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PHAR255 > Kidney Disorders 3 > Flashcards

Kidney Disorders 3 Flashcards

CKD complications

1
Q

What are the complications of CKD related to?

A

the progressive inability of the kidney to perform its functions
-fluid, electrolyte, acid-based balance
-remove metabolic waste products
-remove foreign chemicals
-regulate blood pressure
-secrete hormones

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2
Q

What are the complications of CKD?

A

fluid and electrolyte abnormalities
-sodium and water imbalance
-metabolic acidosis
-hyperkalemia
mineral bone disease
anemia
other: CV, GI, neurological

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3
Q

What increases the likelihood of CKD complications?

A

decreasing GFR
-can be evident as early as stage 2

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4
Q

How does sodium and water imbalance arise in CKD?

A

progressive loss of ability of kidneys to excrete excess water and sodium

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5
Q

What does sodium and water imbalance lead to in CKD?

A

weight gain
hypertension
peripheral and pulmonary edema

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6
Q

When do you typically see the onset of symptoms due to water and sodium imbalance in CKD?

A

stage 4

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7
Q

What is the treatment of sodium and water imbalance in CKD?

A

sodium and water restriction
- < 2g of sodium, 1-2L of fluid/day
-diuretics: furosemide +/- metolazone
-stage 5: dialysis

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8
Q

Why is furosemide preferred for sodium and water retention in CKD?

A

thiazides are less effective for diuresis once GFR < 30ml/min

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9
Q

When would you consider adding metolazone for sodium and water retention in CKD?

A

loop diuretic resistance
-synergistic with loops due to natriuretic action at distal tubule

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10
Q

Describe proper diuretic monitoring.

A

electrolytes
-Na+, K+, Cl-, HCO3, Mg, Ca
-q1-2 weeks initially, q3-6 months when stable
signs and symptoms of dehydration
-especially acute illness (SADMANS)

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11
Q

What is metabolic acidosis?

A

decrease in pH of the blood and a decrease in sodium bicarbonate (< 22mmol/L)

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12
Q

Describe metabolic acidosis in CKD.

A

impaired excretion of acids and/or reabsorption of bicarb
-can still acidify the urine but kidneys produce less ammonia to buffer H+=retention of H+
-exacerbated by hyperkalemia (depresses NH3 production)
result: retained acid is buffered by bicarb, protein in muscle, and phosphate in bone
most prominent in stage 4-5

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13
Q

What is the treatment of metabolic acidosis in CKD?

A

sodium bicarbonate tablets
-325-500mg po BID-TID

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14
Q

What are the benefits of sodium bicarbonate treatment for metabolic acidosis in CKD?

A

delays CKD progression
improves nutritional status

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15
Q

What is the concern with sodium bicarbonate treatment for metabolic acidosis in CKD?

A

sodium loading

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16
Q

What is hyperkalemia?

A

inability to maintain normal serum potassium of 3.5-5.0mmol/L
-due to decreased excretion

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17
Q

What are the exacerbating factors for hyperkalemia in CKD?

A

metabolic acidosis
excessive dietary intake
potassium sparing diuretics
ACEI/ARB
NSAIDs

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18
Q

True or false: many patients with hyperkalemia are symptomatic

A

false

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19
Q

What is the treatment of hyperkalemia in CKD?

A

identify/correct exacerbating factors
most CKD patients with mild hyperkalemia can be managed with dietary restrictions
mild acute or refractory chronic hyperkalemia–> binders
-sodium polystyrene sulfonate
-patiromer
-sodium zirconium cyclosilicate

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20
Q

What is the MOA of Kayexalate?

A

cation exchange resin
-removes K+ ions by exchanging it
not absorbed by GI tract

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21
Q

What are the adverse effects of Kayexalate?

A

GI: constipation, NVD

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22
Q

Differentiate between the different binders based on MOA.

A

sodium polystyrene sulfonate
-nonspecific cation binding (Na+ for K+)
sodium zirconium cyclosilicate
-selective K+ binding (Na+ for K+)
patiromer
-nonspecific cation binding (Ca2+ for K+)

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23
Q

Which binder has the fastest onset of action?

A

sodium zirconium cyclosilicate

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24
Q

Which binder can be administered rectally?

A

sodium polystyrene sulfonate

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25
Q

Differentiate the binders based on their different adverse effects.

A

sodium polystyrene sulfonate
-GI (intestinal necrosis)
sodium zirconium cyclosilicate
-edema
patiromer
-constipation

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26
Q

What is the treatment of severe hyperkalemia?

A

calcium gluconate IV (stabilize myocardium)
glucose + regular insulin
if metabolic acidosis: sodium bicarb IV
salbutamol via nebulizer
kayexalate 30-60g po q4h until K+ normalized
dialysis if stage 5 or acute severe hyperkalemia

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27
Q

What is the goal of therapy for severe hyperkalemia?

A

prevent severe cardiac arrhythmia, death, correct K+ < 5.5mmol/L

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28
Q

What is CKD-MBD?

A

systemic disorder of mineral and bone metabolism due to CKD manifested by either one, or a combo of the following:
-abnormalities of calcium, phosphorus, PTH or vit D metabolism
-abnormalities in bone turnover, mineralization volume, linear growth, strength (bone metabolism)
-vascular or other soft tissue calcification

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29
Q

When do changes in bone and mineral metabolism begin?

A

stage 3 and progresses
-bone abnormalities present in nearly all dialysis patients

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30
Q

What are the mechanisms of CKD-MBD?

A

increased serum phosphate due to decreased exceretion
decreased serum calcium due to decreased GI absorption due to decreased vitamin D
negative feedback leads to increased PTH

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31
Q

How is CKD-MBD diagnosed?

A

biochemical abnormalities
-serum Ca, PO4, PTH, ALP
bone abnormalities
-biopsy or BMD
vascular calcification

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32
Q

At what stage of CKD do we recommend monitoring Ca, PO4, and PTH?

A

CKD G4-G5

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33
Q

What is the risk of increased serum phosphate in CKD G3a-5?

A

increased risk of all-cause mortality

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34
Q

Is there a benefit in treating CKD patients to prevent hyperphosphatemia with normal serum concentrations?

A

no benefit
-possible risk

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35
Q

What do low levels of calcium contribute to in CKD?

A

secondary hyperparathyroidism
renal osteodystrophy
prolonged QT interval

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36
Q

What do elevated levels of calcium contribute to in CKD?

A

higher mortality and risk of CV events

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37
Q

Which severity of hypocalcemia is typically treated in CKD?

A

severe or symptomatic (numbness, tingling, myalgia)
-avoid hypercalcemia (risks are acute)
-mild and asymptomatic may not require tx

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38
Q

What are the risks of severe hyperparathyroidism in CKD?

A

calciphylaxis
CVD
neuromuscular disturbances
death
stages 3-5

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39
Q

What is the optimal PTH level in CKD?

A

unknown in CKD patients NOT on dialysis
-G5: 2-9x upper limit of normal
levels should be progressively rising or persistently high in order to initiate treatment

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40
Q

What are the types of renal osteodystrophy?

A

hyperparathyroid bone disease
-increased bone turnover, increased PTH levels
adynamic bone disease
-decreased bone turnover, normal or low PTH levels
osteomalacia
-decreased vitamin D activity

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41
Q

What is the role of FGF-23?

A

promote PO4 excretion
stimulates PTH to increase PO4 excretion
suppresses formation of calcitriol to decrease PO4 absorption in GI tract

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42
Q

What is the role of PTH?

A

increases Ca reabsorption and PO4 excretion
increases Ca mobilization from bone

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43
Q

What happens to FGF-23 and PTH response in advanced CKD?

A

kidneys fail to respond
=Ca and PO4 abnormalities worsen

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44
Q

What does persistent hyperparathyroidism lead to?

A

persistent calcium resorption from bone
-bone pain and fragility
-bone marrow fibrosis
-refractory pruritis
parathyroid gland hyperplasia and resistance to exogenous calcitriol

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45
Q

What is calciphylaxis?

A

calcification and occlusion of small blood vessels
-leads to ulceration, gangrene, sepsis, high mortality rate

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46
Q

What is the general overview of the treatment of hyperparathyroid bone disease?

A

to decrease phosphate:
-restrict dietary phosphate
-binders (Ca products, Al/Mg products, sevelamer, lanthanum, sucroferric oxyhydroxide)
-intensified dialysis schedules
to suppress PTH
-vitamin D (calcitriol, alfacalcidiol, ergo or cholecalciferol)
-calcimimetics
-parathyroidectomy

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47
Q

Why should a dietician be involved in regulating dietary phosphate of a CKD patient?

A

aggressive PO4 restriction can lead to inadequate intake of other nutrients like protein

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48
Q

How do all phosphate binders work?

A

binding dietary PO4 in GI tract–>eliminated in feces

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49
Q

How should all phosphate binders be taken?

A

within the first few bites of a meal
-multiple times per day with meals
-still requires dietary PO4 restriction

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50
Q

Which phosphate binders are first line therapy for hyperphosphatemia in CKD?

A

calcium-based binders (calcium carbonate)
-not calcium citrate

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51
Q

What is the usual dose of calcium carbonate in CKD?

A

500mg elemental calcium po TID with meals
-total recommended dose unknown

52
Q

What are the adverse effects of calcium carbonate?

A

GI: constipation, cramps
hypercalcemia (esp if co-administered with calcitriol)

53
Q

What is the use of aluminum or magnesium phosphate binders for hyperphosphatemia in CKD?

A

short-term use only
-not recommended for chronic use due to risk of accumulation and toxicity=NOT FIRST LINE

54
Q

Describe sevelamer.

A

phosphate binder
useful in pts with hypercalcemia or when not controlled with Ca-based binders
AE: ++ GI tolerability
expensive (EDS)

55
Q

Describe lanthanum.

A

similar to sevelamer
chewable tab

56
Q

Describe sucroferric oxyhydroxide.

A

newest calcium-free binder
iron-based but negligible contribution to iron intake
AE: black stools and nausea
EDS

57
Q

What are impacts of vitamin D therapy on PTH, Ca, and PO4 levels?

A

supress PTH levels
-stimulates absorption of Ca in GIT
-directly acts on parathyroid gland to suppress PTH
increased risk of hypercalcemia & hyperphosphatemia
-increase in FGF-23 levels

58
Q

What are the impacts of vitamin D therapy on fractures and mortality?

A

uncertain if it decreases fractures or mortality

59
Q

In which CKD population should we initiate vitamin D therapy?

A

severe & progressive HPT
-should NOT be routinely used if not on dialysis

60
Q

What are examples of vitamin D analogues?

A

calcitriol
alfacalcidol

61
Q

What are the usual doses of vitamin D analogues?

A

usual: 0.25-1mcg po OD
IV: 3x weekly with dialysis
adjust doses based on serum Ca, PO4, PTH levels
serum Ca and PO4 should be in range prior to initiating therapy

62
Q

What is the benefit of nutritional vitamin D therapy in HPT?

A

can suppress PTH (esp. G3) with less hyper-Ca/PO4

63
Q

What is the MOA of calcimimetics?

A

increase sensitivity of parathyroid gland to calcium
lowers PTH concentrations without increasing serum Ca or PO4 (useful in hypercalcemia)

64
Q

Are the benefits of calcimimetics certain/well proven?

A

uncertain if they decrease fracture risk, CV events or mortality

65
Q

What is an example of a calcimimetic?

A

cinacalcet

66
Q

What is the use of cinacalcet?

A

dialysis patients +/- vit D therapy

67
Q

What are the adverse effects of cinacalcet?

A

N/V/D
hypocalcemia

68
Q

What is the role of antiresorptive therapy in CKD-MBD?

A

may increase BMD and decrease fracture risk
might use in CKD-MBD if low BMD and/or fragility fracture
-particularly if GFR >30ml/min, CKD G3a-b
CSN 2020 recommends against routine use in G4-5

69
Q

What are examples of antiresorptive therapy?

A

denosumab
-poses risk of hypocalcemia
bisphosphonates
-may induce/exacerbate low bone turnover
-use with caution at CrCl < 35ml/min

70
Q

What are the proper monitoring parameters for HPT?

A

serum Ca, PO4, and PTH levels at least MONTHLY
many drug interactions to be watch for

71
Q

When is a parathyroidectomy used in CKD-MBD?

A

parathyroidectomy=partial removal of parathyroid gland
when PTH, Ca, PO4 abnormalities not medically correctable
-usually stage 5

72
Q

What is a post-op concern with parathyroidectomy?

A

hungry bones syndrome

73
Q

Describe adynamic bone disease.

A

low bone turnover
-lack of osteoblast/osteoclast stimulation
associated with more fractures and calcification
results from Ca and vit D supplementation and over suppression of PTH (overtreated PTH)

74
Q

What is the treatment of adynamic bone disease?

A

stop vitamin D supplementation

75
Q

Describe osteomalacia.

A

inadequate mineralization of Ca and PO4
-due to reduced production and action of calcitriol
can also result from aluminum deposition in bone
results in: fractures, myopathy, neurological deficits, dementia, seizures

76
Q

What is the treatment of osteomalacia?

A

stop aluminum-containing phosphate binders

77
Q

Describe vascular calcification.

A

vascular smooth muscle cells change into osteoblast-like cell
-seen in high and low bone turnover disease
-increased prevalence of CV calcification in CKD

78
Q

Provide a brief review of the labs used for anemia.

A

hemoglobin
-iron based protein in RBC that transports O2
hematocrit
-volume % of RBC in blood
reticulocyte count
-immature RBCs (indicates production from bone marrow)
total iron binding capacity (TIBC)
-amount of iron that can be bound to transferrin
serum iron
-amount of circulating iron bound to transferrin
transferrin saturation (TSAT)
-transfers iron to bone marrow
ferritin
-stored iron

79
Q

What are expected labs of anemia in CKD?

A

RBCs: normochromic, normocytic (stages 3-5)
HgB: < 130g/L (males), < 120g/L (females)
decreased reticulocytes
nearly universal in ESRD

80
Q

What is the primary reason for anemia in CKD?

A

loss of erythropoietin generation by the kidneys
-also decreased RBC t1/2 in uremia, blood loss, bone marrow fibrosis, or iron, folate, vit B12 deficiency

81
Q

Describe iron deficiency in anemia due to CKD.

A

common in stages 4-5 due to decreased GI absorption, inflammation, blood tests, blood loss in HD
-iron demands increase with ESA therapy
absolute iron deficiency:
-decreased TSAT, ferritin
-total iron stores in body are low
functional iron deficiency:
-decreased TSAT, normal or increased ferritin
-might be anemia of chronic disease, adding iron may not help

82
Q

What are the signs and symptoms of anemia in CKD?

A

weakness, lethargy, malaise
shortness of breath on exertion
impaired memory and concentration
feeling cold

83
Q

Why do we treat anemia in CKD?

A

improve QOL
risk factor for adverse outcomes (ex: LVH, CVD)

84
Q

What are the pros of treatment with ESAs?

A

eliminate need for blood transfusions
decreased fatigue, symptoms of anemia (QOL)

85
Q

What are the cons of treatment with ESAs?

A

failed to improve CV outcomes
associated with increased risk of stroke and other thromboembolic events

86
Q

What are the goals of treatment for anemia in CKD?

A

hemoglobin:
-target: 100-110g/L (initiate ESA when < 90g/L)
-optimal HgB is unknown
-risks with higher targets
TSAT:
-maintain > 20% (avoid iron overload)
serum ferritin:
-> 100mcg/L (non-dialysis and PD), > 200mcg/L (HD)
normal serum B12 and folic acid levels

87
Q

Provide an overview of the management of anemia in CKD.

A

correct blood loss
replace vitamin, iron deficiencies
ESA therapy
dialysis to correct uremia (as applicable)
blood transfusions if required (last resort)

88
Q

What should be done before initiating ESA therapy for anemia in CKD?

A

avoid initiating ESA therapy until all correctable causes of anemia (ex: iron deficiency) have been addressed

89
Q

What is the correlation between iron supplementation and ESA therapy for anemia in CKD?

A

iron supplementation may correct anemia without the need for ESA therapy if iron deficiency present
most patients receiving ESA therapy need iron therapy

90
Q

What is the benefit of iron supplementation in functional iron deficiency?

A

questionable benefit

91
Q

Which route of admin is recommended for initial therapy of anemia in CKD?

A

oral iron for 1-3 months prior to initiating IV therapy
-in HD patients, IV is required

92
Q

What is the dose of oral iron for anemia in CKD?

A

100-200mg elemental iron daily
-2 to 3 divided doses

93
Q

What are the adverse effects of oral iron?

A

black stools
N/V/D
cramping
constipation
heartburn
staining of teeth (liquid)

94
Q

When do we use IV iron for anemia in CKD?

A

intolerant, unresponsive, non-compliant to oral iron
-1st line in HD patients

95
Q

What are the injectable formulations of iron?

A

iron dextran (dc)
iron sucrose
iron sodium ferric gluconate
iron isomaltoside

96
Q

What are the adverse effects of IV iron?

A

generally well tolerated
hypersensitivity reactions
hypotension
infection

97
Q

Describe erythropoietin.

A

hormone produced by kidney when they sense decreased blood oxygenation
stimulates development and maturation of RBCs
-increase O2-carrying capacity of blood
-restore tissue oxygenation
production becomes deficient as CKD progresses

98
Q

Differentiate between epoetin alfa and darbepoetin alfa.

A

epoetin alfa:
-resembles endogenous EPO
-shorter t1/2
darbepoetin alfa:
-2nd gen molecule
-longer t1/2

99
Q

What are the doses of epoetin alfa and darbepoetin alfa?

A

epoetin alfa: 50-100 units/kg IV or SC 2-3x/week
darbepoetin alfa: 0.45mcg/kg weekly IV or SC

100
Q

What is the goal with ESA therapy?

A

reach target HgB (~110g/L) within 2-4mo (then maintain)
-gradual increase in HgB by ~10g/L q month, to target

101
Q

Describe the dose adjustments for ESAs.

A

if HgB rise is inadequate (<10g/L) after 4 weeks, increase dose by 25%
if HgB rise is excessive (>10g/L) in 2 weeks, decrease dose by 25%
do not adjust dose more than q1-2 months because of delay in changes in HgB levels (2-6 weeks)

102
Q

Describe the proper monitoring for ESA.

A

serum iron, TIBC, iron sat, ferritin:
-q1-3 months
HgB:
-q1-2 weeks initially, then monthly
-HgB >100g/L (non-HD) or >110g/L (HD): hold/decrease dose

103
Q

What are the adverse effects of ESA?

A

well-tolerated
hypertension (dose-dependent)
flu-like (transient)
thrombosis
MI, stroke, death (avoid >110g/L)
PRCA

104
Q

What is erythropoietin resistance?

A

incomplete or lack of response to ESA
-epoetin alfa > 300U/kg/wk
-darbepoetin alfa > 1.5mcg/kg/wk

105
Q

What are the causes of erythropoietin resistance?

A

iron deficiency (most common)
vitamin deficiency
bleeding
inflammation/infection
aluminum toxicity
inadequate dialysis

106
Q

How do we manage erythropoietin resistance?

A

treat underlying cause if it can be corrected
avoid ESA doses > 4x the initial dose

107
Q

What is the MOA of HIF-PHIs?

A

inhibit enzyme that degrades hypoxia-inducible factor
-improves iron mobilization into serum
-increased EPO production which increases HgB (without causing a spike in EPO)

108
Q

What is an example of a HIF-PHI?

A

daprodustat

109
Q

What are the cardiovascular complications of CKD?

A

hypertension
LVH
heart failure
hyperlipidemia
pericarditis

110
Q

Describe hypertension as a complication of CKD.

A

can be both a cause and consequence of CKD
causes progression of stage 1-4
~90% of patients have hypertension by stage 5
contributes to CV morbidity/mortality

111
Q

What are the contributing factors to hypertension in CKD?

A

water and salt retention
RAAS activation
ESA therapy
HPT
renal vascular disease

112
Q

Do we see typical dosing of hypertension drugs in hemodialysis patients?

A

may see unusual dosing

113
Q

What is the most common structural cardiac abnormality in CKD?

A

LVH

114
Q

What are the risk factors for LVH in CKD?

A

HTN
fluid retention
anemia
DM
age
Ca/PO4 abnormalities
uremia

115
Q

What are the symptoms of LVH in CKD?

A

generally asymptomatic in early stages
leads to: decreased diastolic compliance, IHD, HF

116
Q

What is the treatment of LVH in CKD?

A

manage HTN and fluid overload
treat anemia
manage Ca, PO4, and PTH abnormalities

117
Q

What are the precipitating factors for HF in CKD?

A

anemia
HTN
fluid overload
LVH
CAD

118
Q

What is the treatment of HF in CKD?

A

correct underlying factors
treat as per HF guidelines

119
Q

What are the neurological complications of CKD?

A

peripheral neuropathy
uremic encephalopathy
uremic polyneuropathy
-restless legs
-leg cramps
-numbness/tingling/paraesthesias
-carpal tunnel
-myopathy

120
Q

What is the treatment for the neurological complications of CKD?

A

dialysis or change dialysis prescription

121
Q

How common is chronic pruritis in CKD?

A

~40% of patients with ESRD

122
Q

What are the complications of chronic pruritis?

A

ulcers, infection, QOL, sleep

123
Q

Which part of the body is affected by chronic pruritis in CKD?

A

can affect parts of or whole body

124
Q

What is the cause of chronic pruritis in CKD?

A

no clear cause
-makes treatment a challenge

125
Q

What are the treatment options for chronic pruritis in CKD?

A

gabapentinoids
capsaicin
sertraline
antihistamines
Uremol lotion

126
Q

What is the new option that has been approved for pruritis in CKD?

A

difelikefalin
-MOA: peripheral kappa opioid receptor agonist
-approved by HC for mod-severe pruritis associated with HD in CKD
-dose: IV 3x/wk following HD
-clinically significant decrease in itch
-AE: dizziness, somnolence, mental status change

127
Q

What are normal phosphate levels?

A

0.81-1.45mmol/L
lower levels to normal range in pts with overt hyperphosphatemia
-ND CKD: > 1.49mmol/L
-HD/PD CKD: > 1.78mmol/L

PHAR255 (24 decks)

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