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CVPR > CVPR Week 8: Renal handling of P > Flashcards

CVPR Week 8: Renal handling of P Flashcards

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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
Actions of FGF23 4 listed
* 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
26
FGF23 overall effect
Lowering of serum phosphorus
27
Inhibiting 1α-hydroxylase has what effect?
decreases calcitriol
28
Stimulating 24-hydroxylase has what effect?
Degrades Vitamin D
29
Describe the integrated regulation of renal P excretion
30
Mechanisms of hypophosphatemia
Shift into cells Decreased intestinal absorption Decreased intake (starvation/alcoholism) Increased renal loss of phosphate (phosphate wasting)
31
Mechanisms of hyperphosphatemia 5 listed
* 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
32
Fanconi syndrome and phosphorus
NaP transporter mutation causes phosphate wasting
33
NaP transporter mutation that results in phosphate wasting?
Fanconi Syndrome
34
Alcoholism and phosphate
* will have low phosphorus level * If they are not alcoholic then they might have Fanconi Syndrome
35
When phosphorus is high what should you look for?
Look for tissue release (rhabdomyolysis) or poor kidney function
36
Hypophosphatemia clinical manifestations
* Manifestations depend on the acuity and chronicity * Symptoms due to changes in mineral metabolism * Symptoms due to ATP depletion
37
What are the symptoms due to ATP depletion? 5 listed
* Metabolic encephalopathy, impaired myocardial function * Respiratory failure * myopathy * Dysphagia, ileus * Hemolytic anemia
38
Hyperphosphatemia clinical manifestations
* 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
Tx of Acute severe hypophosphatemia of \< 1 mg/dL
IV phosphate replacement
40
Tx of chronic hypophosphatemia
oral phosphorus with vitamin D
41
Adverse effects of phosphate therapy
* phosphate therapy can aggravate hypocalcemia * in hypercalcemic patients, acute loading may lead to calcium phosphate precipitation and nephrocalcinosis
42
Tx of hyperphosphatemia
* Phosphate binders (CKD) * Dialysis * Tumor lysis * Rhabdomyolysis
43
44
Lab profile calcium and phosphate disorders
45
Hypoparathyroidism PTH
decreased
46
Hypoparathyroidism calcitriol
decreased
47
Hypoparathyroidism calcium
decreased
48
Hypoparathyroidism phosphorus
decreased
49
Hypoparathyroidism eGFR
normal
50
Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome PTH
Increased
51
Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome Calcitriol
decreased
52
Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome Calcium
Decreased
53
Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome Phosphorus
Increased
54
Pseudohypoparathyroidism: Type 1A GNAS mutations/Albright syndrome eGFR
normal
55
Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome PTH
Increased
56
Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome Calcitriol
Decreased
57
Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome Calcium
Decreased
58
Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome Phosphorus
Increased
59
Pseudohypoparathyroidism: Type 1B GNAS mutations/Usually without skeletal defects of Albright syndrome eGFR
Normal
60
Pseudohypoparathyroidism: Type 2 PTH
increased
61
Pseudohypoparathyroidism: Type 2 Calcitriol
decreased
62
Pseudohypoparathyroidism: Type 2 Calcium
Decreased
63
Pseudohypoparathyroidism: Type 2 Phosphorus
Increased
64
Pseudohypoparathyroidism: Type 2 eGFR
65
Pseudopseudohypoparathyroidism PTH
Normal
66
Pseudopseudohypoparathyroidism Calcitriol
Normal
67
Pseudopseudohypoparathyroidism Calcium
Normal
68
Pseudopseudohypoparathyroidism Phosphorus
Normal
69
Pseudopseudohypoparathyroidism eGFR
Normal
70
Vitamin D Deficiency PTH
Increased
71
Vitamin D Deficiency Calcitriol
Decreased
72
Vitamin D Deficiency Calcium
Decreased
73
Vitamin D Deficiency Phosphate
decreased
74
Vitamin D Deficiency eGFR
75
Primary Hyperparathyroidism PTH
Increased
76
Primary Hyperparathyroidism Calcitriol
increased
77
Primary Hyperparathyroidism Calcium
increased
78
Primary Hyperparathyroidism Phosphate
decreased
79
Primary Hyperparathyroidism eGFR
Normal or decreased
80
Secondary Hyperparathyroidism PTH
Increased
81
Secondary Hyperparathyroidism Calcitriol
normal or low
82
Secondary Hyperparathyroidism calcium
normal or low
83
Secondary Hyperparathyroidism phosphate
high
84
Secondary Hyperparathyroidism eGFR
low
85
Tertiary Hyperparathyroidism PTH
high
86
Tertiary Hyperparathyroidism Calcitriol
normal or low
87
Tertiary Hyperparathyroidism Calcium
high
88
Tertiary Hyperparathyroidism phosphate
high or normal
89
Tertiary Hyperparathyroidism eGFR
low

CVPR (93 decks)

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