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Renal > Calcium & Phosphate Metabolism > Flashcards

Calcium & Phosphate Metabolism Flashcards

1
Q

What happens to the pulse wave velocity in calcified stiff arteries?

A

Pulse wave increases. It does a bunch of shit that’s bad.

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2
Q

What is CKD-Bone Mineral Disease?

A

The kidneys fail to maintain proper levels of Ca and PO4 in the blood leading to abnormal bone hormone levels.

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3
Q

What are the 4 functions of phosphorus?

A
  1. key component of bony skeleton
  2. metabolic (i.e. ATP)
  3. component of nucleic acids
  4. blood and urinary pH buffer
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4
Q

What is the normal serum phosphorus concentration?

A

3-4.5 mg/dL

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5
Q

Phosphorus is present in the plasma as what 2 ions?

A
  1. HPO4^2-
  2. H2PO4-
    At pH of 7.4, HPO4 is favored 4:1.
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6
Q

What is the distribution of phosphorus in the body?

A

Bone- 85%
Soft Tissue- 14%
ECF- 1%

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7
Q

What is the metabolic balance of phosphorus?

A

1400 mg from diet each day. 500 mg lost in feces. 900 mg renally excreted. There is a 200 mg/day turnover of phosphorus from bone (resorption/formation occuring in equal amounts).

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8
Q

What is the renal handling of phosphate?

A

90% freely filtered. 80-97% reabsorbed with 80% occuring in the proximal tubule.

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9
Q

T or F. Tubular reabsorption of phosphate is saturable.

A

T: with a GFR<40, hyperphosphatemia results. Note, glucose reabsorption is also saturable.

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10
Q

What is the overall goal of PTH?

A

To increase serum Ca back to normal. It is secreted in response to hypocalcemia. Secreted by parathyroid.

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11
Q

PTH acts on which 3 organs?

A
  1. Kidney
  2. Small Intestine
  3. Bone
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12
Q

What is the result of PTH action on the kidney?

A
  1. Increased 1-alpha-hydroxylase activity, thus more calcitrol
  2. Increased excretion of phosphorus
  3. Increased reabsorption of Ca
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13
Q

What is the result of PTH action on the small intestine?

A

Increased Ca and PO4 absorption.

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14
Q

What is the result of PTH action on bone?

A

Increased Ca and PO4 mobilization from bone.

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15
Q

What trade off occurs with Ca with CKD?

A

High PTH levels in exchange for Ca homeostasis. This is only an adequate correction for a GFR >40.

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16
Q

Hyperphosphatemia isn’t seen in CKD patients until GFR drops below what value?

A

40 mL/min

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17
Q

T or F. Then he shows some bullshit graph with the key point of “the vast majority of patients with Stage 5 CKD have elevated serum phosphorus.”

A

T: no shit Sherlock…thanks Kovesdy.

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18
Q

Hyperphosphatemia initiates a cascade of cellular events that results in what?

A

Calcification of vascular smooth muscle cells.

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19
Q

What is the metabolic balance of Ca?

A

1000 mg dietary intake per day. 700 mg lost in feces. 300 mg renally excreted. 280 mg/day turnover in bone.

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20
Q

What hormone increases Ca absorption in the small intestine?

A

Vitamin D. PTH indirectly does this by stimulating 1-alpha-hydroxylase.

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21
Q

T or F. Most CKD patients have a normal serum calcium but there are small decreases seen with worsening kidney function.

A

T

22
Q

T or F. His next point is confusing as shit b/c he says CKD patients have higher incidences of hypocalcemia AND hypercalcemia with worsening kidney function.

A

T: this is the UT way. FMS.

23
Q

Normally, what percentage of Ca is bound to albumin in the serum?

A

40%. This is the reason serum Ca concentration measurements must be albumin-adjusted.

24
Q

An albumin-adjusted serum Ca concentration measurement is important because?

A

If serum albumin is low, serum Ca could be decreased but if free Ca is normal then the serum concentration would appear to be normal if it wasn’t adjusted.

25
Q

Does K-DIGO (whoever the eff that is) recommend adjusting Ca concentration for albumin in CKD and ESRD patients?

A

Nope.

26
Q

T or F. The risks of both hypo- and hypercalcemia increase with advanced CKD when adjusting for changes in serum albumin and bicarbonate.

A

T. I can’t even begin to explain this. The next graph shows these patients die or something.

27
Q

What side effect is seen in CKD patients with hypocalcemia?

A

Increased neuromuscular excitability.

28
Q

What side effect is seen in CKD patients with hypercalcemia?

A

Cardiovascular and soft tissue calcification.

29
Q

T or F. He then has the gumption to call vitamin D a hormone…involved in the regulation of a wide range of physiologic processes.

A

T. He then asks if it is the holy grail of medicine or rat poison. I can’t make this stuff up.

30
Q

Describe vitamin D metabolism.

A

UVB stimulates vitamin D synthesis. Intake is another source. Then you hydroxylate in the liver. Then hydroxylate again in the kidney (or tissue) to its active form.

31
Q

Describe calcitrol’s MOA.

A

Calcitrol binds VDR. VDR goes to the nucleus and heterodimerizes with RXR. This complex binds DNA and regulates transcription of those genes.

32
Q

Tell me about classical FGFs.

A
  1. paracrine mediators
  2. binds to FGF receptor tyrosine kinases
  3. binding requires heparin as a cofactor
33
Q

Tell me about the FGF19 subfamily.

A
  1. endocrine mediators
  2. heparin INdependent
  3. members are FGF19, FGF21, and FGF23
34
Q

FGF19 is involved in the homeostasis of what?

A

Energy and bile acid.

35
Q

FGF21 is involved in the metabolism of what?

A

Glucose and lipids.

36
Q

FGF23, the one we talk about, is involved in the homeostasis of what?

A

Phosphate and vitamin D.

37
Q

What kind of activity does FGF23 have in vivo?

A

Phosphaturic activity

38
Q

Where is FGF23 expressed?

A

Mainly in osteocytes. Also by ventrolateral thalamic nucleus, central venous sinusoids, and the thymus.

39
Q

What 3 things stimulate FGF23?

A
  1. calcitrol
  2. PTH
  3. bone metabolism
40
Q

What 4 things does FGF23 do?

A
  1. decreases activity (or levels?) of 1-alpha-hydroxylase thus lowering calcitrol
  2. decreases PTH
  3. decreases Klotho expression
  4. decreases renal phosphate reabsorption
41
Q

What is the overall goal of FGF23?

A

To lower serum phosphorus levels back to normal.

42
Q

What is unique about FGF23 in regards to calcitrol?

A

It is stimulated by calcitrol but its activity is to lower calcitrol. Closed feedback loop.

43
Q

T or F. FGF23 levels become very high in CKD patients thus explaining the very low calcitrol levels also seen in those patients.

A

T

44
Q

Panda’s Notes about FGF23.

A
  1. PHEX gene mutation decreases degradation of FGF23
  2. Increased FGF23 downregulates phosphate transporter activity
  3. It also inhibits activation of vitamin D
  4. Inc FGF23 leads to dec calcitrol which inc PTH which leads to hypophosphatemia.
45
Q

T or F. FGF23 measurements may be a sensitive early biomarker of disordered phosphorus metabolism in patients with CKD and normal serum phosphate levels.

A

T. From one of the BS graphs.

46
Q

How does FGF23 lead to hyperparathyroidism in CKD patients?

A

FGF23 lowers calcitrol levels which decreases Ca absorption in the gut. Decreased Ca triggers PTH secretion.

47
Q

T or F. The effects of FGF23 to suppress PTH is blocked by downregulation of FGFR1/Klotho in CKD patients.

A

T: this combined with the decreased Ca culminates in hyperparathyroidism. Moral of the story: CKD patients have hyperparathyroidism. I think.

48
Q

T or F. Increased FGF23 levels are linked to an increased mortality rate in CKD patients.

A

T. Cool story bro. I don’t even think this is proven but it’s part of his crappy research.

49
Q

T or F. Then he shows another graph showing elevated FGF23 levels are associated with LVH in CKD patients.

A

T. Then he found $20.

50
Q

In summary, what 5 bad things does elevated FGF23 levels do? What is the consequence of each?

A
  1. Dec calcitrol: CV disease, metabolic disorders, infections, malignancies
  2. Inc RAAS: CV disease, metabolic disorders
  3. Dec Klotho expression: vascular and metabolic disorders
  4. Inc inflammation: CV disease, protein-energy wasting
  5. Inc LVH: arrhthymias, CV mortality
51
Q

Summary Slide of CKD-MBD. Just watch.

A

Decreased renal function leads to decreased calcitrol production and phosphate retention. This leads to decreased VDR expression, increased PTH, hypo- or hypercalcemia, hyperphosphatemia, elevated FGF23, and increased ALP. The consequences of all that shit= renal osteodystrophy, fractures, calcification, and CV disease. Thus, increased morbidity and mortality.

Renal (33 decks)

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