceeded?

A

coupled transporters/carriers have Michaelis-Mentin kinetics; they are saturable and have a transport capacity. Once the transport capacity is exceeded, no more solute can be reabsorbed.

54
Q

What is considered the proximal nephron?

A

It includes all parts of the nephron from the PCT exiting the glomerulus up to the macula densa ( at the end of the TALH)

55
Q

What is the proximal nephron built for?

A

This entire segment is built for bulk reabsorption

56
Q

By the time the tubular fluid reaches the MD, how much of the total filtrate has been reabsorbed? What does the remaining nephron do?

A

By the time the tubular fluid reaches the MD, 90% of the total filtrate has been reabsorbed, leaving the remaining nephron with a small volume to create fine steep gradients, necessary for precise homeostasis.

57
Q

Why is everything geared toward getting solutes reabsorbed proximally?

A

So that the distal nephron is not overloaded. B/c the distal nephron is not built for bulk reabsorption, any excess delivered solute will be lost in the urine.

58
Q

Where is the PCT located?

A

PCT is located entirely in the cortex

59
Q

what do the peritubular capillaries arise from?

A

Cortical efferent arterioles

60
Q

Where is the PST located?

A

in the cortex, descends to the corticomedullary junction

61
Q

How is the osmolality and composition of the tubular fluid in the proximal tubule changed due to the bulk reabsorption in the proximal tubule? Why/

A

Osmolality is unchanged bc reabs in the PT is ISOTONIC, but the composition of the tubular fluid is altered by SELECTIVE reabsorption.

62
Q

What gets reabsorbed in the PT?

A
  1. Approx. 50-55% of total filtered load (FL) of NaCl and H2O (thru water channels, follows reabs of Na due to changes in osmotic pressure)
  2. Approx 90% of NaHCO3
  3. 100% of organic nutrients (glc, AA’s)
  4. K+
  5. Urea
63
Q

What also happens in the PT?

A

It is also the site of organic anion and cation secretory pathways, including PAH

64
Q

What is the major route of drug excretion?

A

Organic anion and cation secretory pathways in the PT

65
Q

How are PO4, urate, and organic anion reabsorption (lactate, pyruvate, ketoanions) reabsorbed in the PT?

A

linked to sodium coupled transport proteins

66
Q

Where is NH3 produced? What is NH3 important in?

A

NH3 production thru glutamine metabolism in the PT is important in acid/base metabolism

67
Q

How does urea reabsorption in the PT work?

A

it parallels water reabsorption

68
Q

Where does glomerulotubular balance occur?

A

PT (GT balance is different from tubuloglomerular feedback)

69
Q

What does Transport Maximum correspond to?

A

Tm exists for transporters with M-M kinetics bc they can become saturated.

70
Q

What is Glomerulotubular Balance (GTB)?

A

Matching how much of the solute gets reabsorbed at the proximal tubule to how much gets filtered.

71
Q

How much of the FL gets reabsorbed in the PT, regardless of GFR or FL?

A

50-55%

72
Q

Why is 50-55% of the GFR always reabsorbed in the PT?

A

Reabsorption in the PT is load dependent

73
Q

What would happen if the GFR increases 20% after a protein load? How would it affect the distal nephron?

A

There would be a large increase in the absolute amount filtered. If excess filtrate reached the distal nephron, the distal nephron could not handle it and excess solutes would be lost, eventually resulting in shock from hypovolemia.

74
Q

How does the nephron prevent this loss of excess solute after a protein load which increases the GFR by 20%?

A

The PT will continue to reabsorb 50-55% of the FL even when the GFR increases (load-dependent reabsorption). The absolute amount of filtrate reabsorbed by the PT increases, but the fraction of filtrate reabsorbed remains constant

75
Q

What does load dependent reabsorption in the PT mean?

A

filter more→reabsorb more in PT

76
Q

What is the primary active transport step in the PT? What is the purpose of the transporter?

A

the Na/K-ATPase gets it all started; 3 Na pumped out, 2 K pumped in).
This creates the Na+ electrochemical gradient that drives all the secondary transport processes of the PT, limiting the amt of ATP needed to move solutes

77
Q

How does the NKA pump create an electrochemical gradient for Na to enter the cell at the apical membrane?

A

It keeps the intracellular [Na] and makes the cell interior negative

78
Q

What is required for coupled transporters to work?

A

They do not work unless both components bind to the transporter

79
Q

What are some of the transporters used to reabsorb substances in the PT?

A
  1. Cotransporters: Na with Glc, PO4, Urate, AA, organic anion
  2. Na/H-Antiporter (Na into cell, H+ exits cell)
  3. Na channel→not saturable
  4. Water channels (AQP’s) and urea channels
80
Q

What is important about the kinetics of the Na-Glucose co-transporter in the PT?

A

It is a SATURABLE carrier

81
Q

What does it meant that the Na-Glc cotransporter is saturable?

A

As blood Glc increases, the FL of glc increases. The cotransporter will reabsorb more and more up to the point of saturation. After that, further increases in blood glc will still increase the FL, but more glc is not reabsorbed and is instead lost in the urine (glycosuria).

82
Q

In what kind of patients is glycosuria seen? At what blood glucose concentration do the Na-Glc cotransporters saturate?

A

This is seen in uncontrolled diabetics.

The transporters are saturated when blood glc>180-200 mg/dl.

83
Q

In patients with glycosuria, once the excess Glc passes thru the PT, what problems does it cause?

A

The excess glc in the tubular fluid then disturbs the function of the remaining tubular segments, acting as an osmotic diuretic→increased NaCl and water excretion

Renal Module (13 decks)

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