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Clin med A 2 > Chronic Kidney Disease part 1 > Flashcards

Chronic Kidney Disease part 1 Flashcards

1
Q

what is CKD (the definition preferred by jensen)

A

Chronic Kidney Disease (CKD) - Spectrum of disorders associated with abnormal kidney function and/or progressive decline in GFR

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2
Q

reduction of significant number of nephrons cause what response by the kidneys

A
  • hyperfiltration of the remaining nephrons
  • hypertrophy of the remaining nephrons
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3
Q

what is seen in this picture

A

left - normal kidney cross-section
right - scarring d/t chronic inflammation and remodeling in kidneys

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4
Q

in what circumstances would markers such as BUN, Creatinine, and GFR improve in patients with CKD. What does this improvement mean?

A

Recovery from AKI-on-CKD
Removal of toxic substances
Diet changes
Improved hydration
Control of other disease states

This improvement does not reflect the restoration of renal tissue, but rather the removal of disease burden on still-functioning nephrons.

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5
Q

what is the prevalence of CKD in US

A

15%

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6
Q

what is the MCC of late-stage CKD

A

70% due to:
DM or HTN/Vascular disease

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7
Q

what type of CKD increases risk of CV mortality

A

proteinuric CKD

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8
Q

what is the usual cause of death for CKD patients

A

CVD.

CKD is an independent risk factor for CVD and most pts die from CVD before progressing to ESRD

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9
Q

what are patient demographic risk factors for CKD

A
  • older age
  • sub-sarahan african ancestry
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10
Q

what historical factors are risk factors for CKD

A
  • Previous episode of AKI
  • family hx of renal disease
  • Smoking
  • Lead exposure
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11
Q

what GU conditions are comorbidities for CKD

A
  • Structural urinary tract abnormalities
  • Proteinuria
  • Abnormal urinary sediment
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12
Q

What Metabolic conditions are comorbidities for CKD

A

Diabetes Mellitus
Low HDL
Obesity
Metabolic Syndrome

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13
Q

what are “other” conditions that are comorbidities for CKD

A

HTN
Autoimmune disease
Cardiorenal Syndrome

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14
Q

what is cardiorenal syndrome

A

Deterioration of one organ results in deterioration of the other

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15
Q

what are the 5 types of cardiorenal syndrome (renocardiac syndrome)

A
  • Type 1 (Acute CRS) - AKI caused by acute cardiac disease
  • Type 2 (Chronic CRS) - CKD caused by chronic cardiac disease
  • Type 3 (Acute RCS) - Acute cardiac disease caused by AKI
  • Type 4 (Chronic RCS) - Chronic cardiac decompensation caused by CKD
  • Type 5 (Secondary CRS) - Simultaneous heart and kidney dysfunction
    caused by another acute or chronic systemic disorder
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16
Q

what is the newest recommendation on staging CKD

A

GFR
or
Albuminuria

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17
Q

what are the stages of CKD according to GFR

A
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18
Q

what are the stages of CKD according to albuminuria

A
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19
Q

A patient with a GFR of 38 mL/min and urine albumin of 100 mg/g =

A

stage G3B and A2

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20
Q

A patient with a GFR of 96 mL/min and urine albumin of 38 mg/g =

A

stage G1 and A2

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21
Q

A patient with a GFR of 10 mL/min and urine albumin of 350 mg/g =

A

stage G5 and A3

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22
Q

A patient with a GFR of 110 mL/min and urine albumin of 12 mg/g =

A

stage G1 and A1

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23
Q

How does early to mid CKD present

A
  • asymptomatic
  • most common PE finding is HTN.
  • later stages can lead to volume overload
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24
Q

how does late CKD present ( GFR 10 or less)

A

s/s uremia

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25
Q

what are the s/s or uremia

A

just a refresher!

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26
Q

“Please dont waste your time memorizing this chart just realize that waste build up effects every part of your body” - jensen

A
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27
Q

what serum labs are LOW in CKD

A
  • Heme - RBC, H&H (normocytic, normochromic anemia)
  • Lytes/Acid-Base - calcium, sodium, pH (metabolic acidosis)
  • Renal - GFR
  • Others - vitamin D, HDL
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28
Q

what serum labs are HIGH in CKD

A
  • Lytes/Acid-Base - potassium
  • Renal - BUN, serum Cr
  • Others - phosphate, PTH, triglycerides, uric acid
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29
Q

what is seen on a urinalysis in CKD

A
  • Broad, waxy casts (dilated nephrons)
  • Proteinuria often present; glucosuria may be present
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30
Q

what are s/s of stage 1 and stage 2 CKD

A
  • usually no s/s from deceased GFR
  • May see s/s from underlying disease
  • Edema, HTN
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31
Q

what are the S/S of stage 3 and 4 CKD

A
  • Anemia, fatigue, anorexia
  • Abnormal calcium, phosphorus, vitamin D, PTH
  • Abnormal Na, K, water, and acid-base balance
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32
Q

what are the s/s of stage 5 CKD/ESRD

A
  • marked disturbance in ADL, well being, nutrition, water and electrolyte homeostasis
  • uremic syndrome
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33
Q

what type of abnormalities in renal imaging could indicate CKD even if Cr/GFR is normal

A
  • Polycystic kidneys
  • Small kidneys ( < 9-10 cm )
  • Asymmetric kidneys (vascular disease)
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34
Q

what is the function of ACE/ARBs in CKD

A
  • reduce Glomerular HTN
  • Reduce Proteinuria
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35
Q

if a CKD patient is diabetic what specific meds would you consider

A

SGLT-2 inhibitors

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36
Q

what percent of CKD patients die before needing dialysis? why?

A

80% d/t CVD

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37
Q

what are the CV compliations

A
  • Hypertension (HTN)
  • Coronary Artery Disease (CAD) / Hyperlipidemia
  • Heart Failure (HF)
  • Atrial Fibrillation
  • Pericarditis
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38
Q

what is the MC complication of CKD

A

CVD

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39
Q

what is the goal BP of a patient with CKD

A

<130/80

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40
Q

what should you check prior to starting or increasing an ACE/ARB in a CKD patient

A

serum Cr
potassium

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41
Q

what is an indicator to stop ACE/ARBs in CKD patients

A

Hyperkalemia or >30% Cr increase - reduce or stop

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42
Q

what diuretics are more effective in early CKD

A

thiazides

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43
Q

what diuretics are more effective in late CKD

A

loops

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44
Q

what lipid changes do we see in CKD

A
  • abnormal lipid metabolism
  • hypertriglyceridemia
  • normal cholesterol
  • lower HDL and increased lipoprotein A
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45
Q

what vascular disorder is especially accelerated in ESRD

A

atherosclerosis

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46
Q

what is treatment for CAD in CKD

A
  • statins - 1st line (said in class)
  • PSK9 inhibitors and ezetimibe (2nd line in adjunct to statin)
  • fibrates (paired with statins)
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47
Q

why does CKD lead to HF

A
  • increased cardiac workload d/t volume overload and other complications
  • this leads to left ventricular hypertrophy and diastolic dysfunction
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48
Q

what puts CKD patients at a higher risk for HF than non CKD patients

A

the use of digoxin.

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49
Q

what is treatment for HF in CKD

A

Diuretics, ACE/ARB, fluid and salt restriction

ACE/ARB - can help with progression of HF

50
Q

how do you treat Afib in stage 1-4 CKD

A

same as general population

51
Q

what should be kept in mind when treating a stage 5 CKD patient with afib

A

higher bleeding risk with anticoagulation

52
Q

what CV disease is rare but may deveope in uremic patients

A

pericarditis

53
Q

what are s/s of pericarditis

A
  • retrosternal chest pain
  • friction rub
  • cardiac temponade
  • uremic pericardial effusion
54
Q

what is the treatment for CKD with pericarditis

A

Always an indication for hospitalization and initiation of hemodialysis

55
Q

what are the main mineral metabolism complications of CKD

A
  • hyperphosphatemia
  • hypovitaminosis D
  • hypocalcemia
  • abnormal PTH
56
Q

what is the cause of hypocalcemia in CKD

A

￬ gut Ca absorption due to ￬ vitamin D

57
Q

what is the name of CKD bone disease

A

renal osteodystrophy

58
Q

what is the definitive diagnostic study of renal osteodystrophy

A

bone biopsy.

59
Q

what are the three types of renal osetodystrophy

A
  1. osteitis fibrosa cystica (MC)
  2. adynamic bone disease
  3. osteomalacia
60
Q

What is osteitis fibrosa cystica

A

MC form of renal osteodystrophy

caused by hyperparathyroidism leading to osteoclast stimulation. This causes INCREASED rates of bone turnover

61
Q

what are symptoms of osteitis fibrosa cystica

A

bone pain
proximal muscle weakness

62
Q

what is adynamic bone disease

A

decreased bone turnover caused by suppression of PTH or endogenous PTH

(I think this can be caused by treating osteitis fibrosa cystica!)

63
Q

What is osteomalacia

A

lack of bone mineralization

these days MC due to hypovitaminosis D and use of bisphosphonates

64
Q

what is the big risk when a patient develops a renal osteodystrophy?

A

increased fracture risk

65
Q

which renal osteodystrophy is associated with brown tumors on an Xray

A

Osteitis fibrosa cystica

66
Q

what is the first step in treating mineral metabolism disorders

A

control hyperphosphatemia by:
initially - restricing dietary phosphate
later - oral phosphorus binders taken with meals

67
Q

what is considered hyperphosphatemia? what about in ESRD?

A

Phosphorus ≥ 4.5 mg/dL or ≥ 5.5 mg/dL in ESRD

68
Q

what foods are high in phosphate

A
  • meats (especially processed)
  • Colas
  • Baked goods/mixes
  • Fast food
  • Frozen premade foods
69
Q

what are the oral phosphorus binders

A
  • non-calcium based (sevelamer or lanthanum) FIRST LINE
  • Calcium carbonate or calcium acetate
  • aluminum hydroxide
  • iron based agents (ferric citrate or sucroferric oxyhydroxide)
70
Q

what are the SE of calcium carbonate and calcium acetate

A

may cause increased vascular calcification or hypercalcemia

71
Q

what are the SE of aluminum hydroxide

A

osteomalacia and neurologic complications

72
Q

what phosphorus binder is used when there is severe hyperphosphatemia (>7) or during short periods (<3 weeks)

A

aluminum hydroxide

73
Q

what can be combined with a calcium based phosphate binder

A

sevelamer or lanthanum

74
Q

what is the second step in management of mineral metabolism disorders

A

manage PTH by giving vitamin D3 (calcitriol) daily or every other day. or by using cincalet (sensipar).

75
Q

what are the SE of Vitamin D3 (calcitriol)

A

will increase serum calcium and phosphorus so you must monitor routine labs

76
Q

what is the SE of cincalet (sensipar)

A

hypocalcemia

77
Q

when managing PTH in mineral metabolism disorders, which medication should be used if the patient also has hyperphosphatemia

A

cincalet (sensipar) because Vit D3 (calcitriol) has a SE of raising phosphorus

78
Q

what are the PTH level goals in CKD

A

higher than normal!

this is to avoid adynamic bone disease!

79
Q

when does anemia tend to become significant in CKD? What is the main cause of this?

A

stage 3

due to decraesed erythropoitein since this is made in the kidneys!

80
Q

what must you do prior to treating CKD anemia with erythropoiesis-stimulating agents?

A

rule out other causes of anemia such as iron deficiency

81
Q

why does iron deficiency anemia occur in higher rates in CKD

A

hepcidin builds up due to decreased renal clearance.

hepciden blocks GI absorption and mobilization of iron from body stores

therefore low iron!

82
Q

what iron levels would indicate iron deficiency in CKD patients

A

Ferritin < 100-200 ng/mL OR iron saturation < 20% = iron deficiency

DO NOT treat if ferritin >500-800 even if iron saturation is <20%!

83
Q

How would you treat iron deficiency in CKD

A
  • Oral auryxia (ferric citrate) this was bolded! FDA approved for CKD anemia.
  • oral ferrous sulfate, ferrous gluconate or ferrous fumerate.
  • parenteral iron if oral iron isnt tolerated or if patient does not respond to it.
84
Q

what is the goal Hb in CKD

A

10-11g/dL

only higher if patient has risk of CV event. Hb should rise 1g/dL every 3-4 weeks during treatment

85
Q

what are the two agents used for erythropoietin treatment

A

epoetin (1-2x/week)
darbepoetin (2-4 weeks)

both can be IV or SC (SC 30% more effective)

86
Q

ehat is the cause of hypocoagulability in CKD

A

platelet dysfunction

87
Q

when is treatment indicated for hypocoagulability in CKD and how do you treat it

A

only if symptomatic

treat with desmopressin or dialysis.

can also use estrogen or cryoprecipitate (rarely used)

88
Q

when would you see hypercoagulability in CKD

A

severe proteinuria due ot loss of Protein C and protein S in the urine

(Clot Stoppers)

89
Q

at what stage does hypercalemia usually present in CKD

A

stage 4-5

90
Q

What are the possible medication causes for hyperkalemia

A

decrease K+ secretion by using :
- triamterene, spirinolocatone, NSAIDS, ACE/ARB

block K+ cell uptake by using:
- Beta blockers

91
Q

what is treatment for chronic hyperkalemia

A
  • dietary K+ restriction
  • stop medications affecting K+ metabolism
  • loop diuretics
92
Q

what is the cause of metabolic acidosis in CKD

A

loss of ability to excrete acid in urine usually due to loss of renal mass!

93
Q

how does metabolic acidosis contribute to renal osteodystrophy

A

calcium is pulled from the bones to buffer the acidosis

94
Q

how is metabolic acidosis in CKD treated

A

oral sodium bicarbonate given BID

goal serum bicarb is >21

95
Q

what is the cause of uremic encephalopathy in CKD and when in CKD does it occur

A

aggregation of uremic toxins.

not seen until GFR is <5-10 mL

96
Q

what are the s/s of uremic encephalopathy in CKD

A
  • Early - difficulty concentrating
  • Later - lethargy, confusion, seizure, coma
  • Exam - altered mental status, asterixis, weakness
97
Q

how is uremic encephalopathy treated in CKD

A

dialysis

98
Q

what is uremic neuropathy in CKD and what does it indicate

A

Distal, symmetrical, mixed peripheral neuropathy

indication to start dialysis if not already started

99
Q

what are the s/s of uremic neuropathy

A
  • Initial - loss of position and vibration sense in toes, decreased DTRs
  • Sensory - paresthesias, burning, pain, RLS
  • Motor - may lead to muscle atrophy, myoclonus, eventual paralysis

sensory symptoms precede motor symptoms.

100
Q

how do you diagnose and treat uremic neuropathy

A

dx - electrophysiologic studies (EP studies)

tx:
- dialysis
- TCAs or anticonvulsants for pain
- RLS may improve with tx of anemia or iron deficency

101
Q

What is the cause of hypoglycemia in CKD and how is it managed?

A

d/t decraesed renal clearance of insulin

tx - adjust dose of insulin or oral medicaiton
- start metformin if needed but discontinue when serum Cr >1.5 or GFR<30.

102
Q

what reproductive problems are common in CKD

A

decreased libido and ED

(men - decreased testosterone
women - aften anovulatory)

103
Q

what is seen in pregnancies that occur during ESRD

A
  • if serum Cr>1.4 pregnancy may cause CKD to progress faster
  • fetal mortality in 50% ESRD pts
  • surviving infants often premature
104
Q

what dietary changes are commonly needed in CKD
(theres so much im sorry)

A
  • protein restriction to slow progression (avoid if cachectic or low albumin)
  • sodium restriction of 2000mg daily. (>3-4g/day can cause HTN/volume overload, <1g/day can cause hypotenstion and depletion)
  • water restriction (<2L/day)
  • potassium restriction (<2g/d if GFR <10-20 or hyperkalemia)
  • phosphorus restriction (GFR <20-30 usually needs phosphate binders!)
105
Q

what are 5 medication changes that need to be considered in CKD

A
  1. adjust dose of renally excreted drugs - insulin, BB, ABX
  2. AVOID magnesium containing drugs - laxatives/antacids
  3. AVOID phosphorus containing drugs - cathartic laxatives
  4. AVOID nephrotoxic drugs - NSAIDS, IV contrast
  5. stop morphine
106
Q

when GFR reaches 5-10ml what treatment options are available

A

hemodialysis
peritoneal dialysis
transplantation

107
Q

what 4 signs are indications of need for dialysis in CKD patients

A
  1. GFR<10
  2. Uremic symptoms (pericarditis, encephalopathy, neuropathy)
  3. metabolic disturbances (hyperkalemia, hyponatremia, met acidosis, ect)
  4. fluid overload unresponsive to diuretics
108
Q

where are renal transplants obtained from

A
  • 2/3 from deceased donors (1 yr survival 91%, 5 yr survival 71%)
  • 1/3 transplants living donors (1 yr survival 97%, 5 yr survival 85%)
109
Q

what factors determine a transplant match

A
  • ABO blood groups and major histocompatibility
  • age/race or recipient and age of donor.
  • comorbidities
  • length of time on dialysis.
110
Q

After renal transplant what must be done

A

administration of immunosuppressive regimens.

this must balance between avoiding rejection and the risk of SE of immunosuppresents such as cancer, infection, DM ect.

111
Q

describe the process of hemodialysis

A

blood is taken out of the patient and put into a dialyzer where dialysate (cleansing solution) removes unwanted substances and replaces needed substances.

112
Q

what are vascular access options for hemodialysis

A
  • arteriovenous fistula (preferred - requires 6-8 weeks)
  • prosthetic graft ( shorter duration but only 2 weeks to mature, higher risk of infection)
  • indwelling vascular catheter (HIGHEST risk of infection, temporary only!)
113
Q

how often must hemodialysis occur

A

3x/week for 3-5 hrs at hospital
or
3-6x week for shorer duration at home w assistance

114
Q

what is the MC modality of treatment for ESRD

A

hemodualysis (87% ESRD pts in US use it)

115
Q

describe peritoneal dialysis

A

dialysate is put into the peritoneal cavity via indwelling catheter and water/solutes move across capillary bed in peritoneum.

dialysate is periodically drained and replaced.

116
Q

what are the two types of peritoneal dialysis?

A
  • continuous ambulatory peritoneal dialysis (manually exchanges dialysate 4-6x daily)
  • continuous cyclic peritoneal dialysis (automatic exchange of dialysate at night)
117
Q

what are the pros and cons of peritoneal dialysis (4 of each)

A

pros
- increased autonomy
- continuous = less voluem and electrolyte shifts
- less diet restrictions
- stay at home, limited transport

cons
- remove large amounts albumin
- requires physical and mental capability to complete
- risk of peritonitis
- access not possible in sig intra-abdominal adhesions or scarring

118
Q

what is the MC complication of peritoneal dialysis

A

peritonitis

119
Q

what are s/s of peritonitis

A

N/V/D/C
adbominal pain
fever
cloudy dialysate

120
Q

how do you diagnose and treat peritonitis

A

dx - peritoneal fluid >100 WBC
(usually staph bacteria as cause)

tx - abx therapy for appropriate organism

121
Q

what is overall 5 year survival rate for PD and HD

A

Overall 5-year survival - 39%
Estimated life expectancy - 3-5 years

122
Q

what is MCC of death in CKD

A

cardiac disease (>50%)

Clin med A 2 (30 decks)

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