Managing Comorbidities in Pts w/ CKD Flashcards

1
Q

CKD is classified based on what 3 things?

A
  • Cause
  • GFR
  • Extent of proteinuria
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2
Q

What are complications of CKD? (5)

A
  • Altered Na & H2O balance
  • Metabolic acidosis
  • Anemia
  • MBD
  • Cardiac disease
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3
Q

What is the leading cause of CKD & ultimately ESRD?

A

DM

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4
Q

What is the 2nd leading cause of ESRD?

A

HTN

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5
Q

What is the 3rd leading cause of ESRD?

A

Glomerulonephritis

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6
Q

What is the patho of CKD?

A

Irreversible parenchymal damage & ESRD

  • Loss of nephron mass
  • Glomerular HTN
  • Proteinuria
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7
Q

What are 2 contributing concerns of CKD?

A
  • Smoking (decreases GFR & increases albumin excretion)

- Obesity

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8
Q

What is 1st line therapy for diabetes if the urine albumin excretion is >30/24hrs?

A

ACEI or ARB

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9
Q

How long is the ACEI or ARB dose increased for the tx of diabetes?

A

Increased until:

  • Albuminuria is reduced by 30-50% OR
  • Sig. drop in eGFR OR
  • Hyperkalemia
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10
Q

What are the renal changes of ACEIs & ARBs?

A
  • Renal hemodynamics

- Reduction of BP

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11
Q

Define anemia. What is a contributing factor?

A

Deficiency in production of endogenous erythropoietin by the kidney

Iron deficiency

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12
Q

How do you manage anemia?

A
  • Administer erythropoietic-stimulating agents (ESAs)

- Iron supplements (oral or IV)

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13
Q

What are administration limits when treating anemia?

A
  • Higher risk of cardiac events

- When Hgb > 11

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14
Q

What guidelines are used for grading & strength recommendations?

A

KDIGO

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15
Q

KDIGO: Level 1 vs level 2

A

Level 1 = “we recommend”

Level 2 = “we suggest”

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16
Q

KDIGO: Grades

A

A: High
B: Moderate
C: Low
D: Very low

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17
Q

When do you initiate ESA in a ND-CKD pt?

A
  • Hgb < 10

- Consider Hgb rate of fall

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18
Q

When should you NOT initiate ESA in a ND-CKD pt?

A

Hgb ≥10

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19
Q

When do you initiate ESA in a CKD pt who is dialysis dependent?

A

Hgb btwn 9-10

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20
Q

In ND-CKD, do NOT use ESAs to…

A
  • intentionally increase Hgb

- maintain Hgb > 11.5

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21
Q

When do you initiate iron in a ND-CKD pt?

A

TSat ≤ 30% & ferritin ≤ 500

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22
Q

What are examples of ESAs?

A
  • Epoetin alfa
  • Darbepoetin alfa
  • Methoxy PEG-epoetin beta
23
Q

How often should you use epoetin alfa?

A

3 times/wk

24
Q

How often should you use darbepoetin alfa?

A

once every 4 wks

25
Q

How often should you use methoxy PEG-epoetin beta

A

Every 2 wks

26
Q

When do you double the dose of methoxy PEG-epoetin beta?

A

Once Hgb stabilizes, double the dose & administer monthly

27
Q

What is the MOA of ESAs?

A
  • Induce erythropoiesis by stimulating the division of erythroid progenitor cells
  • Induce release of reticulocytes from bone marrow into blood
28
Q

What are clinical indications for ESAs?

A
  • Anemia due to myelosuppresion

- Anemia due to CKD

29
Q

What is the box warning for ESAs?

A

Increased CV & CKD events w/ Hgb > 11

30
Q

What are other ADEs of ESAs?

A
  • CA
  • Shortened survival or progression or recurrence in breast, cervical, head/neck, & non-small cell lung cancer pts ≥ 12
  • Increased risk of DVT
31
Q

What are abnormalities in CKD-MBD?

A
  • PTH
  • Ca, phosphorus & product
  • Vit D
  • Bone turnover
  • Soft tissue calcifications
32
Q

What is the net effect on serum levels w/ PTH?

A

Ca increase, phosphate decrease

33
Q

What is the net effect on serum levels w/ vit D?

A

Both Ca & phosphate increase

34
Q

What is the net effect on serum levels w/ FGF23?

A

Decreased phosphate

35
Q

How do you manage CKD-MBD?

A
  • Phosphorus restriction
  • Phosphate-binding agents
  • Vit D
  • Calcimimetic therapy
36
Q

What phosphate-binding agents can you use for tx of hyperphosphatemia in CKD?

A
  • Ca based binders
  • Iron based binders
  • Resin binders
  • Other elemental binders
37
Q

What are 2 examples of Ca based binders?

A

Ca acetate

Ca carbonate

38
Q

What are 2 examples of iron based binders?

A

Ferric citrate

Sucroferric oxyhydroxide

39
Q

What are the effects of ferric citrate?

A
  • Increase in iron, ferritin, & TSat

- Discolored stools

40
Q

What is an ADE of sucroferric oxyhydroxide?

A

Discolored stools

41
Q

What are 2 examples of resin binders?

A

Sevelamer carbonate

Sevelamer hydrochloride

42
Q

What are the effects of sevelamer carbonate?

A
  • Lowers LDL

- May interact w/ cipro & mycophenolate

43
Q

What are 2 examples of other elemental binders?

A
  • Lanthanum carbonate

- Aluminium hydroxide (not 1st line, short-term use)

44
Q

What are ADEs of lanthanum carbonate?

A
  • Accumulation due to GI absorption
  • N/V/abd pain
  • Bowel obstruction, constipation, dyspepsia
  • Fecal impaction, ileus
45
Q

What are ADEs of aluminum hydroxide?

A
  • Aluminum toxicity
  • Constipation, fecal impaction
  • Hypomagnesmia, hypophosphatemia
46
Q

Do not use aluminum hydroxide w/ ….

A

citrate-containing products

47
Q

What is the MOA of Ca based phosphate binding agents for hyperphosphatemia in CKD pts?

A
  • Binds w/ dietary phosphate to form Ca phosphate

- Excreted in feces

48
Q

What are ADEs of Ca based phosphate-binding agents?

A
  • Hypercalciumia
  • Hypophosphatemia
  • Milk-alkali syndrome
49
Q

What is the MOA of sevelamer hydrochloride (a resin-binder)

A
  • Binds phosphate within intestinal lumen –> decreased absorption & phosphate concentrations
  • Lowers LDL
50
Q

What are ADEs of sevelamer hydrochloride?

A
  • Metabolic acidosis (esp. in children)

- N/V/D & dyspepsia

51
Q

What is the MOA of lanthanum carbonate?

A

Binds dietary phosphate –> insoluble complexes w/ net decreases in phosphate & Ca levels

52
Q

What is the MOA of aluminum hydroxide?

A

Binds phosphate in GI tract, preventing absorption of phosphate

53
Q

What vit D agents can cause hypercalcemia?

A
  • Ergocalciferol D2

- Cholecalciferol D3

54
Q

What is the MOA of ergocalciferol D2 & cholecalciferol D3?

A
  • Stimulate Ca & phosphate absorption from small intestine
  • Promote secretion of Ca from bone to blood
  • Promote renal tubule phosphate resorption