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Renal > CKD > Flashcards

CKD Flashcards

1
Q

The different ways to name CKD

A

CRI = chronic renal insufficiency
Progressive kidney disease
Nephropathy

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2
Q

CKD definition

A

Abnormalities of kidney structure or function, present for > 3 months, with implications for health

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3
Q

Markers of kidney disease

A

1 or more of the following:
Albuminuria
Urine sediment abnormalities (casts)
Electrolyte and other abnormalities d/t tubular disorders
Abnormalities detected by histology (biopsy)
Structural abnormalities detected by imaging (polycystic kidney disease)
Hx of kidney transplant

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4
Q

CKD GFR

A

< 60

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5
Q

CKD susceptibility factors

A 
Older age
Decreased kidney mass
Low birth weight
FH of CKD
US ethnic minority status
Low income or education
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6
Q

CKD initiation factors

A

DM
HTN
Glomerulonephritis

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7
Q

What is the main structural marker for kidney damage?

A

Proteinuria

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8
Q

Albumin excretion rate (AER) classifications

A

Normal-Mildly increased: < 30
Moderately increased: 30-300
Severely increased: > 300

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9
Q

Protein Excretion Rate (PER) classifications

A

Normal-Mildly increased: < 150
Moderately increased: 150-500
Severely increased: > 50

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10
Q

Albumin-to-Creatinine Ratio (ACR) classifications

A

Normal-Mildly increased: < 30
Moderately increased: 30-300
Severely increased: > 300

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11
Q

Protein-to-Creatinine Ratio (PCR) classifications

A

Normal-Mildly increased: < 150
Moderately increased: 150-500
Severely increased: > 500

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12
Q

Protein reagent strip classifications

A

Normal-Mildly increased: negative to trace
Moderately increased: Trace to +
Severely increased: + to greater

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13
Q

Ways to assess renal disease

A 
Proteinuria
SCr (BMP)
GFR
BP
Sx
CBC
Urinalysis
Imaging
Cystatin C
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14
Q

What assessments must be screened annually for high risk patients?

A 
SCr
GFR
BP
Sx
CBC
Urinalysis
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15
Q

Cystatin C

A

Low molecular weight protein
Freely filtered by glomerulus
Completely reabsorbed by tubules then catabolized
Not affected by age, gender, race or muscle mass

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16
Q

CKD G1

A

GFR >/= 90
“Normal or high”
No sx

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17
Q

CKD G2

A

GFR 60 - 89
“Mildly decreased”
No sx

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18
Q

CKD G3

A 
G3a: GFR 45-59
"Mild-moderately decreased"
G3b: GFR 30-44
"Moderately-severely decreased"
Both sx: generally asx; HTN, anemia
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19
Q

CKD G4

A

GFR 15-29
“Severely decreased”
Sx: Nocturia, fatigue, cold intolerance, anorexia, hyperphosphatemia, hypocalcemia, metabolic acidosis

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20
Q

CKD G5

A

GFR < 15 (or dialysis)
“Kidney failure”
Sx: Malaise, lack of energy, pruritus, N/V, myoclonus, asterixis, seizures

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21
Q

Albuminuria A1

A

AER/ACR < 30

“Normal-Mildly increased”

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22
Q

Albuminuria A2

A

AER/ACR 30-300

“Moderately increased”

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23
Q

Albuminuria A3

A

AER/ACR > 300

“Severely increased”

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24
Q

Progression of CKD

A

Small fluctuations in GFR are common
Requires multiple SCr and eGFR measurements over time
Defined as 1 or more of the following:
-Decline in GFR category with a 25% or greater drop in eGFR from baseline
-Sustained decline in eGFR of more than 5

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25
Q

Desired outcomes of renal disease

A

Reverse or delay progression of renal injury
Reduce incidence of stage 5 CKD
Specifically for stage 5 on HD

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26
Q

Nutritional management of renal disease

A 
Dietary protein restriction
Sodium restriction
Smoking cessation
Exercise
Wt loss
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27
Q

Dietary protein restriction in renal disease

A

0.8 g/kg/d

Only for patients with GFR < 30 (G4 and G5)

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28
Q

Sodium restriction in renal disease

A

< 2 g/d

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29
Q

Exercise in renal disease

A

30 minutes for 5 times a week

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30
Q

Weight loss in renal disease

A

BMI between 20-25

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31
Q

Pharmacologic therapy

A

Glycemic control

HTN

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32
Q

Glycemic goals in renal disease

A

A1c: 7.0%
Pre-prandial: 70-130
Post-prandial: < 180

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33
Q

HTN goals in renal disease

A

= 140/90 (DM or non-DM w/ACR < 30)

= 130/80 (DM or non-DM w/ACR > 30)

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34
Q

HTN DOC in renal dz

A

ACR > 30: ACE/ARB
DM w/ACR > 30: ACE/ARB
Any pt w/ACR < 30: diuretic

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35
Q

Smoking cessation in renal dz

A

May limit progression of dz

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36
Q

Complications of CKD

A 
Fluid and electrolyte disturbances
Metabolic acidosis
Anemia
Decreased calcium and Mineral and Bone Disorder
Renal osteodystrophy
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37
Q

Treatment of sodium and fluid balance in renal disease

A

No-added salt diet
Fluid restriction (reserve for dialysis pts between sessions)
Diuretics (Loop +/- thiazide)

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38
Q

Sodium and fluid balance goal

A

Serum Na between 135-145 w/o volume overload or depletion

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39
Q

Sodium and fluid balance in CKD

A

Decreased ability to concentrate or dilute urine

Decreased total renal Na excretion = Increased body fluid = Volume overload

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40
Q

Monitoring of Sodium and fluid balance in CKD

A

BP
Volume status
Serum electrolytes

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41
Q

Potassium homeostasis in CKD

A

Regulated by renal excretion, shifting in and out of cell, GI excretion
G4 - G5 = body can no longer adapt to decreased renal excretion of K = hyperkalemia

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42
Q

Potassium goals in CKD

A

Prevent hyperkalemia and adverse consequences
G2-G3s: K in normal range (3.5 - 5.0)
G4 - G5: K between 4.5-6

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43
Q

Potassium acute treatment

A

same as AKI (calcium gluconate, insulin plus glucose, albuterol)

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44
Q

Chronic potassium treatment in CKD

A 
Dietary restrictions
Prevent constipation
Eliminate medications likely to cause hyperkalemia
Sodium polystyrene sulfonate
Patiromer
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45
Q

Sodium polystyrene sulfonate

A

MOA: exchanges Na for K w/in large intestines
SE: constipation, hypernatremia, interstitial necrosis
Safety alert: Do not take any medications for 6 hours before/after

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46
Q

Patiromer

A

MOA: exchanges Ca for K within the colon = decreased free K in colon = decreased serum levels
Administer w/food
SE: constipation, hypomagnesemia, N/D, ab discomfort, flatulence
Safety alert: Do not take any medications for 6 hours before/after
Comments: Primary use is in patients with CKD receiving at least one RAAS inhibitor medication

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47
Q

Metabolic acidosis

A

pH < 7.35
pCO2 < 35
HCO3 < 24

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48
Q

Metabolic acidosis presentation

A

Fatigue
Decreased exercise tolerance
Hyperkalemia

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49
Q

Metabolic acidosis pathophysiology

A

Decreased ammonia synthesis =
Decreased urinary buffer =
Decreased net H+ excretion =
Decreased pH

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50
Q

Metabolic acidosis goal

A

Normalize pH
Maintain serum HCO3 within normal range (22-28)
Prevent complications of severe acidosis (bone dz, decreased cardiac contractility)

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51
Q

Asx metabolic acidosis treatment

A

Patients with mild acidosis generally do not need emergent treatment

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52
Q

Severe metabolic acidosis

A

pH < 7.2

Serum HCO3 < 15

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53
Q

When to treat metabolic acidosis

A

Serum HCO3 < 22

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54
Q

Metabolic acidosis alkalinizing agents

A

Sodium bicarbonate
Sodium citrate/citric acid
Potassium citrate/citric acid
Citric acid/sodium citrate/potassium citrate

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55
Q

Anemia of CKD

A

Hgb < 13 in males

Hgb < 12 in females

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56
Q

Anemia of CKD contributing factors

A 
Decreased EPO production
Uremic toxins decrease RBC lifespan
Iron deficiency
Blood loss from HD and lab testing
Poor nutrition (decreased folic acid and B vitamins)
Severe mineral and bone disorder
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57
Q

Anemia of CKD patient evaluation

A

RBC indices
Absolute reticulocyte count
Iron indices
Folic acid and vitamin B12

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58
Q

Anemia of CKD goals

A

Increased oxygenation
Improve QOL
Prevent complications
Target Hgb: = 11.5 (KDIGO); = 11 (manuf./FDA)

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59
Q

Anemia of CKD treatment

A

Iron supplementation

Initiate when TSAT = 30% and ferritin = 500

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60
Q

Oral iron supplements

A

10% absorbed in duodenum and upper jejunum
Decreased absorption with food
Convenient for patients without IV access

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61
Q

Oral iron supplement formulations

A 
Ferrous sulfate (20%)
Ferrous sulfate, exsiccated (30%)
Ferrous fumarate (33%)
Ferrous gluconate (12%)
Iron polysaccharide complex (100%)
Heme iron polypeptide (100%)
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62
Q

Oral iron supplementation adverse effects

A

GI: N, constipation, abdominal cramping

63
Q

Oral iron supplementation drug interactions

A

Vitamin C
FQs
PPIs/H2RAs
Tetracyclines

64
Q

IV iron supplementation formulations

A

Iron dextran
Sodium ferric gluconate
Iron sucrose
Ferumoxytol

65
Q

IV iron supplementation ADR

A 
Anaphylaxis (Iron dextran)
-BBW
-Test dose required
Infusion rxns: hypotension, arthralgias, myalgias, fever, flushing, HA
Risk of iron overload
66
Q

Erythropoietin stimulating agents MOA

A

Same biologic activity as endogenous erythropoietin

67
Q

When to initiate Erythropoietin stimulating agents

A

CKD ND: Hgb < 10

CKD 5D: Hgb: 9-10 to avoid falling below 9

68
Q

When to interrupt or reduce ESA dose

A

Hgb approaching/exceeding 11

69
Q

ESA BBW

A

Increased risk of death, MI and stroke

70
Q

ESA drugs

A

Epoetin alfa
Darbepoetin
Peginesatide

71
Q

Epoetin alfa SE

A 
HTN
Arthralfia
Muscle spasm
Pyrexia
Dizziness
72
Q

Darbepoetin SE

A 
HTN
Dyspnea
Peripheral edema
Cough
Procedural hypotension
73
Q

Which ESA(s) were/was removed from the market?

A

Peginesatide

74
Q

Which ESA(s) require adequate iron?

A

Epoetin alfa and Darbepoetin

75
Q

ESA dose adjustment

A

Dose increases: once every 4 weeks
-If hgb has not increased by > 1 after 4 weeks = increase by 25%
Dose reductions: Can be more frequent
-With rapid hgb rise (> 1 in any 2wk period) = reduce by 25%
Use lowest dose possible

76
Q

ESA monitoring

A

Monitor Hgb at least weekly until stable then monthly

77
Q

Mineral and Bone Disorder and Renal Osteodystrophy aka

A

Secondary hyperparathyroidism

78
Q

Renal osteodystrophy classifications

A

Osteomalacia
Osteitis fibrosa cystica
Adynamic bone disease

79
Q

Osteomalacia definition

A

Softening of bones (defective mineralization)

80
Q

Osteitis fibrose cystica definition

A

Replacement of bone with fibrous tissue (high bone turnover)

81
Q

Adynamic bone disease definition

A

Decreased bone formation without a mineralization defect

82
Q

MBD and ROD goals

A

Prevent MBD and ROS and associated consequences

Maintain Ca, PO4, iPTH levels

83
Q

Corrected calcium equation

A

Observed Ca + 0.8 x (4 - albumin level)

84
Q

Corrected calcium levels

A

Normal: 8.5 - 10.8
CKD 3: “Normal”
CKD 4: “Normal”
CKD 5: 8.4 - 9.5

85
Q

Phosphorous levels

A

Normal: 2.7 - 4.6
CKD 3: “Normal”
CKD 4: “Normal”
CKD 5: 3.5 - 5.5

86
Q

Ca x P levels

A

All: < 55

87
Q

Intact PTH (iPTH) levels

A

Normal: 10 - 60
CKD 3: 35 - 70
CKD 4: 70 - 110
CKD 5: 150 - 300

88
Q

Evaluation of a patient for MBD and ROD

A 
Serum Ca
Serum PO4
Vitamin D
BMD
PTH
89
Q

MBD and ROD non-pharm treatment

A

Dietary PO4 restriction

Parathyroidectomy (last line)

90
Q

Major treatment failure with dietary PO4 restriction

A

Non-compliance

91
Q

What foods contain PO4

A 
Meat
Dairy
Nuts
Dried beans
Colas
Peanut butter
Beer
92
Q

MBD and ROD pharm treatment

A

Phosphate binding agents
Vitamin D
Calcimimetics

93
Q

Phosphate binding agents pathophysiology

A

Bind dietary phosphorous in the GI tract = form insoluble salts = excreted in feces

94
Q

Phosphate binding agents

A 
Calcium carbonate
Calcium acetate
Sevelamer
Lanthanum
Sucroferric oxyhydroxide
Aluminum-containing agents
Magnesium-containing agents
95
Q

How must phosphate binding agents be taken?

A

With meals

96
Q

Calcium carbonate SE

A

Constipation
N/V/D
Increased Ca

97
Q

Calcium acetate SE

A

Constipation
N/V/D
Increased calcium

98
Q

Sevelamer SE

A

Pruritus

N/V/D

99
Q

Lanthanum SE

A

N/V/D

100
Q

Sucroferric oxyhydroxide SE

A

Dark colored feces

N/D

101
Q

What % of ca is calcium carbonate

A

40% elemental

102
Q

What % of ca is calcium acetate

A

25% elemental

103
Q

1st line phosphate binding agents

A

Calcium carbonate and Calcium acetate

*Except when vascular or soft-tissue calcifications are present

104
Q

Calcium carbonate and Calcium acetate comments

A

Can increase aluminum absorption

105
Q

Calcium carbonate and Calcium acetate DDI

A

Iron
Zinc
FQs

106
Q

Sevelamer comments

A

Do not crush or chew tablets
Does not affect serum Ca
Initial dose based on serum PO4 level

107
Q

Which phosphate binding agents can be used with calcifications?

A

Sevelamer

108
Q

Lanthanum comments

A

Chewable tablets

Primary use - Stage 5

109
Q

Sucroferric oxyhydroxide comments

A

Only for patients on HD
Chewable
Contains 500mg elemental iron

110
Q

Sucroferric oxyhydroxide DDI

A

Avoid w/vitamin D analogs and levothyroxine

111
Q

Aluminum-containing agents

A

3rd line - increased risk of toxicity
Limit to 4 weeks
SE: bone disease, anemia, encephalopathy

112
Q

Magnesium-containing agents

A

Not generally recommended

SE: severe diarrhea, abdominal cramps, hypermagnesemia, hyperkalemia

113
Q

When to initiate vitamin D therapy?

A

< 30

114
Q

Vitamin D precursors

A

Ergocalciferol

Cholecalciferol

115
Q

Active Vitamin D

A

Calcitriol

116
Q

Vitamin D analogs

A

Paricalcitol

Doxercalciferol

117
Q

Vitamin D precursor MOA

A

Metabolized to active form of vitamin D then same MOA

118
Q

Calcitriol and Paricalcitol MOA

A

Binds to and activates Vitamin D receptor in kidney, parathyroid gland, intestine and bone

119
Q

Doxercalciferol MOA

A

Metabolized to active form of vitamin D then same MOA

120
Q

Ergocalciferol SE

A

GI upset
Hypercalcemia
Hyperphosphotemia

121
Q

Cholecalciferol SE

A

Lipid abnormalities

Hypervitaminosis D

122
Q

Calcitriol SE

A

GI upset
Hypercalcemia
Hyperphosphotemia

123
Q

Paricalcitol SE

A

GI upset
Edema
HTN

124
Q

Doxercalciferol SE

A

Edema
HA
N/V

125
Q

Which vitamin D is primarily used for vitamin D deficiency or insufficiency

A

Ergocalciferol

126
Q

Which vitamin D is primarily used for prevention

A

Cholecalciferol

127
Q

Which vitamin D’s come in both PO and IV form?

A

Calcitriol
Paricalcitol
Doxercalciferol

128
Q

When do patients receive calcitriol IV?

A

Stage 5

129
Q

Calcimimetics

A

Cinacalcet

Etelcalcetide

130
Q

When are calcimimetics used?

A

Dialysis

131
Q

Calcimimetic MOA

A

Works on calcium-sensing receptor of parathyroid gland

Mimics extracellular ionized calcium = decreased PTH = decreased serum calcium

132
Q

Cinacalcet SE

A

GI upset
Hypocalcemia
Myalgia

133
Q

Etelcalcetide SE

A

Hypocalcemia
Worsening HF
GI bleeding

134
Q

How many drugs are needed for HTN in renal disease?

A

Most will need >/= 3

135
Q

Other complications of CKD

A 
Nutrition status
Hyperlipidemia
Uremic bleeding
Gastrointestinal disorders
Immune function
Pruritus
Neurologic abnormalities
Endocrine disorders
136
Q

Protein-energy malnutrition causes

A

Anorexia
Altered taste sensation
Unpalatable food (PO4 and Na restrictions)

137
Q

Protein-energy malnutrition treatment

A

Replace B and C vitamins and folic acid in dialysis patients

138
Q

When to treat hyperlipidemia in CKD?

A

Treat if have other risk factors

139
Q

KDIGO lipid guidelines

A

“Fire and Forget” strategy
Non-dialysis and non-transplant patients only
Only recommend - statin or statin/ezetimibe combo

140
Q

Uremic bleeding contributing factors

A

D/t platelet abnormalities (decreased platelet aggregation and adhesiveness)
Heparin administered with dialysis
Other anticoagulants/antiplatelet agents for other indications

141
Q

Uremic bleeding treatment

A

Cryoprecipitate (has factor VII and fibrinogen which helps decrease bleeding time)
Fresh frozen plasma (FFP)
Desmopressin

142
Q

GI disorders SE

A

Anorexia
Hiccups
Metallic taste in mouth

143
Q

Immune function causes

A

Uremic toxins may alter cell-mediated immunity

HD patients at increased risk with vascular access (exposure to infectious sources)

144
Q

Pruritus contributing factors

A

Inadequate dialysis, dry skin, CKD-MBD, increased histamine levels

145
Q

Pruritus treatment

A

Sufficient dialysis
Oral antihistamines
Topical steroids

146
Q

Neurologic abnormalities causes

A

Uremic encephalopathy

Peripheral neuropathy

147
Q

Uremic encephalopathy

A

Changes in consciousness, thinking, memory, speech, movement, emotion
Less common in earlier initiation of dialysis in stage 5

148
Q

Peripheral neuropathy treatment

A

TCAs

Gabapentin

149
Q

Endocrine disorders

A

Hypothyroidism
Hypothalamus disorders
Glucose management issues

150
Q

Hypothyroidism labs

A

Decreased T4 but TSH usually norma
Decreased T4 to T3 conversion
Replace thyroid hormone if TSH elevated

151
Q

Hypothalamus disorder presentation

A

Hypothermia - 1 degree less than normal

152
Q

Hyperglycemia cause

A

Peripheral insulin resistance

153
Q

Hypoglycemia cause

A

Decreased renal insulin degradation

Renal (8 decks)

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