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CVPR > CVPR Week 7: Renal tubular absorption and secretion > Flashcards

CVPR Week 7: Renal tubular absorption and secretion Flashcards

1
Q

Average GFR

A
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2
Q

Identify

A
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3
Q

Question 1

A
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4
Q

Tubular reabsorption selectivity

A

Tubular reabsorption is highly selective

  • Glucose, amino acids are nearly completely resorbed
  • Majority of sodium, chloride and HCO3- also highly resorbed however their are mechanisms to allow for variability
  • Waste products such as urea and creatinine are poorly resorbed so that large amounts are excreted in the urine
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5
Q

Kidney solute reabsorption summary

A
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6
Q

What is reabsorbed where?

A
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7
Q

What is reabsorbed in the proximal convoluted tubule?

A
  • Glucose 100%
  • Amino acids 100%
  • Urea 50%
  • Sodium 70%
  • Potassium 70%
  • Phosphate 70%
  • Calcium 70%
  • Magnesium 30%
  • H2O 70%
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8
Q

What is reabsorbed in the proximal straight tubule?

A

Phosphate 15%

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9
Q

What is reabsorbed in the thick ascending limb

A
  • Sodium 25%
  • Potassium 20%
  • Calcium 25%
  • Magnesium 60%
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10
Q

What is reabsorbed in the distal convoluted tubule

A

Sodium 5%

Calcium 8%

Magnesium 5%

H2O and urea is variable

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11
Q

What is reabsorbed in the collecting duct?

A

Sodium 3%

H2O and urea are variable

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12
Q

What is reabsorbed in the bladder?

A

Potassium 1-100%

Magnesium 5%

Phosphate 15%

Sodium < 1%

Calcium < 1%

H2O and urea are variable

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13
Q

What is filtered load?

A

Total substance filtered into Bowman’s space per time

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14
Q

Filtered Load equation

A

Filtered Load = GFR x [Plasma concentration S] x % unbound S

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15
Q

What is the excretion rate?

A

The amount of substance excreted per time

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16
Q

Excretion rate equation

A

Excretion rate = V’ x [urine concentration S]

where V’ is the micturation rate

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17
Q

How to determine the rate of absorption or secretion?

A

Reabsorption/Secretion rate = filtered load - Excretion rate

or

Urinary excretion = filtered load - tubular reabsorption + tubular secretion

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18
Q

Examples of net reabsorption and net secretion calculations

A
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19
Q

Types of reabsorption (transport mechanisms)

A

Active transport

Passive transport

carrier-mediated transport

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20
Q

Types of active transport

A

Primary active transport

Secondary active transport

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21
Q

Active transport description

A

requires energy expenditure for transport which is usually in the form of ATP

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22
Q

Primary active transport

A

direct energy expenditure to facilitate transport

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23
Q

Secondary active transport

A

Transport which is due to an ion gradient indirectly created by ATPase pump

Typically 2 or more substances are coupled across a membrane protein one moving down its concentration gradient to move the other substance

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24
Q

Example of primary active transport

A

Na+ via Na-K-ATPase pump present throughout the renal tubule

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25
Example of secondary active transport
Glucose via the SGLT1 and SGLT2 pumps
26
Passive transport description
no energy required, substance moves along its concentration gradient
27
Example of passive transport
Water reabsorption by tubules is passive and follows Na+ reabsorption
28
Na-K-ATPase pathway
29
Sodium reabsorption mechanisms in the renal system
* Na-K-ATPase is extensively located on the basolateral membranes throughout the renal tubule * there is an extensive brush border on the luminal membrane in the proximal tubule to increase surface area for diffusion of Na+ into the proximal tubular cells (20-fold increase) * Sodium co-transporters on the luminal membrane pull sodium, along with carrier substances, into the proximal tubular cells (amino acids, glucose)
30
What is reabsorbed or secreted in the early proximal tubule?
31
Features of carrier-mediated transport
* There is a limit because a limited number of carriers exist on a cell membrane and therefore the system can become saturated maximizing reabsorption or secretion * Carriers are stereospecific such as recognizing d-glucose but not I-glucose * Competition similar sized and shaped molecules can compete for transporter space such as lithium for sodium
32
Carrier-mediated transport speed of transport
There is a limit because a limited number of carriers exist on a cell membrane and therefore the system can become saturated maximizing reabsorption or secretion
33
Carrier-mediated transport specificity
Carriers are stereospecific such as recognizing d-glucose but not I-glucose
34
Carrier-mediated transport competition
Competition similar sized and shaped molecules can compete for transporter space such as lithium for sodium
35
Kinetics of carrier-mediated transport
36
Facilitated glucose transport (transport type)
Secondary active transport
37
Facilitated glucose transport mechanism
is a two-step process Step 1 * Glucose is initially reabsorbed from the luminal epithelial cells via SGLT cotransporter * 2 Na+ molecules transported for each one molecule of glucose * Protein rotates in the cell membrane and releases the Na+ and glucose into the ICF * Electrochemical gradient of Na+ drives reaction (from Na-K-ATPase) Step 2 * Glucose transported from cell to capillary by faciliated diffusion * GLUT 1 and GLUT 2 transporter * Moving down concentration gradient, no energy required
38
Glucose filtered loads
Glucose is freely filtered at the basement membrane filtered load rises with increasing serum concentration
39
At what levels can all the glucse be reabsorbed?
200 mg/dL
40
Glucose levels and reabsorption
Levels \> 200 mg/dL some of the glucose is unable to be reabsorbed and once \> 350 mg/dL, all of the glucose co-transporters are saturated thus reaching the transport maximum Tm
41
Question 2
42
Glucose titration curves
43
How is urea reabsorbed?
Passive urea reabsorption * Urea is reabsorbed and secreted in different segments of the nephron * driven by passive diffusion * Concentration gradient between tubular fluid and blood and epithelial cell membrane permeability to urea
44
Where is urea reabsorbed?
About half is reabsorbed in the proximal tubule
45
Urea rate of diffusion
Urea diffuses at slightly a slower rate than water
46
Passive urea reabsorption mechanism
* The urea is secreted in the descending loop of Henle due to high medullary urea concentrations reaching 110% of filtered urea load and bend of loop * Ascending loop of Henle distal convoluted tubule and cortical collecting ducts impermeable to urea * Inner medullary collecting ducts there facilitated urea reabsorption via urea transporter 1 which is upregulated in presence of ADH * Thus the final excretion of filtered urea is variable
47
Regulation of urea transporter 1 levels
upregulated in the presence of ADH
48
Urea handling in the nephron
49
Secretion of para-aminohippuric acid
example of secretion of an organic anion in promimal tubular cells transporter responsible for secretion of penicillin many transporters exist within promal tubular cells for secretion of organic acids and bases
50
Question 3
51
PAH titration curve
52
Question 4
53
How is HCO3- reabsorbed in the kidney?
the majority of filtered HCO3- is reabsorbed via secondary active transport
54
Na+ - H+ exchanger
Na+ - H+ exchanger is responsible for reclamation
55
Reabsorption of filtered HCO3-
56
Question 5
57
Sodium balance
58
What percentage of sodium is usually secreted?
1% of sodium is typically excreted
59
Positive Na+ balance results in
expanded extracellular fluid volume, hypertension and potentially edema but does not equal a change in serum Na concentration
60
How are changes in serum Na+ concentration reflected?
Changes in serum Na+ concentration are reflected by increases or decreases in total body water composition rather than Na+ balance
61
Where is most of the Na+ reabsorbed?
approximately 2/3 of Na+ in the proximal tubule where water reabsorption follows sodium reabsorption
62
Where does sodium reabsorption occur?
* approximately 2/3 of Na+ in the proximal tubule where water reabsorption follows sodium reabsorption * 25% is reabsorbed in the thick ascending loop of Henle which is impermeable to water by the Na/K/2Cl- cotransporter * 5% is absorbed in the early distal convoluted tubule which is also impermeable to water * 3% is absorbed in the late distal convoluted tubule and collecting duct
63
Explain Na+ handling in the nephron
64
Explain reabsorption and secretion in the late proximal tubule
65
Question 6
66
Permeability of the thin descending loop of Henle
The thin descending loop of Henle is permeable to small solutes, urea and water
67
Permeability of the thin ascending loop of Henle
The thin ascending loop of Henle remains permeable to small solutes but is no longer permeable to water
68
Describe the osmolarity of the ultrafiltrate throughout the loop of Henle
In the thin descending loop of Henle the osmolarity of ultrafiltrate increases towards the bottom of the loop of Henle In tthe ascending thin loop of Henle small solutes leave and the ultrafiltrate becomes more hypo-osmolar
69
Describe secretion and reabsorption in the thick ascending limb of the loop of Henle
Secondary active reabsorption of Na+ via the Na/K/2Cl- cotransporter energy driven by Na/K/ATPase
70
Diuretic effect on diuresis
diuretic blocking reabsorption in the proximal tubule has a small effect on diuresis
71
Loop diuretics bind to?
loop diuretics bind to the chloride portion of the Na/K/2Cl- cotransporter inactivating the channel
72
Sodium balance in the early distal tubule
5% of Na+ is reclaimed here via the Na/Cl cotransporter secondary active transport driven by Na/K/ATPase
73
Early distal tubule permeability to water
Remains impermeable to water
74
Thiazide-type diuretics bind to?
the Cl- portion of the Na/Cl cotransporter in the distal tubule and inactivate this channel
75
Describe reabsorption and secretion in the early distal tubule
76
What binds to the Na/Cl cotransporter in the early distal tubule
thiazide diuretics
77
What binds to the Na/K/2Cl cotransporter in the thick ascending limb of the loop of Henle?
Loop diuretics (i.e. Furosemide)
78
Types of cells in the late distal tubule 2 listed
* Principal cells * α-intercalated cells
79
Principal cells of the late distal tubule function
* Na+ and water reabsorption * K+ secretion
80
α-intercalated cells in the late distal tubule function
* K+ reabsorption * H+ secretion
81
The importance of the late distal tubule and collecting duct in sodium balance
Though the cells of the DCT and collecting duct only account for 3% of Na+ reabsorption they are hormonally influenced and are a major determinant of overall Na+ balance
82
How much sodium reabsorption do the distal convoluted tubule and the collecting ducts account for?
DCT and collecting duct only account for 3% of Na+ reabsorption but play a major role in determining the overall Na+ balance through hormones
83
ENaC AKA
Epithelial Sodium Channel
84
Amilorone site of action
ENaC
85
Triamterene site of action
ENaC
86
Aldosterone effect on principal cells
* Aldosterone causes an upregulation ENaC channels and the Na/K/ATPase in the principal cells
87
How do principal cells reabsorb Na+
reabsorb Na+ via the Epithelial Sodium Channel (ENaC) which is the site of action for amiloride and triamterene
88
Drugs that target ENaC
* Amiloride * Triamterene
89
Drugs that target the aldosterone receptor on principal cells
* Spironolactone * Eplerenone
90
Spironolactone site of action
Aldosterone receptor of principal cells
91
Where are principal cells located?
the late distal tubule
92
What do principal cells do?
* Na+ and water reabsorption * K+ secretion
93
Antidiuretic hormone release results in?
Aquaporin2 channel insertion into the luminal membranes of the DCT and collecting duct increasing their permeability to water
94
What happens when the Aquaporin-2 channel inserts into the luminal membranes of the DCT and collecting duct
Increased permeability to water
95
Describe reabsorption and secretion in the DCT and collecting duct
96
Early proximal tubule major functions
Isosmotic reabsorption of solute and water
97
Early proximal tubule cellular mechanisms
* Na+/glucose * Na+ /amino acid * Na+ /phosphate cotransport * Na+/H+ exchange
98
Early proximal tubule Hormone actions
* PTH inhibits Na+ phosphate cotransport * Angiotensin II stimulates Na/H exchange
99
Early proximal tubule diuretic classes w/ actions
* osmotic diuretics * carbonic anhydrase inhibitors
100
Late proximal tubule major functions
Isosmotic reabsorption of solute and water
101
Late proximal tubule cellular mechanisms
NaCl reabsorption driven by Cl- gradient
102
Late proximal tubule hormone actions
none
103
Late proximal tubule diuretic classes w/ actions
Osmotic diuretics
104
Thick ascending limb of the loop of Henle major actions
* Reabsorption of NaCl without water * Dilution of tubular fluid * single effect of countercurrent multiplication * Resorption of Ca2+ and Mg2+ driven by lumen-positive potential
105
Thick ascending limb of the loop of Henle cellular mechanisms
Na/K/2Cl cotransport
106
Thick ascending limb of the loop of Henle hormone actions
ADH stimulates Na/K/2Cl cotransport
107
Thick ascending limb of the loop of Henle diuretic w/ actions
Loop diuretics
108
Early distal tubule major functions
* Reabsorption of NaCl without water * Dilution of tubular fluid
109
Early distal tubule Cellular mechanisms
NaCl cotransport
110
Early distal tubule hormone actions
PTH stimulates Ca2+ reabsorption
111
Early distal tubule diuretics w/ actions
Thiazide diuretics
112
Late distal tubule and collecting ducts (principal cells) major functions
* Reabsorption of NaCl * K+ secretion * Variable water reabsorption
113
Late distal tubule and collecting ducts (principal cells) cellular mechanisms
* Na+ channels (ENaC) * K+ channels * AQP2 water channels
114
Late distal tubule and collecting ducts (principal cells) hormone actions
* Aldosterone stimulates Na+ reabsorption * Aldosterone stimulates K+ secretion * ADH stimulates water reabsorption
115
Late distal tubule and collecting ducts (principal cells) diuretics w/ actions
K+ sparring diuretics
116
Late distal tubule and collecting ducts (α-intercalated cells) major functions
* Reabsorption of K+ * Secretion of H+
117
Late distal tubule and collecting ducts (α-intercalated cells) cellular mechanisms
* H/K/ATPase * H/ATPase
118
Late distal tubule and collecting ducts (α-intercalated cells) hormone actions
Aldosterone stimulates H+ secretion
119
Late distal tubule and collecting ducts (α-intercalated cells) diuretics w/ actions
K+ sparring diuretics
120
Major mechanisms affecting Na+ balance 4 listed
* SNS * ANP * Starling forces in peritubular capillaries * Renin-Angiotensin-Aldosterone System
121
How does the SNS affect the Na+ balance? 2 listed
* Decreased blood volume detected by carotid baroreceptors * vasoconstriction of afferent arterioles and increased proximal tubule Na+ reabsorption
122
How does ANP affect Na+ balance? 3 listed
* Stretch of atria * Vasodilation of afferent arterioles and vasoconstriction of efferent arterioles (increase GFR) * Decreases Na+ reabsorption in DCT and collecting duct
123
How do Starling forces in peritubular capillaries affect Na+ balance?
* Glomerulotubular balance - expansion of ECF decreases oncotic pressure minimizing fluid reabsorption
124
How does the Renin-Angiotensin-Aldosterone System affect Na+ balance?
* Activated in response to decreased renal perfusion pressure
125
Increased Na+ intake results in?
126
Reduced Na+ intake results in?
127
Question 7
128
Mechanism of isosmotic reabsorption in the proximal tubule
129
Question 8
130
Question 9
131
Potassium balance
132
Describe K+ handling in the nephron
133
Describe K+ handling in the late distal tubule and collecting duct
134
Question 10
135
Clearance of weak acid/base
136
Clearance of weak acid/base and urine pH
137
Clinical considerations of diuretics
138
Clinical considerations of SGLT inhibitors
Treatment of diabetes
139
Clinical considerations of ACE-inhibitors/Angiotensin receptor blockers
management of hypertension
140
Clinical considerations of carbonic anhydrase inhibitors
Acetazolamide - acidifying agent for severe alkalosis
141
Disease Clinical considerations

CVPR (93 decks)

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