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Renal by Minnie: AH Version > SM 198a - Calcium and Phosphate > Flashcards

SM 198a - Calcium and Phosphate Flashcards

1
Q

FGF-23 will ___________ production of 1,25-OH2 Vitamin D3 (active) by [stimulating/inhibiting] __________________.

A

FGF-23 will decrease production of 1,25-OH2 Vitamin D3 (active) by inhibiting 25 alpha hydroxylase .

FGF-23 is secreted in response to too much serum phosphorous

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2
Q

What belongs in box E?

A

1,25-OH2-D3

The active form of vitamin D3

PTH upregulates 1 alpha hydroxylase activity -> more 1,25-OH2-D3 -> works to increase serum Ca2+

FGF23 inhibits 1 alpha hydroxylase activity -> less 1,25-OH2-D3 -> works to decrease serum Ca2+

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3
Q

Which enzyme belongs in box B?

Where does it act?

A

25 alpha-hydroxylase

Acts in the liver to covert cholecalciferol to 25-hydroxy-D3

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4
Q

What is claudin 16?

What deos it do?

A

Claudin 16 is a protein between the epithelial cells of the thick ascending limb of the loop of Henle

It allows for paracellular reabsorption of Ca2+ down its concentration and electrical gradient

(The lumen in thick ascending loop is positively charged due to the action of ROMK)

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5
Q

Which 3 enzymes are important for the synthesis of active vitamin D?

A
  • 25 alpha hydroxylase (liver)
    • Cholecalciferol -> 25-OH-D3
  • 24 alpha hydroxylase (renal PCT cell)
    • 25-OH-D3 -> inactive 24,25-OH2-D3
  • 25 alpha hydroxylase (renal PCT cell)
    • 25-OH-D3 -> active 1,25-OH2-D3

Also: UV light to convert 7-dehydrocholesterol to cholecalciferol

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6
Q

What belongs in box A?

A

7-dehydrocholesterol

This is the starting material for active vitamin D synthesis

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7
Q

Which enzyme belongs in box C?

A

24 alpha-hydroxelase

Converts 25-OH-D3 to the inactive 24,25-hydroxy-D3​

This enzyme is upregulated when serum calcium levels are too high

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8
Q

What is the effect of PTH on Ca2+ reabsorption in the intsetine?

A

PTH has no direct effect on Ca2+ reabsorption in the intestine

Vitamin D (1,25 Hydroxy-D3) is the primary regulator of Ca2+ reabsorption in the intestine

However, PTH secreted in response to low Ca2+ increases activation of vitamin D in the kidney, thus indirectly increaseing Ca2+ reabsorption in the intestine

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9
Q

When you are re-feeding a patient with starvation, why would you need to give phosphorus as well?

A

Feeding -> increased metabolism -> increased PO4 demand

This uses up the phosphorous that is available in the blood

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10
Q

How does FGF-23 affect phosphorous homeostasis?

A

FGF-23 promotes the excretion of phosphorous to lower serum phosphorous levels

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11
Q

What factors regulate PTH secretion from the chief cells of the parathryroid gland?

A
  • Promote PTH synthesis and release
    • Low Ca2+ levels
  • Inhibit PTH synthesis and release
    • High Ca2+ levels
    • High vitamin D
    • FGF-23
    • Phosphorous
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12
Q

What belongs in box B?

A

Cholecalciferol

Created when UV light acts on 7-dehydrocholesterol in the skin

Dietary sources of vitamin D can also enter the vitamin D synthesis pathway here

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13
Q

What is the effect of gastric acid on Ca2+ reabsorption?

A

Gastric acid enhances Ca2+ absorption

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14
Q

Low PTH is a physiological response to ____________

A

Low PTH is a physiological response to high Ca2+

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15
Q

Describe Ca2+ reabsorption in the thick ascending limb of the loop of Henle

A
  • K+/Na+/2Cl- cotransporter (NKCC2) in the apical membrane gets these ions from the lumen to the epithelial cell
  • Na+/K+ ATPase on the basolateral membrane moves Na+ into the interstitium and K+ into the epithelial cell – electrically neutral
  • Chloride channels on the basolateral membrane transport Cl- ions are into the insterstitium
  • ROMK on the apical membrane pumps K+ back into the lumen -> positive charge in the lumen
  • This positive charge drives paracellular Ca2+ reabsorption through claudin 16
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16
Q

Which enzyme belongs in box A?

A

No enzymes!

UV light hits the skin and converts 7-dehydrocholesterol to colecalciferol (pre-vitamin D)

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17
Q

Which enzyme blelongs in box D?

A

1-alpha hydroxylase

Converts 25-OH-D3 to the active 1,25-hydroxy-D3

This enzyme is upregulated when serum Ca2+ levels are low

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18
Q

Increased bone mineralization will result in [high/low] phosphate in the blood

A

Increased bone mineralization will result in low phosphate in the blood

Bone mineralization moves phosphate from serum -> bone

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19
Q

What is the most common cause of hypocalcemia?

A

Low PTH

  • Usually post-surgical
    • Thyroidectomy, parathyroidectomy, radial neck dissection
  • Autoimmune or genetic possible
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20
Q

Where in the kidney tubule is the majority of phosphorous reabsorbed?

A

Proximal convluted tubule

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21
Q

Describe the clinical manifestation of hyposphosphatemia

A
  • Neuro
    • Lethergy
    • Paraesthesia
    • Siezure
  • Cardiac
    • Arrhythima
    • Hypotension
  • Hematologic
    • Hemolysis
  • Skeletal
    • Bone demineralization (to increase serum phosphate)
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22
Q

What is the active form of vitamin D?

A

1,25 Hydroxy-D3

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23
Q

______ is the single most important factor that affects PTH secretion

A

Serum Ca2+ level is the single most important factor that affects PTH secretion

  • High Serum Ca2+
    • Ca2+ binds to CaSR on the chief cells of the parathyroid gland
    • Inhibits PTH production and secretion
  • Low Serum Ca2+
    • Ca2+ does not bind to CaSR
    • PTH is produced and released from the chief cells of the parathyroid gland
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24
Q

What stimulus promotes the secretion of FGF-23?

What is the effect?

A

FGF-23 is secreted in response to too much serum phosphorous

FGF-23 -> Decreased Vitamin D synthesis -> decreased phosphorous absorption from the intestine

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25
Q

In primary hyperparathyroidism, would you expect the following serum levels to be high or low?

Calcium:

Phosphorous:

1,25-OH2-D3:

A
  • Calcium: High
    • ​Increased renal reabsorption
    • Increased active vitamin D -> increased intestinal reabsorption
    • Increased resorption from bone
  • Phosphorous: Low
    • ​Decreased renal reabsorption
  • 1,25-OH2-D3: Varies
    • Increased vitamin D synthesis in the kidney, but some studies have shown that primary hyperparathyroidism is associated with vitamin D deficiency
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26
Q

What is the role of CaSR on Ca2+ reabsorption in the distal convoluted tuble?

A

In the DCT, CaSR is located on the apical membrane

  • CaSR senses increased Ca2+ in the urine
    • If Ca2+ in the urine is high, CaSR stimulates increased reabsorption of PO4 to prevent kidney stone formation
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27
Q

What factors affect GI absorption of calcium?

A
  • Increase absorption
    • Vitamin D (1,25-OH2-D3)
      • PTH indirectly, by increasing Vitamin D syntheisis
    • Gastric acid
  • Decrease abosrption
    • Billiary and pancratic insufficiency
      • Ca2+ binds to unabsorbed fat and is excreted
    • Serum hypercalcemia
      • Via CaSR, which binds to Ca2+ and inhibits the effects of vitamin D
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28
Q

What is a “pseudo-state” as it refers to an electrolyte?

A

Low total electrolyte, but no change in the level of its active form

Ex: Low albumin causes a pseudo-decrease in calcium. The amount of protein-bound Ca2+ decreases which decreases total Ca2+, but the levels of ionized (active) Ca2+ remain the same

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29
Q

What is the effect of biliary and pancreatic insufficiency on Ca2+ absorption in the gut?

A

Biliary and pancreatic insufficiency -> decreased Ca2+ absorption in the gut

  • Biliary and pancreatic insufficiency -> trouble absorbing fat
  • Ca2+ loves fat. If there is more fat in the intestine, Ca2+ will bind to it and be excreted.
  • Therefore, Ca2+ will not be absorbed
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30
Q

How does tumor lysis lead to hypocalcemia?

Would you expect high or low PTH?

A
  • Cell lysis -> PO4 release
  • PO4 in the blod binds to Ca2+, creating a Ca2+/PO4 product
  • This decreases the amount of ionized Ca2+ in the blood

You would expect high PTH, since the body is “seeing” low Ca2+ levels due to low ionized Ca2+

High PTH = physiological response to low Ca2+

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31
Q

Which forms of Ca2+ are filtered in the glomerulus?

A

Ionized Ca2+ only

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32
Q

Describe the management of hypercalcemia

A
  • Improve excretion
    • Saline fluids
    • Loop diuretics
    • Dialysis (last resort)
  • Decrease production
    • ​Give calcitonin and bisphosphates
  • Treat the underlying cause
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33
Q

What is the effect of PTH on reabsorption of Ca2+ in the kidney?

A

PTH is secreted when Ca2+ is low, and workds to increase reabsorption of Ca2+ in the thick ascending limb of the loop of Henle

  • PTH increases Claudin 16 production
  • Ca2+ must pass through Claudin 16 in order to be reabsobed paracellularly in the thick ascending limb
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34
Q

Describe the process of intestinal absorption of phosphorous

A

Transcellular transport:

  • NaPi-IIb: Lumen -> intestinal cell
    Absorbs HPO4- with 2 Na+
  • Unknown channel: Intestinal cell -> interstitium

There is also a paracellular pathway

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35
Q

How does immobilization affect Ca2+ homeostasis?

A

Immobilization impairs bone formation

  • Physical, mechanical load is required to promote bone formation
  • Immobilization can result in hypercalcemia
    • Less Ca2+ moving into bone = more remains in the serum
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36
Q

A 50 year old male with chronic kidney disease stage 5, DM type 2, and hypertension presents for routine follow-up with his nephrologist. Labs reveal markedly elevated serum phosphorous. All of the following interventions would help treat his hyperphosphatemia except:

  1. Low phosphorous diet
  2. Low sodium diet
  3. Vitamin D supplementation
  4. Dietary phosphorous binders
A

c. Vitamin D supplementation

37
Q

What substance regulates Calcium absoprtion in the intestine?

A

1,25 Hydroxy-D3 (The active form of vitamin D)

  • If Ca2+ levels are high, Ca2+ binds to the Ca2+ sensing receptor (CaSR)
    • CaSR downregulates 1,25 Hydroxy-D3 synthesis
    • Decreased 1,25 Hydroxy-D3 -> decreased Ca2+ absorption
  • If Ca2+ levels are low, CaSR does not downregulate 1,25 Hydroxy-D3 synthesis
    • The presence of 1,25 Hydroxy-D3 -> Ca2+ absorption
38
Q

How do antacids affect Ca2+ absorption?

A

Gastric acid enhances Ca2+ absorption

Antacids decrease gastric acid, and therefore decrease Ca2+ absorption

39
Q

Which form of Ca2+ is biologically active?

A

Ionized Ca2+

40
Q

What belongs in box D?

A

24,25-OH2-D3

This is a waste product, created when the body does not need more active vitamin D3 (ex: when calcium levels are normal or high)

41
Q

What is the effect of CaSR activation on the epithelial cells of the thick ascending loop?

A

CaSR binds to Ca2+ when serum Ca2+ levels are elevated

Binding of Ca2+ to CaSR downregulates Ca2+ reabsorption:

  • Decreased ROMK activity
    • -> Decreased liminal positivity
    • -> Decreased driving force for Ca2+ reabsorption
  • Decreased Claudin 16 production
    • -> Fewer channels for paracellular Ca2+ reabsorption in the thick ascending limb of the loop of Henle
42
Q

Describe the clinical manifestation of hyperphosphatemia

A
  • Symptoms of hypocalcemia
    • Phosphorous binds to Ca2+, thus reducing the amount of ionized Ca2+
    • Bone fractures, stomach cramps, dysrhythmia, irritability, anxiety, carpopedal spasm, siezure
  • Itching
  • Metastatic calcifications
43
Q

Describe the management of hypophosphatemia

A

Eat high-phosphate foods!

  • Replete phosphorous
    • Eat high-phosphate foods
    • IV if severe or patient cannot eat
  • Treat underlying cause
44
Q

What are the expected levels for a patient with hyperparathyroidism?

Calcium:

Phosphorous:

A

Calcium: high

Phosphorous: low

PTH = increased renal Ca2+ reabsorption and phosphorous excretion

45
Q

What is Milk alkali syndrome?

A

Milk consumption -> loss of regulation of GI Ca2+ absorption -> hypercalcemia

46
Q

Describe the process of phosphorous reabsorption in the renal tubules

A
  • NaPi-IIa and NaPi-IIc: Lumen -> Tubular epithelial cell
  • Unknown channel: Tubular epithelial cell -> interstitium
47
Q

Which diuretics are known for causing hypercalcemia?

Describe the mechanism

A

Thiazides

  • Decrease Na+ reabsorption in the distal convoluted tubule (Inhibit Na+/Cl- cotransporter)
  • -> Decreased intracellular Na+
  • -> Increased Na+/Ca2+ antiporter activity on the basolateral membrane; Na+ into the cell, Ca2+ into the interstitium
  • -> Decreased intracellular Ca2+ promotes reabosrption of Ca2+ from the lumen via TRPV5
48
Q

What factors regulate phosphorous reabsorption in the renal tubules?

A
  • FGF-23
    • ​Acts on FGFR-1 and Klotho to promote the excretion of phosphorous
  • PTH
    • ​Promotes the excretion of phosphorous by preventing reabsorption
49
Q

What is the effect of vitamin D on PTH in the parathyroid cell?

A

When Vitamin D reaches a threshold level in the serum, it binds to VDR in the chief cell and inhibits production of PTH.

-> decreased GI absorption, renal reabsorption of Vitamin D

50
Q

How would low albumin affect the calcium homeostasis in the blood

A

Low albumin would decrease the protein-bound calcium, thus lowering total calcium levels in the body

However, there would be no change in ionized Ca2+, and therefore no difference in biological funciton

This means you have to determine low serum Ca2+ levels in the context of albumin

51
Q

What is Calbindin? What does it do?

A

Calbindin is a protein produced in intestinal epithelial cells

Within the cell, it moves Ca2+ from the luminal side to the serum side

52
Q

FGF-23 plays a very important role in the regulation of vitamin D and PTH.

How?

A

FGF-23 is the key negative feedback mechanism -
basically FGF-23 is yelling
“CALM DOWN WE HAVE ENOUGH SERUM CA2+”

  • Vitamin D
    • Increases FGF-23 expression in bone
    • -> FGF-23 acts on the kidney to decease vitamin D synthesis
  • PTH
    • Increases FGF-23 express
    • -> FGF-23 acts on teh parathyroid to decrease PTH
53
Q

What factors affect HPO4- absorption in the intestine?

A

Vitamin D (1,25 Hydroxy-D3) increases abosrption of HPO4- in the intestine

54
Q

How does vitamin D affect Ca2+ homeostasis?

A

Increased levels of active vitamin D (1,25 Hydroxy-D3) increase Ca2+ absorption in the intestinal epithelium

  • 1,25 Hydroxy-D3 binds to the Vitamin D Receptor (VDR)
  • VDR acts on the nucleus to increase production of TRPV6, Calbindin, Ca2+ ATPase or Na+/Ca2+
    • All of these proteins are required for Ca2+ reabsorption in the intestine
55
Q

Describe the management of hyperphosphatemia

A
  • Low phosphorous diet (this is hard)
  • Give Phosphorous binders
    • Bind to and excrete dietary phosphorous
    • Common for ESRD and dialysis patients
  • Hemodialysis
  • Treat underlying cause
56
Q

Why is it important to take Ca2+ supplements with food?

A

Gastric acid enhances Ca2+ absorption in the gut

Food increases gastric acid secretion, which increases Ca2+ absorption

57
Q

What are the clinical manifestations of hypocalcemia?

A
  • Neuro
    • Anxiety, irritability, tetany, twitching, carpopedal spasm, seizure
  • Bone
    • Fractures
  • GI
    • Cramps
  • Cardiac
    • Prolonged QT, dysrhythmia
  • Blood
    • Hypercoagulable state
58
Q

What is the biggest Ca2+ reservoir in the body?

A

Bone

59
Q

What is the effect of calcitonin on serum Ca2+?

A

Calcitonin lowers serum Ca2+

  • Increases renal excretion
  • Decreases bond resorption
60
Q

What is the effect of estrogen on Ca2+ homeostasis

A

Estrogen decreases bond resorption

It decreases the movement of Ca2+ from bone to serum

61
Q

What is the DDx for hypercalcemia with low PTH?

A

Low PTH is a normal response to high Ca2+ - the CaSR system is working to suppress PTH secretion

So, what could be causing persistent high Ca2+ in the setting of low PTH?

  • If PTHrP is elevated, malignancy is likely
  • If 1,25-OH2-D3 is elevated, tumor or granulomatous disorder
    • Produces 25 alpha hydroxylase that activates vitamin D
  • If 25-OH-D3 is elevated, vitamin D intake is too high
  • If Vitamin D and PTHrP are normal, consider myeloma, Vitamin A, or thyrotropin
62
Q

Where in the intestine is Ca2+ absorbed?

A

Duodenum and jejunum

63
Q

What percentage of filtered Ca2+ is reabsorbed by the kidney tubule?

In which segments of the kidney tubule?

A

95-99% of filtered Ca2+ is reabsorbed

  • Proximal convoluted tubule: Most (50-60%) Ca2+ is reabsorbed (Ca2+ follows Na+)
  • Thick ascending limb: 20-25%
  • Distal convoluted tuble: 5-10%
  • Collecting tubule = fine tuning

This is not super different from general reabsorption in the kidney tubules

64
Q

What belongs in box C?

A

25-OH-D3

Created when 25 alpha hydroxylase acts on cholecalciferol in the liver

25-OH-D3 binds to D-binding protein, is exported to the blood and absorbed by a proximal tubular cell (via megalin mediated endocytosis), where it is either activated to 1,25-OH2-D3 or turned into the waste product 24,25-OH2-D3, depending on the needs of the body

65
Q

What is the most common cause of hyperphosphatemia?

A

Decreased kidney function resulting in impaired phosphorous excretion

Exacerbated by…

  • Excess intake
  • Cellular breakdown (cells contain a lot of phosphorous)
66
Q

What factors regulate Ca2+ reabsorption in the DCT?

A
  • Vitamin D (1,25 Hydroxy-D3)
    • Increases Ca2+ reabsorption
  • PTH
    • Increases Ca2+ reabsorption
  • CaSR on the luminal epithelium
    • Senses increased Ca2+ in the filtrate
    • If Ca2+ is high, CaSR will derease reabsorption of PO4
      • This will protect against stone formation
67
Q

How does hypoerphosphatemia lead to hypocalcemia?

A

Hyperphosphatemia

  • -> Increased FGF-23 + Reduced 1,25-OH2-D3
    • Increased FGF-23 further reduces 1,25-OH2-D3 synthesis
  • Low active vitamin D -> Hypocalcemia
68
Q

Decreased bone mineralization will result in [high/low] phosphate in the blood

A

Decreased bone mineralization will result in high phosphate in the blood

Bone mineralization moves phosphate from serum -> bone

69
Q

What are the major causes of hypercalcemia?

A
  • Parathyroid mediated (too much PTH)
  • Non-parathyroid mediated
    • Malignancy
    • Vitamin D intoxication
    • Chronic granulomatous disease
  • Medications
    • Thiazides
    • Lithium
  • Misc
    • Hyperthyroid
    • Immobilization
    • Milk alkali syndrome
70
Q

What is the effect of androgens (testosterone) on Ca2+ homeostasis?

A

Testosterone = increased bone formation

Promotes the movement of Ca2+ from the serum to the bone

71
Q

What is secondary hypothyroidism?

What are the most common causes?

A

Secondary hypothyroidism = hypocalcemia in the setting of high PTH

(PTH is not doing its job increasing serum Ca2+ - think of this like reduced effect of PTH, rather than low PTH)

Causes:

  • Vitamin D deficiency
  • Loss of Ca2+ from the circulation
    • Ca2+ is being used up by something else
  • Drugs or medications that affect Ca2+ binding
  • Disorders of Mg2+ metabolism: Low Mg2+ leads to low Ca2+
    • Mg2+ is preferentially reabsorbed, resulting in decreased Ca2+ reabsorption
72
Q

Describe the clinical presentation of hypercalcemia

A
  • Painful bones
    • Weakness, bone pain, osteopenia
  • Renal stones
    • Polyuria, nephrolithiasis, AKI
  • Abdominal groans
    • Nausea, vomiting, constipation, pancreatitis
  • Psychic moans
    • Confusion, fatigue
  • Heart
    • Bradycardia, short QT
73
Q

Describe the management of hypocalcemia

A
  • Ca2+ supplementation
  • Thiazide diuretics
    • Increase Ca2+ reabsorption
  • Treat the underlying cause
    • Replenish Mg2+ or vitamin D if necessary
    • Stop drugs that are binding Ca2+
74
Q

Is the lumen in thick ascending limb of the loop of Henle positively charged or negatively charged?

Why?

A

Positively charged

  • The K+/Na+/2Cl- cotransporter (NKCC2) in the apical membrane gets these ions from the lumen to the epithelial cell is electrically neutral, but ROMK in the apical membrane pumps K+ into the lumen to recycle it
  • This creates a positively charged lumen
    • Creates an electrical gradient that pushes Ca2+ through claudin 16 into the interstitium (Drives Ca2+ reabsorption)
75
Q

How do bisphosphates treat hypercalcemia?

A

Bisphosphates inhibit osteoclast-mediated bone resorption

(Prevents mobilization of Ca2+ from bone -> serum)

76
Q

How do PTH and FGF-23 affect 1-alpha-hydroxylase activity?

A
  • PTH stimulates 1 alpha hydroxylase
    • Works to create more active vitamin D3
    • -> Works to increase serum Ca2+
  • FGF-23 inhibits 1 alpha hydroxylase
    • Works to decrease active vitamin D3
      • Increased synthesis of the waste product
        24,25-OH2-D3
    • -> Decrease serum Ca2+
      *
77
Q

If serum phosphorous levels are high, how would you expect FGF-23 levels to change?

A

High serum phosphorous

  • -> Increased FGF-23
    • ​-> decreased reabsorption of phosphorous
      • -> Increased excretion of phosphorous
78
Q

What percentage of Ca2+ absorption in the intestine is through paracellular transport?

A

5%

79
Q

Describe the process of Ca2+ reabsorption in the DCT

A

Very similar to Ca2+ reabsorption in the intestine

Difference = PTH has a direct effect on Ca2+ reabsorption in the kidney

  • TRPV5: Lumen -> Epithelial cell
  • Calbindin: Luminal side of cell -> basolateral side of cell
  • Na+/Ca2+ exchanger and Ca2+ ATPase: Basolateral side of the cell -> interstitium
    • Both are active transport mechanisms
80
Q

What drives Ca2+ reabsorption in the thick ascending limb?

A

Positive charge in the lumen

  • Created by K+ secretion through ROMK
  • This pushes Ca2+ reabsorption via paracellular transport
81
Q

Where in the body is biologically active phosphorous in the body found?

A

In the blood

82
Q

What is the typical picture of a chronic kidney disease patient?

  • Phosphate:
  • FGF23:
  • Active Vitamin D:
  • Calcium:
A
  • Phosphate: high
  • FGF23: high
  • Active Vitamin D: low
  • Calcium: low
83
Q

PTH will ___________ production of 1,25-OH2 Vitamin D3 (active) by [stimulating/inhibiting] __________________.

A

PTH will increase production of 1,25-OH2 Vitamin D3 (active) by stimulating 25 alpha hydroxylase

84
Q

What are the functions of phosphorous in the body?

A
  • Phosphorous is a part of ATP; we need it for energy and metabolism
    • It is super important for cell function
  • Helps RBCs carry oxygen
  • Minor role in blood buffering system for acid-base balance
  • Structural component of bone and teeth when combined with Ca2+
85
Q

How does 25-OH-D3 get into the proximal tubular cells of the kidney?

A

Megalin-mediated endocytosis

25-OH-D3 bound to D binding protein in the blood is not freely filtered through the glomerular filtration barrier

86
Q

Describe the process of Calcium absorption in the intestine

A
  • TRPV6: Lumen -> intestinal epithelial cell
  • Calbindin: Luminal side of cell -> serum side of the cell via
    (still stays inside of the intestinal epithelial cell)
  • Ca2+ ATPase or Na+/Ca2+ exchange:
    Serum side of the cell -> serum
    • Both are active transpor mechanisms; Intracellular [Ca2+] is lower than extracellular [Ca2+]
87
Q

What is the effect of PTH on Ca2+ homeostasis?

A

PTH is the major regulator of Ca2+ movement in and out of the bones

  • Hypocalcemia -> PTH secretion -> increased Ca2+ resorption from the bones -> Ca2+ levels return to normal
  • Hypercalcemia -> Decreased PTH secretion -> more bone formation
88
Q

How does chronic kidney disease affect phosphorous homeostasis?

How does this effect Vitamin D, Calcium, PTH, and FGF23?

A

Chronic kidney disease ->

  • Reduced renal phosphate clearance
  • -> Hyperphosphatemia
  • -> Increased FGF-23 + Decreased 1,25-OH2-D3 synthesis
    • Increased FGF-23 further reduces 1,25-OH2-D3 synthesis
  • -> Reduced renal Ca2+ reabsorption and GI absorption
  • -> Hypocalcemia
  • -> Increased PTH in response to hypocalcemia, but without increase in Ca2+ levels
    • = secondary hyperparathyroidism

Renal by Minnie: AH Version (27 decks)

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