CKD Flashcards
(153 cards)
1
Q
The different ways to name CKD
A
CRI = chronic renal insufficiency
Progressive kidney disease
Nephropathy
2
Q
CKD definition
A
Abnormalities of kidney structure or function, present for > 3 months, with implications for health
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
4
Q
CKD GFR
A
< 60
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
6
Q
CKD initiation factors
A
DM
HTN
Glomerulonephritis
7
Q
What is the main structural marker for kidney damage?
A
Proteinuria
8
Q
Albumin excretion rate (AER) classifications
A
Normal-Mildly increased: < 30
Moderately increased: 30-300
Severely increased: > 300
9
Q
Protein Excretion Rate (PER) classifications
A
Normal-Mildly increased: < 150
Moderately increased: 150-500
Severely increased: > 50
10
Q
Albumin-to-Creatinine Ratio (ACR) classifications
A
Normal-Mildly increased: < 30
Moderately increased: 30-300
Severely increased: > 300
11
Q
Protein-to-Creatinine Ratio (PCR) classifications
A
Normal-Mildly increased: < 150
Moderately increased: 150-500
Severely increased: > 500
12
Q
Protein reagent strip classifications
A
Normal-Mildly increased: negative to trace
Moderately increased: Trace to +
Severely increased: + to greater
13
Q
Ways to assess renal disease
A
Proteinuria SCr (BMP) GFR BP Sx CBC Urinalysis Imaging Cystatin C
14
Q
What assessments must be screened annually for high risk patients?
A
SCr GFR BP Sx CBC Urinalysis
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
16
Q
CKD G1
A
GFR >/= 90
“Normal or high”
No sx
17
Q
CKD G2
A
GFR 60 - 89
“Mildly decreased”
No sx
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
19
Q
CKD G4
A
GFR 15-29
“Severely decreased”
Sx: Nocturia, fatigue, cold intolerance, anorexia, hyperphosphatemia, hypocalcemia, metabolic acidosis
20
Q
CKD G5
A
GFR < 15 (or dialysis)
“Kidney failure”
Sx: Malaise, lack of energy, pruritus, N/V, myoclonus, asterixis, seizures
21
Q
Albuminuria A1
A
AER/ACR < 30
“Normal-Mildly increased”
22
Q
Albuminuria A2
A
AER/ACR 30-300
“Moderately increased”
23
Q
Albuminuria A3
A
AER/ACR > 300
“Severely increased”
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
25
Desired outcomes of renal disease
Reverse or delay progression of renal injury
Reduce incidence of stage 5 CKD
Specifically for stage 5 on HD
26
Nutritional management of renal disease
```
Dietary protein restriction
Sodium restriction
Smoking cessation
Exercise
Wt loss
```
27
Dietary protein restriction in renal disease
0.8 g/kg/d
| Only for patients with GFR < 30 (G4 and G5)
28
Sodium restriction in renal disease
< 2 g/d
29
Exercise in renal disease
30 minutes for 5 times a week
30
Weight loss in renal disease
BMI between 20-25
31
Pharmacologic therapy
Glycemic control
| HTN
32
Glycemic goals in renal disease
A1c: 7.0%
Pre-prandial: 70-130
Post-prandial: < 180
33
HTN goals in renal disease
= 140/90 (DM or non-DM w/ACR < 30)
| = 130/80 (DM or non-DM w/ACR > 30)
34
HTN DOC in renal dz
ACR > 30: ACE/ARB
DM w/ACR > 30: ACE/ARB
Any pt w/ACR < 30: diuretic
35
Smoking cessation in renal dz
May limit progression of dz
36
Complications of CKD
```
Fluid and electrolyte disturbances
Metabolic acidosis
Anemia
Decreased calcium and Mineral and Bone Disorder
Renal osteodystrophy
```
37
Treatment of sodium and fluid balance in renal disease
No-added salt diet
Fluid restriction (reserve for dialysis pts between sessions)
Diuretics (Loop +/- thiazide)
38
Sodium and fluid balance goal
Serum Na between 135-145 w/o volume overload or depletion
39
Sodium and fluid balance in CKD
Decreased ability to concentrate or dilute urine
| Decreased total renal Na excretion = Increased body fluid = Volume overload
40
Monitoring of Sodium and fluid balance in CKD
BP
Volume status
Serum electrolytes
41
Potassium homeostasis in CKD
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
42
Potassium goals in CKD
Prevent hyperkalemia and adverse consequences
G2-G3s: K in normal range (3.5 - 5.0)
G4 - G5: K between 4.5-6
43
Potassium acute treatment
same as AKI (calcium gluconate, insulin plus glucose, albuterol)
44
Chronic potassium treatment in CKD
```
Dietary restrictions
Prevent constipation
Eliminate medications likely to cause hyperkalemia
Sodium polystyrene sulfonate
Patiromer
```
45
Sodium polystyrene sulfonate
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
46
Patiromer
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
47
Metabolic acidosis
pH < 7.35
pCO2 < 35
HCO3 < 24
48
Metabolic acidosis presentation
Fatigue
Decreased exercise tolerance
Hyperkalemia
49
Metabolic acidosis pathophysiology
Decreased ammonia synthesis =
Decreased urinary buffer =
Decreased net H+ excretion =
Decreased pH
50
Metabolic acidosis goal
Normalize pH
Maintain serum HCO3 within normal range (22-28)
Prevent complications of severe acidosis (bone dz, decreased cardiac contractility)
51
Asx metabolic acidosis treatment
Patients with mild acidosis generally do not need emergent treatment
52
Severe metabolic acidosis
pH < 7.2
| Serum HCO3 < 15
53
When to treat metabolic acidosis
Serum HCO3 < 22
54
Metabolic acidosis alkalinizing agents
Sodium bicarbonate
Sodium citrate/citric acid
Potassium citrate/citric acid
Citric acid/sodium citrate/potassium citrate
55
Anemia of CKD
Hgb < 13 in males
| Hgb < 12 in females
56
Anemia of CKD contributing factors
```
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
```
57
Anemia of CKD patient evaluation
RBC indices
Absolute reticulocyte count
Iron indices
Folic acid and vitamin B12
58
Anemia of CKD goals
Increased oxygenation
Improve QOL
Prevent complications
Target Hgb: = 11.5 (KDIGO); = 11 (manuf./FDA)
59
Anemia of CKD treatment
Iron supplementation
| Initiate when TSAT = 30% and ferritin = 500
60
Oral iron supplements
10% absorbed in duodenum and upper jejunum
Decreased absorption with food
Convenient for patients without IV access
61
Oral iron supplement formulations
```
Ferrous sulfate (20%)
Ferrous sulfate, exsiccated (30%)
Ferrous fumarate (33%)
Ferrous gluconate (12%)
Iron polysaccharide complex (100%)
Heme iron polypeptide (100%)
```
62
Oral iron supplementation adverse effects
GI: N, constipation, abdominal cramping
63
Oral iron supplementation drug interactions
Vitamin C
FQs
PPIs/H2RAs
Tetracyclines
64
IV iron supplementation formulations
Iron dextran
Sodium ferric gluconate
Iron sucrose
Ferumoxytol
65
IV iron supplementation ADR
```
Anaphylaxis (Iron dextran)
-BBW
-Test dose required
Infusion rxns: hypotension, arthralgias, myalgias, fever, flushing, HA
Risk of iron overload
```
66
Erythropoietin stimulating agents MOA
Same biologic activity as endogenous erythropoietin
67
When to initiate Erythropoietin stimulating agents
CKD ND: Hgb < 10
| CKD 5D: Hgb: 9-10 to avoid falling below 9
68
When to interrupt or reduce ESA dose
Hgb approaching/exceeding 11
69
ESA BBW
Increased risk of death, MI and stroke
70
ESA drugs
Epoetin alfa
Darbepoetin
Peginesatide
71
Epoetin alfa SE
```
HTN
Arthralfia
Muscle spasm
Pyrexia
Dizziness
```
72
Darbepoetin SE
```
HTN
Dyspnea
Peripheral edema
Cough
Procedural hypotension
```
73
Which ESA(s) were/was removed from the market?
Peginesatide
74
Which ESA(s) require adequate iron?
Epoetin alfa and Darbepoetin
75
ESA dose adjustment
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
ESA monitoring
Monitor Hgb at least weekly until stable then monthly
77
Mineral and Bone Disorder and Renal Osteodystrophy aka
Secondary hyperparathyroidism
78
Renal osteodystrophy classifications
Osteomalacia
Osteitis fibrosa cystica
Adynamic bone disease
79
Osteomalacia definition
Softening of bones (defective mineralization)
80
Osteitis fibrose cystica definition
Replacement of bone with fibrous tissue (high bone turnover)
81
Adynamic bone disease definition
Decreased bone formation without a mineralization defect
82
MBD and ROD goals
Prevent MBD and ROS and associated consequences
| Maintain Ca, PO4, iPTH levels
83
Corrected calcium equation
Observed Ca + 0.8 x (4 - albumin level)
84
Corrected calcium levels
Normal: 8.5 - 10.8
CKD 3: "Normal"
CKD 4: "Normal"
CKD 5: 8.4 - 9.5
85
Phosphorous levels
Normal: 2.7 - 4.6
CKD 3: "Normal"
CKD 4: "Normal"
CKD 5: 3.5 - 5.5
86
Ca x P levels
All: < 55
87
Intact PTH (iPTH) levels
Normal: 10 - 60
CKD 3: 35 - 70
CKD 4: 70 - 110
CKD 5: 150 - 300
88
Evaluation of a patient for MBD and ROD
```
Serum Ca
Serum PO4
Vitamin D
BMD
PTH
```
89
MBD and ROD non-pharm treatment
Dietary PO4 restriction
| Parathyroidectomy (last line)
90
Major treatment failure with dietary PO4 restriction
Non-compliance
91
What foods contain PO4
```
Meat
Dairy
Nuts
Dried beans
Colas
Peanut butter
Beer
```
92
MBD and ROD pharm treatment
Phosphate binding agents
Vitamin D
Calcimimetics
93
Phosphate binding agents pathophysiology
Bind dietary phosphorous in the GI tract = form insoluble salts = excreted in feces
94
Phosphate binding agents
```
Calcium carbonate
Calcium acetate
Sevelamer
Lanthanum
Sucroferric oxyhydroxide
Aluminum-containing agents
Magnesium-containing agents
```
95
How must phosphate binding agents be taken?
With meals
96
Calcium carbonate SE
Constipation
N/V/D
Increased Ca
97
Calcium acetate SE
Constipation
N/V/D
Increased calcium
98
Sevelamer SE
Pruritus
| N/V/D
99
Lanthanum SE
N/V/D
100
Sucroferric oxyhydroxide SE
Dark colored feces
| N/D
101
What % of ca is calcium carbonate
40% elemental
102
What % of ca is calcium acetate
25% elemental
103
1st line phosphate binding agents
Calcium carbonate and Calcium acetate
| *Except when vascular or soft-tissue calcifications are present
104
Calcium carbonate and Calcium acetate comments
Can increase aluminum absorption
105
Calcium carbonate and Calcium acetate DDI
Iron
Zinc
FQs
106
Sevelamer comments
Do not crush or chew tablets
Does not affect serum Ca
Initial dose based on serum PO4 level
107
Which phosphate binding agents can be used with calcifications?
Sevelamer
108
Lanthanum comments
Chewable tablets
| Primary use - Stage 5
109
Sucroferric oxyhydroxide comments
Only for patients on HD
Chewable
Contains 500mg elemental iron
110
Sucroferric oxyhydroxide DDI
Avoid w/vitamin D analogs and levothyroxine
111
Aluminum-containing agents
3rd line - increased risk of toxicity
Limit to 4 weeks
SE: bone disease, anemia, encephalopathy
112
Magnesium-containing agents
Not generally recommended
| SE: severe diarrhea, abdominal cramps, hypermagnesemia, hyperkalemia
113
When to initiate vitamin D therapy?
< 30
114
Vitamin D precursors
Ergocalciferol
| Cholecalciferol
115
Active Vitamin D
Calcitriol
116
Vitamin D analogs
Paricalcitol
| Doxercalciferol
117
Vitamin D precursor MOA
Metabolized to active form of vitamin D then same MOA
118
Calcitriol and Paricalcitol MOA
Binds to and activates Vitamin D receptor in kidney, parathyroid gland, intestine and bone
119
Doxercalciferol MOA
Metabolized to active form of vitamin D then same MOA
120
Ergocalciferol SE
GI upset
Hypercalcemia
Hyperphosphotemia
121
Cholecalciferol SE
Lipid abnormalities
| Hypervitaminosis D
122
Calcitriol SE
GI upset
Hypercalcemia
Hyperphosphotemia
123
Paricalcitol SE
GI upset
Edema
HTN
124
Doxercalciferol SE
Edema
HA
N/V
125
Which vitamin D is primarily used for vitamin D deficiency or insufficiency
Ergocalciferol
126
Which vitamin D is primarily used for prevention
Cholecalciferol
127
Which vitamin D's come in both PO and IV form?
Calcitriol
Paricalcitol
Doxercalciferol
128
When do patients receive calcitriol IV?
Stage 5
129
Calcimimetics
Cinacalcet
| Etelcalcetide
130
When are calcimimetics used?
Dialysis
131
Calcimimetic MOA
Works on calcium-sensing receptor of parathyroid gland
| Mimics extracellular ionized calcium = decreased PTH = decreased serum calcium
132
Cinacalcet SE
GI upset
Hypocalcemia
Myalgia
133
Etelcalcetide SE
Hypocalcemia
Worsening HF
GI bleeding
134
How many drugs are needed for HTN in renal disease?
Most will need >/= 3
135
Other complications of CKD
```
Nutrition status
Hyperlipidemia
Uremic bleeding
Gastrointestinal disorders
Immune function
Pruritus
Neurologic abnormalities
Endocrine disorders
```
136
Protein-energy malnutrition causes
Anorexia
Altered taste sensation
Unpalatable food (PO4 and Na restrictions)
137
Protein-energy malnutrition treatment
Replace B and C vitamins and folic acid in dialysis patients
138
When to treat hyperlipidemia in CKD?
Treat if have other risk factors
139
KDIGO lipid guidelines
"Fire and Forget" strategy
Non-dialysis and non-transplant patients only
Only recommend - statin or statin/ezetimibe combo
140
Uremic bleeding contributing factors
D/t platelet abnormalities (decreased platelet aggregation and adhesiveness)
Heparin administered with dialysis
Other anticoagulants/antiplatelet agents for other indications
141
Uremic bleeding treatment
Cryoprecipitate (has factor VII and fibrinogen which helps decrease bleeding time)
Fresh frozen plasma (FFP)
Desmopressin
142
GI disorders SE
Anorexia
Hiccups
Metallic taste in mouth
143
Immune function causes
Uremic toxins may alter cell-mediated immunity
| HD patients at increased risk with vascular access (exposure to infectious sources)
144
Pruritus contributing factors
Inadequate dialysis, dry skin, CKD-MBD, increased histamine levels
145
Pruritus treatment
Sufficient dialysis
Oral antihistamines
Topical steroids
146
Neurologic abnormalities causes
Uremic encephalopathy
| Peripheral neuropathy
147
Uremic encephalopathy
Changes in consciousness, thinking, memory, speech, movement, emotion
Less common in earlier initiation of dialysis in stage 5
148
Peripheral neuropathy treatment
TCAs
| Gabapentin
149
Endocrine disorders
Hypothyroidism
Hypothalamus disorders
Glucose management issues
150
Hypothyroidism labs
Decreased T4 but TSH usually norma
Decreased T4 to T3 conversion
Replace thyroid hormone if TSH elevated
151
Hypothalamus disorder presentation
Hypothermia - 1 degree less than normal
152
Hyperglycemia cause
Peripheral insulin resistance
153
Hypoglycemia cause
Decreased renal insulin degradation
