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10. Renal Test 2 > 6. Regulation of Ca, Pi, and Mg Balance > Flashcards

6. Regulation of Ca, Pi, and Mg Balance Flashcards

1
Q

What is the function of the calcium sensing receptor (CaSR)?

Where is it located?

A

CaSR is the primary means by which the body detects calcium. When it detects high plasma calcium levels, it inhibits NKCC2 transporters on the apical side of the cell, disturbing the positive electrochemical gradient – and preventing calcium absorption.

CaSR are located on the interstitial side of the cell – in order to detect calcium levels in the ECF.

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2
Q

Where is calcitriol activated?

A

In the epithelial cells of the proximal tubule.

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3
Q

What percentage of calcium is filterable?

A

60%

(The other 40% is the protein-bound form.)

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4
Q

What regulatory step for calcium reabsorption is featured in the thick ascending limb of the loop of Henle?

A

CaSR (calcium sensing receptor) regulation of NKCC2

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5
Q

How will acidosis affect the concentration of plasma calcium?

A

Acidosis will increase plasma calcium concentration.

(This occurs because the increased number of hydrogen ions will displace more ionic calcium from the binding sites on the albumin)

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6
Q

Through what route is the majority of calcium excreted?

A

Through the feces.

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7
Q

What is the primary site of calcium reabsorption in the kidney?

A

Proximal tubule

(through mostly passive transport)

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8
Q

How is magnesium reabsorbed in the distal tubule?

A

Active transport, via TRPM6.

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9
Q

What is likely to cause phosphaturia?

A

The action of parathyroid hormone on the cells of the proximal tubule.

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10
Q

What up regulates calcitriol activation by the kidneys?

A

Low plasma phosphate and/or calcium, as well as high plasma parathyroid hormone

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11
Q

What important difference is there between the distal tubule and the thick ascending limb of the loop of Henle in regards to calcium absorption?

A

The distal tubule has a lumen negative transepithelial potential difference. This requires active transport for calcium.

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12
Q

What is the effect of insulin on plasma phosphate levels?

A

Insulin decreases plasma phosphate levels

(This is by increasing cellular uptake of phosphate – much the same as insulin increases the cellular uptake of potassium by stimulating the Na/K ATPase pump)

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13
Q

What down regulates calcitriol activation by the kidneys?

A

High plasma calcium – detected by CaSR

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14
Q

Which forms of calcium are considered biologically active?

A

The ionized form, and the nonionized complex form.

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15
Q

What is the general function of calcitonin?

A

Decreases plasma calcium and phosphate levels by slowing bone resorption (inhibits osteoclast activity) and increasing renal secretion of phosphate and calcium.

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16
Q

What is the function of calbindin, and where is it located?

A

Calbindin binds calcium in order to prevent otherwise adverse consequences (apoptosis) of excessive intracellular calcium.

It is located in the tubular cells of the distal tubule.

17
Q

What is the effective calcitonin on the bone and the kidney?

A

Bone: decreases osteoclast activity

Kidney: increases calcium and phosphate secretion

(Overall decreases plasma calcium levels)

18
Q

How does calcium enter the cells of the distal tubule from the tubular lumen?

A

TRPV5 channels

19
Q

What epithelial calcium channel is regulated by 1,25-dihydroxycholecalciferol?

Where is it located?

A

TRPV5

The distal tubule

20
Q

What is the effect of ADH on the reabsorption of calcium in the thick ascending limb?

A

ADH increases reabsorption of calcium in the thick ascending limb.

(ADH increases reabsorption of NaCl from the thick ascending limb in order to increase the osmolality of the medullary interstitium. Because calcium follows sodium, calcium reabsorption is also increased)

21
Q

How does volume expansion affect calcium reabsorption?

A

Volume expansion decreases calcium reabsorption.

(In the proximal tubule calcium follows salt and water. So, if you think about what is happening to the water and salt – in terms of volume expansion/contraction – you can determine what happens with calcium reabsorption)

22
Q

How is phosphate reabsorbed in the proximal tubule?

Where does the “power” come from?

A

Phosphate is reabsorbed with sodium (many other solutes) via a sodium – phosphate symporter.

The power comes from the gradient established by the Na/K ATPase.

23
Q

What do we need to know about the production of calcitriol?

A

UV light strikes the skin “kicking off” the process, and presenting its product to the liver.
The liver the makes a modification, and sends an inactive form of calcitriol to the kidney.
The kidney then activates the product into true, active calcitriol via activity of an enzyme that primarily exists in the proximal tubule.

24
Q

How do parathyroid hormone and calcitriol (vitamin D) stimulate reabsorption of calcium?

A

They stimulate the TRPV5 transporter in the distal tubule.

25
Q

What is the effect of chronic alkalosis and acidosis on phosphate excretion?

A

Chronic acidosis increases phosphate excretion.

Chronic alkalosis decreases phosphate excretion.

26
Q

What is the normal range of plasma calcium?

How much of that is biologically active?

A

Total plasma level = 5.0 mEq/L

Biologically active = 2.4 mEq/L

27
Q

What is the effect of acidemia and alkalemia on calcium reabsorption?

What is the mechanism by which this occurs?

A

Acidemia decreases calcium reabsorption, and alkalemia increases calcium reabsorption.

TRPV5 is inhibited by acid, and stimulated by an alkalotic state.

28
Q

Where is the majority of magnesium reabsorbed?

A

The thick ascending limb.

(Only 20% is absorbed in the proximal tubule – 70% is reabsorbed in the thick ascending limb)

29
Q

To what calcium-related condition are individuals with alkalosis more predisposed?

A

Hypocalcemic tetany

(Less hydrogen bound to albumin means more calcium bound to albumin. This results in hypocalcemia, which makes it more likely for the patients to go into tetany)

30
Q

When calcium is transported out of the cells of the proximal tubule, what two transporters eject it?

A

Calcium ATPase

or

Calcium sodium exchanger

31
Q

How does the reabsorption of sodium and water in the proximal tubule affect the reabsorption of calcium in the proximal tubule?

A

They are parallel, when water and sodium reabsorption increases – so does calcium, and vice versa

32
Q

What happens when vitamin D is filtered at the glomerulus?

A

It is endocytosed by the cells of the proximal tubule.

33
Q

Why is active transport of magnesium required in the distal tubule?

A

Because the concentration of magnesium intracellularly and extracellularly is roughly equal. Therefore the only driving factor is transepithelial potential difference – and the distal tubule has a lumen negative TEPD.

34
Q

What percentage of phosphate is reabsorbed in the proximal tubule?

A

80%

35
Q

What are the functions of parathyroid hormone on the bone, intestine, and kidney?

A

Bone: increases osteoclastic resorption of calcium and phosphate

Intestine: increases absorption of calcium and phosphate (indirectly increases absorption of phosphate through activation of calcitriol)

Kidney: increases reabsorption of calcium, but decreases reabsorption of phosphate.

(PTH causes the secretion of FGF-23 by bone which inhibits sodium/phosphate symporters)

36
Q

What are the four names for vitamin D we are responsible for?

A

Calcitriol

1,25-dihydroxycholecalciferol

1,25 hydroxy vitamin D

1,25(OH)2D3

37
Q

What are the effects of calcitriol on the bone, intestine, and kidney?

A

Bone: promotes osteoid mineralization by controlling ratios of phosphate and calcium, stimulates resorption of calcium and phosphate from bone via stimulation of osteoclasts.

Intestine: stimulates absorption of calcium and phosphate.

Kidney: stimulates reabsorption of calcium and phosphate

10. Renal Test 2 (9 decks)

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