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Renal Week 1 > Lecture 8: Transport in the Distal Nephron > Flashcards

Lecture 8: Transport in the Distal Nephron Flashcards

1
Q

What is the character of fluid entering the thin limb of Henle’s Loop?

A
  1. Na is same as concentration as plasma
  2. Cl in higher concentration compared to plasma due to HCO3 reabsorption in PT
    • because of HCO3/Cl antiporter
  3. No glucose, AA or protein (unless diseased states)
  4. Rich in K as it is secreted into the pars recta (PST)
  5. Rich in NH4+ as it is synthesized in the PT
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2
Q

How much active transport activity is present in the THIN limbs of LoH?

A

Not a lot of active transport taking place
Mostly passive
Hardly any Na/K ATPase in thin descending and ascending loops

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3
Q

Where is Na/K ATPase activity lowest?

A

In the descending and ascending loops of LoH

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4
Q

What is the distal nephron?

A

Everything after the pars recta is considered the distal nephron

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5
Q

What is the function of the thin limbs of LoH?

A
  1. Descending thin limb epithelium is permeable to water but has a low permeability to Na and Cl
    • Allows water to be extracted from the tubule fluid as thin limb descends
    • Leads to hypertonic interstitium of medulla
  2. Ascending thin limb is largely IMPERMEABLE to water
    • highly permeable to Na and Cl
    • causes salt to diffuse out of the tubule
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6
Q

What is the INTEGRATED function of the thin limbs?

A

To reabsorb water and sodium isotonically that is in about same net concentration as Na/water in blood or glomerular filtrate
Allows one to reabsorb both the water and salt components of blood

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7
Q

What is the tubular fluid content by the end of the thin limbs?

A 
A. 75% of filtered NaCl reabsorbed
	-60% in PT
	-15% in thin limbs
B. 75% of filtered water reabsorbed
	-60% in PT
	-15$ in thin limbs
C. 90% of filtered potassium is reabsorbed (although there is still a lot of K because of K secretion)
D. 100% of filtered glucose reabsorbed
E. 90% of filtered phosphate reabsorbed
F. 20% of filtered magnesium reabsorbed
G. 100% of filtered HCO3- reabsorbed
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8
Q

What is the function of the thick ascending limb?

A
  1. Powerful NaCl transporter to dilute the urine
  2. Water impermeable
  3. Lumen positive potential difference vs blood side of tubule
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9
Q

What is the key transporter for thick ascending limb function?

A

The NKCC2 transporter
NKCC2 = Na-K-2Cl symporter
So brings in 1 mol of Na and K and 2 mol of Cl into the lumen
NKCC2 transporter has no limit as to how much sodium they can reabsorb

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10
Q

Why are furosemide diuretics (the ones that block NKCC2) so poor?

A

Because even though they block most NKCC2 channels, they don’t block them all
The transporters remaining have no saturation point so can take up as much solute as they see

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11
Q

What are the characteristics of the transporters in thick ascending limb?

A
  1. NKCC2 absorbs Na-K-2Cl and has no saturation point (can take up as much as comes by)
  2. There exists a ROMK (renal outer medullary potassium) channel on the apical membrane of thick ascending limb
    • ROMK pumps potassium (absorbed into lumen by NKCC2) back into the lumen
  3. Mg2+ and Ca2+ will go into the lumen because of K+ leaving the lumen
    • ROMK thus creates the electric gradient necessary for Ca and Mg to enter the cell
  4. there exists CLC-Kb/CLC-Ka channels on basolateral membrane that pump Cl- into circulation and away from the lumen
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12
Q

What happens to urinary calcium excretion when a patient has a defect in Renal Outer Medullary Potassium (ROMK) transporter?

A

Increased urinary calcium excretion because there is less of an electrogenic gradient

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13
Q

What ions are excreted in greater volume due to furosemide ?

A

Increases excretion of Na by blocking NKCC2

Also increases excretion of Ca and Mg because + charges stay in the lumen (K is not absorbed)

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14
Q

What is the character of reabsorption in THICK ascending limb of henle?

A 
The diluting section of the kidney
25% of filtered NaCl is reabsorbed
0% of filtered water is reabsorbed (ABSORBS NO WATER)
20% of filtered calcium reabsorbed
0% of glucose, Pi and HCO3- reabsorbed
70% of Mg reabsorbed
90% of synthesized NH3 reabsorbed
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15
Q

What are the consequences to patient with defect in thick ALH?

A
  1. failure to thrive (volume depletion)
  2. Low BP (volume depletion)
  3. Hypokalemia (No potassium uptake by NKCC2)
  4. Calcium deposits in the kidney (because not enough Ca uptake)
  5. High alkali content of the blood
    -depletion of ECF volume = increased aldosterone secretion
    -high aldosterone = increased K and H+ EXCRETION so less K and H in body
    -that’s why you get hypokalemia and excess alkali in body
    Receptors are all fucked inthis case
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16
Q

What is the normal character of fluid entering the distal tubule?

A
  1. Hypotonic due to powerful NaCl reabsorption in thick ALH
  2. Dilution due to concomitant H2O impermeability in thick ALH
  3. Very little K and NH4
  4. No HCO3-
  5. Moderate amount of Ca and Mg
  6. About 10% of filtered NaCl
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17
Q

What is the distal tubule made up of?

A

Early DCT or DCT1
Late DCT or DCT2
Connecting Tubule or CNT
Experiments show that transporters can change to meet body demand but more research required

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18
Q

What is the nature of distal nephron transport?

A
  1. steep chemical gradients established between lumen and cell/blood
  2. Hormonally regulated transport pathways serving systemic needs
  3. Separate pathways for sodium and other ion transport systems although sodium dependence often present
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19
Q

What is the key apical membrane transporter in the DCT?

A

The NCCT (Na-Cl cotransporter)
Na-Cl symporter
Takes up 5% of sodium
Blocked by thiazide

20
Q

What is the membrane potential at the DCT?

A

Slightly positive because of Cl- being reabsorbed

At the basolateral membrane and K+ cycling

21
Q

Where does Active Mg2+ absorption take place?

A

DCT1 and DCT2

22
Q

Where does active Ca2+ absorption take place?

A

DCT2 and CNT (connecting tubule)

23
Q

What region of the DCT actively absorbs both Ca and Mg?

A

DCT2

24
Q

What is the mechanism of Mg2+ reabsorption?

A 
In DCT1 and DCT2, TRPM6 lets Mg diffuse
Down its gradient
Gradient is established by efflux of K
Cells through Kv1.1 channel into the lumen
Efflux of K cells means intracellular is
Slightly negatively charged
NCC transporter is isoeletric
25
Q

What is TRPM6?

A

Transient Receptor Potential Magnesium

Ion channel

26
Q

What is EGF?

A

Epidermal growth factor
The first magnesiotropic hormone to regulate Mg2+ reabsorption through the TRPM6
EGF stimulates Mg reabsorption by activating the TRPM6

27
Q

What is the significance of HNF1B?

A

Stands for hepatocyte nuclear factor 1 homeobox B

Regulates the function of the Na/K ATPase by determining its expression

28
Q

What is the mechanism of Ca absorption?

A 
In DCT2 and CNT, 3 steps occur
1. entry of luminal Ca via the
TRPV5 channel on apical membrane
2. Calbindin (CaBP) buffers Ca and 
Ca diffuses to basolateral membrane
3. Ca is extruded by PMCA1b and NCX1
29
Q

What regulates calcium absorption

At the distal tuble?

A

Calciotropic hormones like

PTH and 1,25(OH)2D3

30
Q

What is the significance of calbindin

A

In the active transport absorption of calcium, it serves to buffer the calcium levels…too much calcium = apoptosis or worse

31
Q

What is PMCA?

A

Plasma membrane Ca ATPase

32
Q

What is NCX?

A

Sodium calcium exchanger

33
Q

What is 1,25(OH)2D3?

A

1,25 vitamin D or calcitriol
Promotes calcium absorption
PTH also promotes calcium reabsorption
PTH upregulates expression of vitamin D

34
Q

What is the character of fluid leaving DCT?

A
  1. Hypotonic
  2. Less sodium and chloride
  3. Little if any potassium
  4. Minimal calcium and magnesium (close to final urine amounts)
  5. Acidic (because no bicarb)
35
Q

What is the MRCT?

A

Medullary ray collecting tubule
Yellow = Distal Tubule
Blue = collecting duct

36
Q

What is the principal cell in the CCD (cortical collecting duct) epithelium?

A

One of two cell types of collecting duct
ENa is located in apical surface of principal cell
Na/K on basolateral membrane
K channel on both apical and basolateral membrane to pump K out
Sodium transport with steep gradients

37
Q

What are the two cell types in collecting duct?

A
  1. Principal cell (as seen below)
  2. Intercalated cells)
    • alpha intercalated cells
    • beta intercalated cells
38
Q

What is the function of alpha intercalated cells?

A

Secretes bicarbonate via pendrin (a specialized apical Cl/HCO3-)
Absorbs Acid through basal H+ATPase

39
Q

What are the effects of aldosterone? Consequences?

A

Upregulates ENac and the Na/K ATPase in collecting duct
Stimulates Alkalosis and hypokalemia (potassium wasting!)
Because so much Na is taken up, you have to counter that with excreting potassium
H/K antiports also work harder so you lose H+ as well

40
Q

What are the clinical consequences of excess sodium transport

A
  1. Hypertension (volume expansion)
  2. Hypokalemia
  3. Alkalosis
41
Q

What is potassium wasting?

A

When you excrete too much potassium and have hypokalemia

42
Q

What is Liddle’s syndrome?

A

A syndrome in which there is a gain of function in the ENaC leading to too much sodium absorption

43
Q

What are the two causes of excess sodium transport from the collecting tubule?

A
  1. hyperaldosteronism

2. Liddle’s syndrome (gain of function of ENaC)

44
Q

Why do H+ ions get secreted into the lumen during sodium excess?

A

Because chloride ions are taken up much more slowly from the lumen
Therefore this “lag” creates a temporary electric gradient that forces H+ towards the lumen, thereby depleting the cell of H+ and leading to alkalosis

45
Q

Where do H+ ions come from?

A

The combination of H2O and CO2 to form HCO3- and H+

46
Q

What are the intercalated cells?

A

The cells in collecting duct that produce H+

One of the two cell types of collecting duct

47
Q

What are the functions of collecting duct?

A
  1. Regulates the final urine composition for sodium, potassium and bicarb or H+
  2. Allows water retention or elimination depending on needs of the organism
  3. Allow the formation of a high osmolality in the renal interstitium so that concentration of the urine is possible

Renal Week 1 (15 decks)

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