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CKD Flashcards

1
Q

How is chronic kidney disease defined?

A

markers of kidney damage for at least 3 months OR GFR <60 mL/min/1.73 m2 for 3+ months

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2
Q

What sort of markers of kidney damage may be present?

A

abnormalities in composition of blood or urine, or abnormalities in imaging tests

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3
Q

Spectrum of disorders associated with abnormal kidney function and/or progressive decline in GFR

A

chronic kidney disease

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4
Q

What happens if you remove the underlying cause in chronic kidney disease? Why?

A

decline in function persists, nephron overwork injury

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5
Q

What pathophysiology leads to CKD?

A

reduction in number of functional nephrons –> hyperfiltration and hypertrophy of remaining nephrons due to RAAS –> glomerular architecture distorted hindering filtering –> inflammation and fibrosis

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6
Q

In some circumstances, markers can improve such as BUN, creatinine, and GFR after CKD called the “renal rebound”. What are these circumstances (5)?

A

recovery from AKI on CKD
removal of toxic substances
diet changes
improved hydration
control of other disease state

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7
Q

Nephrons can’t regenerate once they are replaced with scar tissue. So, why can the renal rebound occur?

A

removal of disease burden on still-functioning nephrons

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8
Q

What is the cause of the majority of cases of late-stage CKD (70%)?

A

HTN/vascular disease or CVD

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9
Q

CKD is an independent risk factor for _____. What type of CKD increases risk of CV mortality?

A

CV disease, proteinuric CKD

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10
Q

What are the demographic risk factors for CKD?

A

Demographics: older age, sub-saharan african ancestry

Comorbid conditions:
GU: structural urinary tract abnormalities, proteinuria, abnormal urinary sediment
Metabolic conditions: diabetes mellitus, low HDL, obesity, metabolic syndrome
Other conditions: HTN, autoimmune disease, cardiorenal syndrome

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11
Q

What historical factors predispose a patient to chronic kidney disease?

A

Historical factors: previous episode of AKI, + family history of renal disease, smoking, lead exposure

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12
Q

What comorbid conditions can predispose a patient to chronic kidney disease?

A

GU: structural urinary tract abnormalities, proteinuria, abnormal urinary sediment
Metabolic conditions: diabetes mellitus, low HDL, obesity, metabolic syndrome
Other conditions: HTN, autoimmune disease, cardiorenal syndrome

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13
Q

What is cardiorenal syndrome?

A

Deterioration of one organ (heart or kidney) results in deterioration of the other

Staged based on cardiac or renal causing acute or chronic

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14
Q

How is chronic kidney disease staged?

A

formerly KDOQI guidelines based on GFR
Now based on GFR and albuminuria

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15
Q

If a patient has a high level of albuminuria, what does that lead to?

A

Higher mortality risk, higher CKD progression, higher risk of ESRD regardless of GFR

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16
Q

What does CKD stage 1, 2, and 3a/b mean?

A

GFR >90 with markers of kidney damage
GFR 60-89 with mildly decreased GFR
3a: GFR 45-59
3b: GFR 30-44

1: Early CKD with kidney damage but normal GFR
2: kidney damage with mildly decreased GFR
3a: mildly to moderately decreased GFR
3b: moderately to severely decreased GFR

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17
Q

What are stages 4 and 5 of CKD?

A

GFR 15-29
GFR <15

4: severely decreased GFR
5: kidney failure/ESRD, may add D if treated with dialysis

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18
Q

What are the albuminuria stages?

A

A1, A2, and A3
A1: <30
A2: 30-300
A3: >300

only take into account if have decreased GFR

A1: normal to mildly increased
A2: moderately increased
A3: severely increased

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19
Q

What GFR stage is a patient with a GFR of 38 mL/min and urine albumin of 100 mg/g

A

3b

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20
Q

What stage is a patient with a GFR of 96 mL/min and urine albumin of 38 mg/g?

A

G1 A2

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21
Q

What stage is a patient with a GFR of 10 mL/min and urine albumin of 350 mg/g

A

G5 A3

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22
Q

What stage is a patient with a GFR of 110 mL/min and urine albumin of 12 mg/g

A

normal

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23
Q

What are symptoms of early-mid CKD?

A

Asymptomatic

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24
Q

What are the eventual symptoms of CKD?

A

slow onset of nonspecific s/s

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25
Q

what is the most common PE finding of CKD overall?

A

HTN that worsens as disease progresses and volume overload in later stages

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26
Q

What are the signs and symptoms of late CKD?

A

GFR 10 mL/min/1.73 m2
S/S of uremia

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27
Q

If a patient has s/s of uremia, what does that warrant?

A

admission and dialysis consult
dialysis generally improves uremic syndrome

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28
Q

Scalp symptom related to uremia

A

Uremic frost

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29
Q

What are common serum lab findings in CKD?

A

Vary based on underlying cause and stage of disease

Low
Heme: RBC, H&H (normocytic normochromic anemia)
Lytes/acid base: calcium, sodium, pH (metabolic acidosis)
Renal: GFR
Others: vitamin D, HDL

High
Lytes/acid-base: potassium
renal: BUN, serum Cr
others: phosphate, PTH, triglycerides, uric acid

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30
Q

What will be seen on a urinalysis of a patient with CKD?

A

broad, waxy casts (dilated nephrons)
Proteinuria often present; glucosuria may be present

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31
Q

What are signs/symptoms of stage 1 and 2 of CKD?

A

usually no symptoms
May see s/s of underlying disease
Edema, HTN

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32
Q

What are s/s of stage 3/4 of CKD?

A

All organ systems effects
MC: anemia, fatigue, anorexia
Abnormal calcium, phosphorus, vitamin D, PTH
Abnormal Na, K, water, and acid-base balance

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33
Q

What are s/s of stage 5/ESRD of CKD?

A

marked disturbance in ADL, well being, nutrition, water and electrolyte homeostasis

Uremic syndrome

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34
Q

_____ can indicate CKD even if there is normal Cr/GFR

A

abnormal renal imaging

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35
Q

What indicates CKD on imaging?

A

polycystic kidneys
small kidneys
asymmetric kidneys

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36
Q

What are the treatment goals of CKD?

A

slow progression
control underlying process
reduce intraglomerular HTN
reduce proteinuria
avoid further injury
if diabetic-control blood glucose (A1C <7%)
adjust medication doses as needed

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37
Q

what can you use to reduce intraglomerular HTN and proteinuria?

A

Intraglomerular HTN: ACE/ARB
reduce proteinuria: ACE/ARB, dietary protein restriction

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38
Q

What can we control that can cause further injury in CKD?

A

obstruction, nephrotoxins, flare of underlying disease

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39
Q

If a patient is diabetic and has CKD, waht medication would we consider?

A

SGLT-2 inhibitors

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40
Q

80% of CKD pts die before needing dialysis, primarily due to ____

A

CV disease

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41
Q

What are the most common CV complications of CKD?

A
  • Hypertension
  • Coronary artery disease
  • Heart failure
  • Atrial fibrillation
  • Pericarditis
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42
Q
A
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43
Q

What is the MC complication of CKD?

A

HTN

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44
Q

What is the goal BP for someone with CKD?

A

<130/80 mmHg

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45
Q

What nonpharmacologic treatment can be used to treat HTN with CKD?

A
  • diet
  • exercise
  • weight loss
  • treatment of OSA
  • low sodium diet (2300 mg/day)
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46
Q

Which BP medications should be used for HTN with early CKD and what will you monitor?

A
  • ACE inhibitors: Check serum Cr and K in 7-14 days when starting or increasing dose. Reduce or stop if hyperkalemia or >30% increase in Cr occurs
  • Diuretics almost always needed: thiazides
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47
Q

What BP medications should be used for HTN with late CKD and what will you monitor?

A
  • ACE inhibitors or ARBs: check serum Cr and K+ in 7-14 days when starting or increasing dose. If hyperkalemia or >30% Cr increase reduce or stop
  • Loop diuretics
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48
Q

If too much diuretics are given with CKD leading to low vascular volume/overdiuresis, what can occur?

A

AKI

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49
Q

In addition to ACE/ARB, diuretics, what BP meds can be used in CKD?

A

CCBs, BBs

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50
Q

What are common CAD/hyperlipidemia findings in CKD?

A
  • Hypertriglyceridemia
  • Normal total cholesterol
  • Low HDL and increased lipoprotein
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51
Q

What related to CAD/hyperlipidemia occurs with CKD, particularly with ESRD?

A

Accelerated atherosclerosis

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52
Q

What is treatment for CAD/hyperlipidemia associated with CKD?

A
  • Agressive CAD risk factor modification through:
  • Lifestyle changes
  • Statins (recommended for most patients with CKD)
  • PSK9 inhibitors and ezetimibe can be used as adjunct to statin
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53
Q

What medication used for cardiovascular risk increases rhabdomyolysis in CKD when paired with statins and is not known to reduce mortality risk?

A

Fibrates

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54
Q

Why can heart failure occure due to CKD?

A

increased cardiac workload due to HTN, volume overload, anemia, and atherosclerosis

Leads to LVH and diastolic dysfunction, systolic dysfunction can also develop

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55
Q

What medication for heart failure has a higher risk of toxicity in CKD patients than non-CKD due to electrolyte disturbances

A

Digoxin

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56
Q

How is HF treated in CKD?

A

Diuretics, ACE/ARB, fluid and salt restriction

Diuretics for early CKD: thiazides
Diuretics for late CKD: loop

Monitor for hyperkalemia with ACE/ARB

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57
Q

When are CKD patients at a disproportionately high risk for atrial fibrillation?

A

Late and end stage CKD

58
Q

How are stage 1-4 CKD patients treated for a fib? Stage 5/ESRD?

A

same as general population
stage 5/ESRD: higher bleeding risk with anticoagulation

59
Q

What population of patients are you worried about pericarditis in related to CKD?

A

Uremic patients

60
Q

What are s/s of pericarditis?

A
  • retrosternal chest pain
  • friction rub
  • Uremic pericardial effusion: pulsus paradoxus, enlarged cardiac silhouette, low voltage QRS
  • Cardiac tamponade may develop

Effusions are generally hemorrhagic and anticoagulants should be avoided

61
Q

How is pericarditis in CKD managed?

A

hospitalization and initiation of hemodialysis

62
Q

How is cardiorenal syndrome treated?

A

euvolemia and control of underlying disease

63
Q

what are mineral metabolism complications of CKD?

A
  • hyperphosphatemia: decreased excretion
  • hypovitaminosis D: decreased production
  • Hypocalcemia: phosphorus complexes with C –> soft tissue deposits, decreased gut absorption due to decreased vit D
  • secondary hyperparathyroidism due to low calcium
64
Q

what bone disease can occur as a complication of CKD?

A
  • Renal osteodystrophy
65
Q

What is the most common form of renal osteodystrophy?

A

osteitis fibrosis cystica

66
Q

what is osteitis fibrosa cystica?

A
  • hyperparathyroidism causes osteoclast stimulation to increase
  • high rates of bone turnover
  • leads to bone pain, proximal muscle weakness
  • Brown tumors on x-ray
67
Q

What are types of renal osteodystrophy?

A
  • osteitis fibrosa cystica
  • adynamic bone disease
  • osteomalacia
68
Q

what causes adynamic bone disease?

A
  • low bone turnover
  • suppression of PTH or low endogenous PTH
69
Q

What causes osteomalacia in kidney disease?

A
  • lack of bone mineralization due to hypovitaminosis D, bisphosphonates
70
Q

How is renal osteodystrophy diagnosed? Why is it a problem?

A
  • diagnosed by bone biopsy
  • increases risk of fracture
71
Q

what is the treatment of mineral metabolism issues in CKD?

A
  1. Control hyperphosphatemia, phosphorus >4.5 mg/dL or >5.5 mg/dL in ESRD
  2. Manage PTH
72
Q

How would you control hyperphosphatemia initially?

A
  • Dietary phosphorus restriction of meats, colas, baked goods/mixes, fast food, frozen premade foods
73
Q

after attempting to control hyperphosphatemia with diet, what would you do?

A

Oral phosphorus binders

74
Q

what are oral phosphorus binders that can be used for hyperphosphatemia treatment?

A
  • calcium carbonate or calcium acetate
  • non-calcium-based: sevelamer or lanthanum first line therapy
  • aluminum hydroxide
  • iron-based agents: ferric citrate, sucroferric oxyhydroxide
75
Q

what is the mechanism of action and drawbacks of calcium carbonate or calcium acetate?

A
  • MOA: blocks absorption of phosphorus in GI tract; dosed TID with meals
  • may increase vascular calcification, hypercalcemia
76
Q

what is the mechanism of action of sevelamer or lanthanum?

A

Block absorption of phosphorus in GI tract; dosed TID with meals

Safe to combine with a calcium-based phosphate binder

77
Q

why is aluminum hydroxide not used as much for treatment of hyperphosphatemia?

A
  • SE of osteomalacia, neurologic complications
  • Only used if severe hyperphosphatemia (>7 mg/dL) or short periods (<3 weeks)
77
Q

this medication for hyperphosphatemia has limited evidence

A

iron-based agents: ferric citrate, sucroferric oxyhydroxide

78
Q

how is high pth managed in CKD?

A
  • vitamin D3 (calcitriol)
  • Cinacalcet (sensipar)
79
Q

what is the mechanism of action of vitamin D3?

A

increases serum calcium and phosphorus

80
Q

which patients can be given calcitriol? What do you need to monitor?

A

secondary hyperparathyroidism in stages 3-5 CKD
measure vitamin D before using, routine labs for monitoring

81
Q

what is the mechanism of action of cinacalcet?

A
  • Targets calcium-sensing receptors of parathyroid gland
82
Q

when would cinacalcet be a good option for treatment of PTH levels in CKD? what do you need to monitor?

A

if increased phosphorus or Ca prohibit use of calcitriol
labs, may cause hypocalcemia

83
Q

When treating late CKD, goal PTH levels are ____

A

higher to prevent adynamic bone disease

84
Q

what are hematologic complications of CKD?

A
  • anemia
  • coagulopathy
85
Q

why does anemia occur in CKD?

A

not making EPO
iron deficiency

85
Q

how would you treat anemia in CKD?

A
  1. R/O other causes of anemia before treatment with EPO stimulating agent
  2. treat iron deficiency before EPO stimulating treatment
86
Q

why do patients with CKD often have iron deficiency?

A

Hepcidin is elevated and blocks GI iron absorption and mobilization from storage

87
Q

What is considered iron deficiency in CKD?

A
  • Ferritin <100-200 ng/mL
  • Iron saturation <20%
88
Q

how would you treat iron deficiency in a pre-ESRD CKD patient?

A
  • Oral ferrous sulfate, ferrous gluconate, or ferrous fumarate
  • Auryxia (ferric citrate)
  • If oral iron isn’t tolerate or has poor response –> parenteral iron
  • Do not give iron if ferritin >500-800 even if iron <20%
89
Q

what is the Hb goal with EPO treatment of anemia in CKD?

A
  • 10-11 g/dL
  • Higher Hb goal –> increased risk of CV events, should rise at most 1 g/dL every 3-4 weeks
  • No benefit to treatment if Hb >9 g/dL
90
Q

What EPO treatment can be used for patients with CKD?

A
  • Epoetin
  • Darbepoetin
  • Can be given IV or SQ
91
Q

What side effect is seen in 20% of patients using a EPO treatment?

A

HTN

92
Q

Why can hypocoagulopathy occur in CKD?

A

Platelet dysfunction

93
Q

How does hypocoagulopathy present in CKD?

A

Prolonged bleeding time, petechiae, purpura

94
Q

When would you treat hypocoagulopathy? How?

A

Only if symptomatic
Desmopressin
Dialysis
Conjugated estrogens, cryoprecipitate (rarely used)

95
Q

In addition to hypocoagulopathy, what coagulopathy can occur?

A

If severe proteinuria, hypercoagulability

96
Q

What acid base dysfunctions can occur due to CKD?

A

hyperkalemia
metabolic acidosis

97
Q

when does hyperkalemia usually present?

A

stages 4-5
earlier in high potassium diet, DM, hemolysis, rhabdomyolysis, medications

98
Q

which medications decrease K secretion? Which block K uptake by cells?

A

triamterene, spironolactone, NSAIDs, ACE, ARB
BBs

99
Q

how do you treat chronic hyperkalemia due to CKD?

A

dietary K restriction
reduce or stop medications that affect K metabolism
loop diuretics (if not volume-depleted)

100
Q

why can metabolic acidosis be a complication of CKD?

A
  • Loss of ability to excrete acid
  • Primarily due to loss of renal mass
  • Distal tubules unable to help excrete
101
Q

What can metabolic acidosis contribute to?

A

Renal osteodystrophy

calcium pulled from bones to help buffer acidosis

102
Q

how is metabolic acidosis treated?

A

maintain serum bicarb at >21 mEq/L
Oral sodium bicarbonate given BID and titrated to maintain normal level

103
Q

What are neurologic complications of CKD?

A

uremic encephalopathy
uremic neuropathy

104
Q

What causes uremic encephalopathy in CKD?

A

aggregation of uremic toxins

not seen until GFR <5-10 mL/min/1.72 m2

104
Q
A
105
Q

What are signs and symptoms of uremic encephalopathy?

A
  • Early- difficulty concentrating
  • Later- lethargy, confusion, seizure, coma
  • Exam- altered mental status, asterixis, weakness
106
Q

what is treatment of uremic encephalopathy?

A

dialysis

107
Q

what is uremic neuropathy?

A
  • distal, symmetrical, mixed peripheral neuropathy
  • indication to start dialysis
108
Q

what are s/s of uremic neuropathy?

A
  • initial- loss of position and vibration sense in toes, decreased DTRs
  • Sensory- paresthesias, burning, pain, RLS
  • Motor- muscle atrophy, myoclonus, eventual paralysis
109
Q

how is uremic neuropathy diagnosed?

A

electrophysiologic studies

110
Q

how is uremic neuropathy treated?

A
  • dialysis
  • symptomatic treatments for neuropathic pain (TCAs, anticonvulsants)
  • RLS- may improve with treatment of anemia, iron deficiency
111
Q

what are endocrine complications of CKD?

A
  • hypoglycemia
  • decreased libido and ED
  • faster CKD progression in pregnancy
112
Q

why can CKD increase risk of hypoglycemia?

A
  • Decreases renal clearance of insulin

May need dose adjustment of oral medication, exogenous insulin

113
Q

When should metformin be discontinued in CKD? Why?

A
  • After serum Cr >1.4-1.5 or GFR <30
  • Increased risk of lactic acidosis
114
Q

How does CKD impact men?

A

decreased testosterone –> decreased libido and ED

115
Q

How does CKD impact men?

A
  • often anovulatory
  • if serum Cr >1.4 CKD may progress faster in pregnancy
  • Fetal mortality almost 50% in ESRD patients
  • Surviving infants are often premature

transplant = best odds for healthy pregnancy

116
Q

what are diet changes for CKD?

A
  • Protein restriction may slow CKD progression (avoid if cachectic or low albumin)
  • sodium restriction to 2 g/d
  • water restriction to 2 L/d
  • K restriction to <2 g/d (if GFR <10-20 mL/min or Hyperkalemia)
  • Phosphorus restriction and binders if GFR <20-30 mL/min

> 3-4 g sodium –> hypertension, fluid overload
<1 g/day sodium –> hypotension, volume depletion

117
Q

What are medication changes in CKD?

A
  • Renally excreted drugs: adjust dose based on pts GFR and clinical presentation
  • Magnesium-containing drugs: avoid use (laxatives, antacids, etc)
  • Phosphorus-containing drugs: avoid use
  • Nephrotoxic drugs (NSAIDs, contrast, etc): avoid use
  • Morphine: avoid

Morphine metabolites can accumulate in late CKD

118
Q

What are indications for dialysis in CKD?

A
  • GFR 10 mL/min/1.73 m2
  • Uremic symptoms
  • Persistent metabolic disturbances refractory to medical therapy
  • Fluid overload unresponsive to diuretics

can be hemodialysis, peritoneal dialysis, or transplant

119
Q

when should CKD patients be followed by a nephrologist?

A
  • no later than late stage 3 or if rapidly progressing
120
Q

what is the ideal method of renal replacement therapy?

A
  • renal transplantation
121
Q

what factors determine match with renal transplantation?

A
  • ABO blood groups and major histocompatibility
  • Age and race of recipient, age of donor
  • Comorbidities
  • Length of time on dialysis
122
Q

What must be used after transplantation?

A

immunosuppressive regimens

transplant nephrologist usually also follow patient to manage

123
Q

what is hemodialysis?

A
  • flow of blood on one side of membrane
  • dialysate on other side
  • diffusion and convection to remove unwanted substances in blood
124
Q

how can vascular access be done to perform hemodialysis?

A
  • AV fistula
  • Prosthetic graft
  • Indwelling vascular catheter
125
Q

what is the longest lasting vascular access for hemodialysis? shortest? Which has the highest risk of infection?

A
  • Longest: AV fistula
  • Shortest: prosthetic but higher risk of infection, thrombosis, aneurysm
  • High risk of infection: indwelling vascular catheter
126
Q

How often do patients need to do hemodialysis?

A

3x/week for 3-5 hrs at hemodialysis center
3-6x/week for shorter sessions at home

127
Q

what is the MC dialysis modality in the US?

A

hemodialysis

128
Q

what is peritoneal dialysis?

A
  • peritoneal membrane is dialyzer
  • dialysate put into peritoneal cavity
  • water and solutes move into dialysate
  • dialysate periodically drained
129
Q

what are types of peritoneal dialysis?

A
  • continuous ambulatory peritoneal dialysis: manually exchanges 4-6x/day
  • continuous cyclic peritoneal dialysis: cycler automatically exchanges at night
130
Q

what are the benefits of peritoneal dialysis?

A
  • increased patient autonomy
  • continuous
  • poorly dialyzed compounds are better cleared
  • may be better for pts with limited transport
  • allows pt to stay in home
131
Q

what are risks of peritoneal dialysis?

A
  • removed large amounts of albumin
  • requires mental/physical ability to understand and complete exchanges
  • access may not be possible in patients with significant intra-abdominal adhesions or scarring
  • risk of peritonitis
132
Q

what is the most common complication of peritoneal dialysis and how does it present?

A

peritonitis
* N/V/D/C
* abdominal pain
* fever
* cloudy dialysate

133
Q

how is peritonitis diangosed?

A

peritoneal fluid >100 WBC/mcl
may culture

134
Q

what are the most common organism in peritonitis due to peritoneal dialysis?

A

MCC: staph aureus
gram negative rods, streptococcus

135
Q
A
136
Q

how is peritonitis due to peritoneal dialysis treated?

A

antibiotic therapy

137
Q

ESRD and dialysis prognosis

A
  • higher mortality than transplant
  • estimated life expectancy 3-5 years
  • MCC death: cardiac disease
138
Q

what are poor prognostic indicators for ESRD with dialysis?

A
  • DM
  • advanced age
  • hypoalbuminemia
  • low socioeconomic status
  • inadequate dialysis
  • high fibroblast growth factor

GU (3 decks)

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