Pharmacotherapy III > CKD Updated > Flashcards

CKD Updated Flashcards

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1
Q

Chronic kidney disease (CKD)

A
  • Abnormalities in kidney structure or function, present
    for ≥3 months, with implications for health
  • Progressive and irreversible loss of kidney function
    characterized by a significant reduction in glomerular
    filtration rate (GFR)
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2
Q

End stage renal disease (ESRD):

A
  • GFR <15 mL/min/1.73 m²
  • Chronic dialysis or kidney transplantation
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3
Q

Complications of CKD and Management

A

Electrolyte abnormalities, anemia, acidosis, secondary parahyperthyroidism, CKD progression, HTN, CVD

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4
Q

CKD electrolyte abnormalities

A
  • Hyperkalemia, hyperphosphatemia
  • Decreased sodium excretion → water retention/volume overload → systemic hypertension/pulmonary edema
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5
Q

Causes of anemia

A
  • Decreased erythropoietin synthesis
  • Decreased GI absorption of iron
  • Iron and vitamin B12 deficiency
  • Blood loss
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6
Q

Anemia diagnosis/definition

A
  • Hemoglobin <13 g/dL in males
  • Hemoglobin <12 g/dL in females
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7
Q

How often to check hemoglobin in CKD Stage 3

A

Annually

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8
Q

How often to check hemoglobin in CKD Stages 4-5

A

Biannually

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9
Q

How often to check hemoglobin in CKD Stage 5

A

Every 3 months

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10
Q

TSat (transferrin saturation)

A

available iron

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11
Q

Ferritin

A

stored iron

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12
Q

In CKD 5PD (Peritoneal Dialysis), start iron if…

A
  1. TSat ≤40% AND ferritin ≤100 ng/mL
    OR
  2. TSat <25% AND ferritin 100–300 ng/mL
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13
Q

In CKD 5HD (Hemodialysis), start iron if…

A

TSat ≤30% AND ferritin ≤500 ng/mL

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14
Q

When should iron be held?

A

If ferritin is above 700 ng/mL

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15
Q

Should anemia be treated before or after dialysis?

A

Before dialysis

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16
Q

What are erythropoiesis-stimulating agents (ESA)?

A

Drugs like epoetin that stimulate RBC production (replace missing EPO in CKD)

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17
Q

When do you START an ESA?

A

Start when Hgb is ~9–10 g/dL

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18
Q

When should you NOT use ESA?

A

If Hgb ≥10 g/dL

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19
Q

Target hemoglobin
Aim for:

A

~11.5 g/dL (safe zone) to avoid stroke, CV events and thrombosis

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20
Q

Things to consider along with Hgb before initiating ESA

A

Consider rate of fall of Hgb, prior response to iron, risk of needing transfusion

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21
Q

Special case: ESA use in CKD 5HD (dialysis)

A

Start around 9–10 g/dL to prevent Hgb from dropping <9

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22
Q

Fill in the blanks

Do not use ESAs to intentionally increase Hgb to > ____ or to maintain Hgb > ____

A
  • Hgb > 13 g/dL
  • Hgb > 11.5 g/dL
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23
Q

Iron supplementation MOA

A

Provides elemental iron to produce Hgb

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24
Q

Iron supplementation preference in non-HD patients

A
  • Either oral or IV recommended in non-HD patients
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25
When is IV iron preferred over oral?
In patients with CKD Stage 5
26
Adverse effects of oral iron
GI (constipation, nausea, abdominal cramping), dark colored stools
27
Adverse effects of IV iron
Hypotension, dizziness, dyspnea, headaches, lower back pain, anaphylaxis
28
Which iron supplementation is no longer used in practice?
Iron dextran
29
What is ferric carboxymaltose used for and how is it administered?
Used in adult CKD patients NOT on dialysis; given IV push or diluted
30
What is ferumoxytol used for and how is it administered?
Used for iron-deficiency anemia in CKD patients; must be diluted in NS or D5
31
When is iron dextran used and what is important before giving it?
Used when oral iron is not effective or not possible; requires a test dose due to risk of reaction
32
What patients can receive iron sucrose and how is it given?
Used in adult and pediatric CKD patients (including CKD 5D ≥2 years); given IV push or diluted
33
What is sodium ferric gluconate used for and how is it administered?
Used in adult and pediatric CKD 5D patients ≥6 years on ESA therapy; given as slow IV push or diluted
34
Which IV iron requires a test dose?
Iron dextran
35
Which IV iron is commonly used in non-dialysis CKD patients?
Ferric carboxymaltose
36
Which IV iron must be diluted before administration?
Ferumoxytol
37
Why is iron important in CKD anemia management?
Iron is required for hemoglobin production and improves response to ESAs
38
Adverse effects of ESAs
* Hypertension/hypertensive encephalopathy * Seizures * Thrombosis * Antibody-associated pure red cell aplasia (PRCA)
39
What does HIF-PHI stand for?
Hypoxia-inducible factor prolyl hydroxylase inhibitors
40
What physiologic condition do HIF-PHI agents mimic?
Hypoxia (low oxygen state)
41
How do HIF-PHI agents increase red blood cell production?
Stimulate the body’s natural EPO production by activating hypoxia signaling pathways
42
Name two HIF-PHI medications
* Daprodustat (Jesduvroq) * Vadadustat (Vafseo)
43
How do HIF-PHI agents differ from ESAs?
HIF-PHIs stimulate endogenous EPO production; ESAs provide exogenous EPO
44
Why is FDA approval limited for HIF-PHI agents?
Cardiovascular safety concerns restrict use mainly to patients on maintenance dialysis
45
What is the overall effect of HIF-PHI agents on anemia in CKD?
Increase endogenous EPO → increase RBC production → improve anemia
46
What can occur as a result of persistent hypocalcemia and hyperphosphatemia?
Renal osteodystrophy
47
Parathyroid hormone is released in response to....
Hypocalcemia or hyperphosphatemia
48
How does reduced kidney function result in impaired vitamin D?
* Reduces vitamin D production * Reduces intestinal calcium absorption * Increases mobilization of calcium from the bone
49
CKD-mineral and bone disorders (CKD-MBD) is also referred to as...
Secondary hyperparathyroidism
50
Non-pharmacologic management of secondary hyperparathyroidism
1. Dietary phosphate restriction ; Goal: 800–1000 mg/day **first line** 2. Dialysis (removes phosphate, toxins) 3. Parathyroidectomy
51
Pharmacologic therapy management of secondary hyperparathyroidism
1. Phosphate binding agents (take with meals) 2. Calcimimetic therapy 3. Vitamin D
52
Phosphate binders reduce absorption of certain drugs due to their cations (calcium, aluminum, iron) binding/chelating to drugs in the gut. How do you fix this?
separate dosing by at least 2 hours
53
MOA of phosphate binders
* Binds to dietary phosphorous in the GI tract * Phosphate salt complex → excreted in the feces
54
Vitamin D and Vitamin D analogs **indirect** effect on PTH secretion suppression
Through stimulating absorption of serum calcium from the gut → raises serum calcium → suppresses PTH
55
Vitamin D and Vitamin D analogs **direct** effect on PTH secretion suppression
Direct activity on parathyroid gland; decreases PTH synthesis
56
Vitamin D analogs adverse effects
Hypercalcemia, Hyperphosphatemia
57
Most vitamin D analogs are metabolized in the liver by which key enzymes?
* CYP3A4 * CYP24 * UGT1A4
58
What is the overall effect of vitamin D therapy in CKD?
Increases calcium and suppresses PTH
59
What is the main drug in the calcimimetic class?
Cinacalcet (Sensipar)
60
Where do calcimimetics act?
Calcium-sensing receptor (CaSR) on parathyroid chief cells
61
What do calcimimetics mimic?
Extracellular ionized calcium
62
How do calcimimetics affect the calcium-sensing receptor?
Increase its sensitivity to calcium
63
What is the final effect of calcimimetics on PTH?
Decrease PTH secretion
64
How should cinacalcet be taken?
With food or shortly after a meal
65
What are common side effects of calcimimetics?
Nausea, vomiting, hypocalcemia
66
Why can calcimimetics cause hypocalcemia?
They suppress PTH, which lowers calcium levels
67
How is cinacalcet metabolized?
Extensively by CYP450 enzymes (CYP3A4, 2D6, 1A2) and glucuronidation
68
How do calcimimetics differ from vitamin D in CKD treatment?
Calcimimetics lower PTH without increasing calcium, while vitamin D raises calcium
Pharmacotherapy III
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