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Renal Final > Renal Transport Mechanisms > Flashcards

Renal Transport Mechanisms Flashcards

1
Q

What fraction of filtered water is reabsorbed by the PT?

A

2/3

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2
Q

Why do the lines for Na and K superimpose on the 1.0 line on TF:P graphs?

A

They are reabsorbed at the same rate as water

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3
Q

What does it mean to have a TF:P ratio of >1?

A

More water is reabsorbed than solutes, or solute is being secreted

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4
Q

What does it mean to have a TF:P ratio of <1?

A

More solute is being reabsorbed than water

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5
Q

Sodium uptake across the apical membrane in the early PT is coupled with another molecule. What molecules might sodium be reabsorbed with?

What about exchanged with?

A

Primarily with HCO3

Can also be with glucose, amino acids, Pi, and lactate

May be reabsorbed in exchange for H+ or organic solutes

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6
Q

The reabsorption of Na and its buddies in the PT generates a transtubular osmotic gradient. Osmolality of tubular fluid is slightly ______ than that in the ISF outside the basolateral membrane, which provides the driving force for ______ diffusion of water from the tubule to ISF and the blood.

A

Lower

Passive

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7
Q

More water than Cl is reabsorbed in the early PT, so tubular [Cl] rises by the time we come to the late PT. How does this drive reabsorption of Na and Cl?

A

By creating a positive transepithelial potential difference, driving paracellular reabsorption of Na and Cl

There is also a modest concentration gradient created by sodium and water reabsorption, as Cl and urea become more concentrated along the length of the PT

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8
Q

Na+uptake across the apical membrane of the LATE PT is coupled with ____ via _________ route

[what other transporters must be operating simultaneously?]

A

Cl; transcellular

Requires operation of parallel transports in Na/H antiporter and Cl-base antiporters

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9
Q

What forces push water from interstitial fluid into the peritubular capillary?

A

Hydrostatic pressure pushes fluid and solute from ISF into peritubular capillary space

In addition, protein oncotic pressure in peritubular capillary is elevated bc of glomerular filtration, which helps pull water in

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10
Q

Describe transport mechanism and cellular path for glucose reabsorption

A

Secondary active transport along trancellular path across SGLT in apical membrane using gradient set up by Na/K ATPase in basolateral membrane

Glucose then exits through basolateral membrane via facilitated diffusion through GLUT transporter

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11
Q

What happens in filtered amount of glucose exceeds a certain rate?

A

If filtered load exceeds a certain rate, SGLTs become saturated and capacity to reabsorb all glucose is exceeded (Tm); glucose appears in the urine

[same principle applies to protein]

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12
Q

Where in the nephron is secretion most active?

A

PT

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13
Q

Describe transporters utilized for organic anion secretion

A

OATs in basolateral membrane - OA’s are taken across basolateral membrane in exchange for a-KG moving down its gradient.

OA’s cross the apical membrane via ATP dependent MRP2/4 or BCRP; or via OAT4 in exchange for a-KG

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14
Q

Describe transporters utilized for organic cation secretion

A

OCT’s in basolateral membrane - cations taken across basolateral membrane driven by magnitude of cell-negative potential difference

OCT’s in apical membrane (ATP dependent), or in exchange for H+

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15
Q

T/F: PAH is both filtered and secreted

A

True

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16
Q

What type of molecule is creatinine, and what transporters does it utilize?

A

An organic cation; utilizes organic cation and anion transporters

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17
Q

What occurs in the kidneys with aspirin poisoning, and how might this be treated?

A

Aspirin has a weak acid metabolite (salicylic acid), dropping the pH of the urine.

Treatment goal is to make the urine more alkaline with sodium bicarb in order to increase ionization of salicylic acid and increase its excretion from the body. Activated charcoal and IV sodium bicarb are used to keep HCO3 from being reabsorbed, or to take more H+ out of the tubule.

[ionization makes it harder for the salicylic acid to be reabsorbed back into the cell]

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18
Q

What are some factors the shift K+ into cells (thus potentially causing hypokalemia)

A

Insulin
Aldosterone
B-adrenergic stimulation
Alkalosis

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19
Q

What are some factors that shift K+ out of cells (thus potentially causing hyperkalemia)

A 
Insulin deficiency
Aldosterone deficiency
B-adrenergic blockade
Acidosis
Cell lysis
Strenuous exercise
Increased extracellular fluid osmolality
20
Q

Variations in [K+] alter membrane potential of skeletal muscle and can result in cardiac arrhythmias. What effect does hyperkalemia have on these 2 cell types?

A

Skeletal muscle: increases resting potential, thus making it easier to generate a muscle contraction

Cardiac muscle: PR interval prolonged, T wave “tenting”, P wave may become indiscernable, possible Vfib. Becomes lethal at high concentrations

21
Q

Variations in [K+] alter membrane potential of skeletal muscle and can result in cardiac arrhythmias. What effect does hypokalemia have on these 2 cell types?

A

Skeletal muscle: shifts resting potential more negative, making muscle contraction more difficult

Cardiac muscle: flattened T wave, may depress ST segment

22
Q

What is reabsorbed vs. secreted by the principal cells?

A

Reabsorb: Na+ and H2O

Secrete: K+

23
Q

What is reabsorbed vs. secreted by the alpha-intercalated cells?

A

Reabsorb: K+ and HCO3

Secrete: H+

24
Q

What is reabsorbed vs. secreted by the beta-intercalated cells?

A

Reabsorb: H+ and Cl-

Secrete: K+ and HCO3-

25
Q

What are the 3 most important factors that stimulate potassium secretion?

A
  1. Increased ECF [K+]
  2. Aldosterone
  3. Increased tubular flow rate
26
Q

What are the 2 most important factors that stimulate potassium reabsorption?

A
  1. K+ deficiency, low K+ diet, hypokalemia

2. K+ loss through SEVERE diarrhea

27
Q

Describe the K+ shift caused by acidosis

A

Decreased activity of Na/K pump

Decreased [K] in the cell

Decreased passive diffusion of K into tubule lumen

Decreased K+ channels

Decreased K+ secretion

End result = hyperkalemia

28
Q

Acute acidosis causes a decrease in potassium secretion with the end result of hyperkalemia. What are the effects of chronic acidosis on potassium?

A

Chronic acidosis stimulates K+ secretion

[because chronic acidosis decreases reabsorption of water and solutes by the PT by inhibiting the Na/K pump which increases tubular flow to DT and CD. Meanwhile RAAS is stimulated d/t lack of water reabsoprtion and subsequent decrease in ECF volume. These changes offset the reabsorptive effects of acute acidosis and K+ secretion rate rises]

29
Q

What effects do hypoalbuminemia vs. hyperalbuminemia have on plasma Ca?

A

Hypoalbuminemia increases plasma Ca

Hyperalbuminemia decreases plasma Ca

30
Q

T/F: in alkalosis, there is more free calcium in circulation

A

False; this is true of acidosis

Alkalosis results in more calcium bound to plasma proteins

31
Q

Alkalosis results in more calcium bound to plasma proteins, which predisposes to what condition?

A

Hypocalcemic tetany

32
Q

What effect does a decreased [Ca++] have on PTH levels? What are the downstream effects?

A

Decreased [Ca] –> increased PTH

Increased PTH increases Vit D3 activation, increases Ca release from bones, and increases renal Ca reabsorption

33
Q

What is the mechanism of reabsorption of Ca in the proximal tubule?

A

Primarily paracellular

May also be transcellular by diffusion gradient into cell, exits via Ca ATPase and Na/Ca antiporter

34
Q

What change in ECF causes an increase in Ca reabsorption in the PT?

A

Volume contraction

35
Q

Describe Ca reabsorption in TAL

A

Primarily paracellular; reabsorption parallels Na

[dependent upon TEPD - lumen positive voltage; ADH stimualtes reabsorption]

36
Q

How are loop diuretics able to treat hypercalcemia?

A

They inhibit Na reabsorption in the TAL, thus reducing the TEPD, reducing Ca paracellular reabsorption (increasing Ca excretion)

37
Q

The DT has a lumen-______ transepithelial voltage. Ca reabsorption is active transcellular transport; it crosses the apical membrane via _______ and the basolateral membrane via Na/Ca exchanger

A

Negative; TRPV5

38
Q

What 2 compounds stimulate Ca reabsorption in the DT?

A

PTH and thiazide diuretics (also Vit D and calcitriol)

39
Q

What effect does acidemia have on TRPV5 in the DT?

A

Acidemia increases Ca excretion by inhibiting TRPV5

[alkalemia decreases Ca excretion by stimulating TRPV5]

40
Q

Calcitonin’s 3 effects on calcium renal regulation

A

Opposes PTH

Stimulated by hypercalcemia

Decreases serum phosphorus and calcium concentrations

41
Q

Decreased ECV effect on Ca renal regulation

A

+ sympathetics –> Na reabsorption in PCT

Ca reabsorption depends on transepithelial voltage and solvent drag, which depend on Na reabsorption

42
Q

What are the major regulatory factors for renal handling of phosphate

A

FGF23 - increases excretion

PTH - increases excretion

Vit D3 - increases serum Pi by increasing intestinal absorption

Insulin - lowers serum levels by shifting into cells

43
Q

How is Pi reabsorbed in the PT

A

Across apical membrane via Na/Pi symporters

Across basolateral membrane via unknown transporter

44
Q

What effect does PTH have on Pi excretion

A

PTH inhibits Na/Pi transporters and Na/H antiporter in apical membrane of PT cells, thus increasing excretion

45
Q

What effect does acidosis vs. alkalosis have on Pi excretion?

A

Chronic acidosis increases Pi excretion

Chronic alkalosis decreases Pi excretion

46
Q

Magnesium reabsorption pathways

A

PT: 20%, paracellular, follows Na and H2O

TAL: 70%, paracellular, depends on uptake of Na and K via NKCC2 and lumen positive voltage of TAL

DCT: 10%, fine-tuning, electric potential = primary driver, crosses apical border via TRPM6, no known mechanism for shuttling or crossing basolateral membrane

47
Q

What effect do diuretics have on Mg reabsorption

A

Decrease reabsorption

Renal Final (10 decks)

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