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CVPR Week 8: Renal handling of P Flashcards

1
Q

Phosphorus flux between body compartments

A
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2
Q

Why is keeping phosphate levels in the normal range important

A

It is required to permit normal calcium deposition and retrieval from bone

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3
Q

Mechanisms of intestinal phosphorus absorption

A
  • Between cells (paracellular)
  • through cells (intracellular)
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4
Q

Features of paracellular intestinal phosphorus absorption

A
  • Passive process
  • Quantitatively significant when intake is high
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5
Q

Features of transcellular intestinal phosphorus absorption

A
  • Active process
  • Influenced by calcitriol
  • Calbindin: acts as an intracellular sink to reduce the microvilli [Ca]
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6
Q

Describe renal handling of phosphorus

A
  • PCT 85%
  • TAHL 10%
  • DCT 3%
  • CD 2%
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7
Q

Main mechanism of proximal tubule phosphorus transport

A

entirely transcellular driven by sodium transport

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8
Q

What gets absorbed in the proximal tubule?

A

Most stuff (glucose, phosphorus, calcium, amino acids, ketoacids) get absorbed with sodium in the proximal tubule

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9
Q

What is the mechanism of volume depletion and depleted potassium stores in diabetic ketoacidosis?

A

(ketoaciduria -> increased ketone body reabsorption in the PT -> reduced availability of Na+ for the reabsorption of proximal tubule substrates)

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10
Q

Proximal tubule phosphorus handling

A
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11
Q

Factors that increase renal absorption of phosphorus

3 listed

A
  • Low-phosphate diet
  • 1, 25-Vitamin D3
  • Thyroid hormone
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12
Q

Factors that decrease renal absorption of phosphorus

9 listed

A
  • Parathyroid hormone
  • Phosphatonins (e.g FGF23)
  • High-phosphate diet
  • Metabolic acidosis
  • Potassium deficiency
  • Glucocorticoids
  • Dopamine
  • Hypertension
  • Estrogen
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13
Q

Describe Paraneoplastic tumor-induced osteomalacia

A

Release of FGF23 by cancer cells: bone pain/fractures/weakness from hypophosphorus

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14
Q

What is FGF23?

A

Fibroblast growth factor 23 is a phosphantonin and is a key regulator of phosphorus homeostasis

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15
Q

FGF23 AKA

A

Fibroblast Growth Factor 23

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16
Q

What is a phosphatonin?

A

i.e. hormone regulating Phosphorus excretion

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17
Q

Where is FGF23 produced?

A

exclusively in osteocytes and bone-lining cells

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18
Q

FGF23 synthesis is influenced by?

A

Synthesis increases by

  • Phosphorus
  • PTH
  • Calcitriol
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19
Q

The most rapid inducer of FGF23 expression is?

A

Calcitriol

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20
Q

How can diet effect FGF23?

A

A high phosphorus dietary intake can stimulate FGF23 expression

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21
Q

Where is the FGF23 receptor

A

FGF23R is in the kidney

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22
Q

Describe the FGF23-R

A

found in the kidney and requires the coreceptor Klotho (which is found in the parathyroids) which decrease in number in aging and CKD

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23
Q

FGF23-R coreceptor

A

Klotho

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24
Q

CKD AKA

A

Chronic Kidney Disease

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25
Q

Actions of FGF23

4 listed

A
  • Downregulates luminal sodium/phosphate cotransporters in the proximal tubule
  • Inhibits 1α-hydroxylase which decreases calcitriol
  • Stimulates 24-hydroxylase which degrades vitamin D
  • Inhibits PTH secretion

Resulting in:

Lowering of serum phosphorus

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26
Q

FGF23 overall effect

A

Lowering of serum phosphorus

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27
Q

Inhibiting 1α-hydroxylase has what effect?

A

decreases calcitriol

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28
Q

Stimulating 24-hydroxylase has what effect?

A

Degrades Vitamin D

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29
Q

Describe the integrated regulation of renal P excretion

A
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30
Q

Mechanisms of hypophosphatemia

A

Shift into cells

Decreased intestinal absorption

Decreased intake (starvation/alcoholism)

Increased renal loss of phosphate (phosphate wasting)

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31
Q

Mechanisms of hyperphosphatemia

5 listed

A
  • Drop in renal function (acute or CKD)

or more common causes

  • Increased intake (oral sodium laxatives)
  • Increased tubular reabsorption of phosphate
  • increased tissue release
  • Shift out of cells
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32
Q

Fanconi syndrome and phosphorus

A

NaP transporter mutation causes phosphate wasting

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33
Q

NaP transporter mutation that results in phosphate wasting?

A

Fanconi Syndrome

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34
Q

Alcoholism and phosphate

A
  • will have low phosphorus level
  • If they are not alcoholic then they might have Fanconi Syndrome
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35
Q

When phosphorus is high what should you look for?

A

Look for tissue release (rhabdomyolysis) or poor kidney function

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36
Q

Hypophosphatemia clinical manifestations

A
  • Manifestations depend on the acuity and chronicity
  • Symptoms due to changes in mineral metabolism
  • Symptoms due to ATP depletion
37
Q

What are the symptoms due to ATP depletion?

5 listed

A
  • Metabolic encephalopathy, impaired myocardial function
  • Respiratory failure
  • myopathy
  • Dysphagia, ileus
  • Hemolytic anemia
38
Q

Hyperphosphatemia clinical manifestations

A
  • Acute elevation of phosphorus may lead to acute kidney injury and failure (phosphate nephropathy)
  • Chronic elevations (CKD) lead to cardiovascular calcification and increased cardiovascular morbidity and mortality
39
Q

Tx of Acute severe hypophosphatemia of < 1 mg/dL

A

IV phosphate replacement

40
Q

Tx of chronic hypophosphatemia

A

oral phosphorus with vitamin D

41
Q

Adverse effects of phosphate therapy

A
  • phosphate therapy can aggravate hypocalcemia
  • in hypercalcemic patients, acute loading may lead to calcium phosphate precipitation and nephrocalcinosis
42
Q

Tx of hyperphosphatemia

A
  • Phosphate binders (CKD)
  • Dialysis
    • Tumor lysis
    • Rhabdomyolysis
44
Q

Lab profile calcium and phosphate disorders

45
Q

Hypoparathyroidism PTH

46
Q

Hypoparathyroidism calcitriol

47
Q

Hypoparathyroidism calcium

48
Q

Hypoparathyroidism phosphorus

49
Q

Hypoparathyroidism eGFR

50
Q

Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome

PTH

51
Q

Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome

Calcitriol

52
Q

Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome

Calcium

53
Q

Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome

Phosphorus

54
Q

Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome

eGFR

55
Q

Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome

PTH

56
Q

Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome

Calcitriol

57
Q

Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome

Calcium

58
Q

Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome

Phosphorus

59
Q

Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome

eGFR

60
Q

Pseudohypoparathyroidism: Type 2

PTH

61
Q

Pseudohypoparathyroidism: Type 2

Calcitriol

62
Q

Pseudohypoparathyroidism: Type 2

Calcium

63
Q

Pseudohypoparathyroidism: Type 2

Phosphorus

64
Q

Pseudohypoparathyroidism: Type 2

eGFR

65
Q

Pseudopseudohypoparathyroidism

PTH

66
Q

Pseudopseudohypoparathyroidism

Calcitriol

67
Q

Pseudopseudohypoparathyroidism

Calcium

68
Q

Pseudopseudohypoparathyroidism

Phosphorus

69
Q

Pseudopseudohypoparathyroidism

eGFR

70
Q

Vitamin D Deficiency

PTH

71
Q

Vitamin D Deficiency

Calcitriol

72
Q

Vitamin D Deficiency

Calcium

73
Q

Vitamin D Deficiency

Phosphate

74
Q

Vitamin D Deficiency

eGFR

75
Q

Primary Hyperparathyroidism

PTH

76
Q

Primary Hyperparathyroidism

Calcitriol

77
Q

Primary Hyperparathyroidism

Calcium

78
Q

Primary Hyperparathyroidism

Phosphate

79
Q

Primary Hyperparathyroidism

eGFR

A

Normal or decreased

80
Q

Secondary Hyperparathyroidism

PTH

81
Q

Secondary Hyperparathyroidism

Calcitriol

A

normal or low

82
Q

Secondary Hyperparathyroidism

calcium

A

normal or low

83
Q

Secondary Hyperparathyroidism

phosphate

84
Q

Secondary Hyperparathyroidism

eGFR

85
Q

Tertiary Hyperparathyroidism

PTH

86
Q

Tertiary Hyperparathyroidism

Calcitriol

A

normal or low

87
Q

Tertiary Hyperparathyroidism

Calcium

88
Q

Tertiary Hyperparathyroidism

phosphate

A

high or normal

89
Q

Tertiary Hyperparathyroidism

eGFR

CVPR (93 decks)

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