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GU: Clin Med IIA > CKD pt 1 > Flashcards

CKD pt 1 Flashcards

1
Q

official definition of CKD

A
  1. presence of markers of kidney damage for 3+ months
    - Structural or functional abnormalities of the kidney (+/- a current decrease in GFR) that can ultimately lead to decreased GFR
    - Manifested by either pathological abnormalities or other markers of kidney damage, including abnormalities in the composition of blood or urine, or abnormalities in imaging tests.
    OR
  2. The presence of GFR <60 mL/min/1.73 m2 for 3+ months with or without other signs of kidney damage
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2
Q

what is CKD (short definition)

A

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

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3
Q

Decline in function usually _____ even if cause is removed
CKD is due to _____

A

persists
nephron overwork injury

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4
Q

pathophys of CKD

A

Kidneys respond to a reduction in the number of functional nephrons by signaling changes that lead to:
1. hyperfiltration
2. hypertrophy
3. RAAS plays a role in these changes

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5
Q

how does hypertrophy change glomerular architecture? result?

A

Glomerular architecture becomes distorted with hypertrophy, hindering filtering abilities
Inflammation and fibrosis ensue

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6
Q

what is “the renal rebound”

A
  1. may see an improvement in markers like BUN, Creatinine, and GFR in some circumstances!
    - Recovery from AKI-on-CKD
    - Removal of toxic substances
    - Diet changes
    - Improved hydration
    - Control of other disease states
    does NOT reflect the restoration of renal tissue, but rather the removal of disease burden on still-functioning nephrons.
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7
Q

Over 70% of cases of late-stage CKD (Stage 5 or ESRD) are due to ?

A

DM
HTN/vascular disease
Other cases - glomerulonephritis, polycystic kidney disease,
chronic tubulointerstitial disease, etc.

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8
Q

CKD is an independent risk factor for ?

A

CVD

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9
Q

what type of CKD can ↑ risk of CV mortality

A

proteinuric CKD

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10
Q

risk factors for CKD

A
  1. Patient Demographics
    - Older age
    - sub-Sarahan African ancestry
  2. Historical Factors
    - Previous episode of AKI
    - FHx of renal disease
    - Smoking
    - Lead exposure
  3. GU Conditions
    - Structural urinary tract abnormalities
    - Proteinuria
    - Abnormal urinary sediment
  4. Metabolic Conditions
    - DM
    - Low HDL
    - Obesity
    - MetS
  5. Other Conditions
    - HTN
    - Autoimmune disease
    - Cardiorenal Syndrome
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11
Q

Deterioration of one organ results in deterioration of the other

A

Cardiorenal Syndrome (Renocardiac Syndrome)

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12
Q

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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13
Q

Newer recommendation of staging CKD

A

GFR and albuminuria

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14
Q

Higher levels of albuminuria =____ mortality risk, ____ CKD progression, _____ risk of ESRD - regardless of GFR

A

higher

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15
Q

Early CKD
Kidney damage with normal GFR
GFR >90
what staging?

A

1

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16
Q

Kidney damage with mildly decreased GFR
GFR 60-89
what staging?

A

2

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17
Q

Mildly to moderately decreased GFR
GFR 45-59
what staging?

A

3a

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18
Q

Moderately to severely decreased GFR
GFR 30-44
what staging

A

3b

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19
Q

Severely decreased GFR
GFR 15-29
what staging

A

4

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20
Q

Kidney failure / ESRD
May add D if treated with dialysis
GFR <15
what staging

A

5

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21
Q

albumin Normal to mildly increased
AER < 30
what is the staging?

A

A1

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22
Q

Moderately increased (microalbuminuria)
AER 30-300
what staging?

A

A2

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23
Q

Severely increased (macroalbuminuria)
May be subdivided into nephrotic and non-nephrotic
AER >300
what staging?

A

A3

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24
Q

s/s of early-mid CKD

A

asx

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25
Q

eventual s/s of early-mid CKD

A

slow onset of nonspecific s/s

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26
Q

MC PE finding of CKD overall

A

HTN
Present in early CKD, and worsens as CKD progresses
Later stages - volume overload

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27
Q

Late CKD s/s

A

waste build up - GFR ~10 mL/min/1.73 m2
Leads to S/S of uremia
S/S of uremia warrants admission and dialysis consult
Dialysis normally improves uremic syndrome

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28
Q

what specific sign can be seen in uncontrolled prolonged CKD?

A

Uremic Frost: crystallized urea excreted in sweat

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29
Q

low serums seen in CKD

A

Heme - RBC, H&H (normocytic, normochromic anemia)
Lytes/Acid-Base - Ca, Na, pH (Met. acidosis)
Renal - GFR
Others - vitamin D, HDL

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30
Q

high serums seen in CKD

A

Lytes/Acid-Base - K
Renal - BUN, sCr
Others - phosphate, PTH, triglycerides, uric acid

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31
Q

Broad, waxy casts in UA is seen in what condition?

A

CKD

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32
Q

what is often present in CKD UA?

A

proteinuria
glucosuria may be present

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33
Q

stage 1 and 2 CKD s/s

A

Usually no symptoms from decreased GFR
May see s/s from underlying disease
Edema, HTN

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34
Q

Anemia, fatigue, anorexia
Abnormal calcium, phosphorus, vitamin D, PTH
Abnormal Na, K, water, and acid-base balance
what stage of CKD could they be in?

A

stage 3 and 4
More likely to have S/S, abnormal labs
All organ systems usually affected by this point

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35
Q

marked disturbance in ADL, well being, nutrition, water and electrolyte homeostasis
uremic syndrome
what stage of CKD

A

stage 5/ESRD

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36
Q

does an abnormal renal imaging indicate CKD?

A

Yes!
Abnormal renal imaging can
indicate CKD even if there is
normal Cr/GFR
- Polycystic kidneys
- Small kidneys ( < 9-10 cm )
- Asymmetric kidneys (vascular disease)

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37
Q

main tx goal of CKD

A

slow progression
1. Control underlying process
2. Reduce intraglomerular HTN - ACE/ARB
3. Reduce proteinuria - ACE/ARB, dietary protein restriction
4. Avoid further injury - Obstruction, nephrotoxins, flare of underlying disease
5. If DM - control glucose (HbA1c <7%) - SGLT-2 inhibitors
6. Adjust medication doses as needed

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38
Q

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

A

CV disease
MC complication of CKD

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39
Q

CV complications of CKD include:

A

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

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40
Q

HTN can be Exacerbated by ___ and ____ for CKD

A

hyperreninemia, exogenous EPO

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41
Q

goal bp for HTN complication of CKD

A

< 130/80 (or 140/90) mmHg

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42
Q

nonpharm tx for HTN - CKD

A

diet, exercise, wt loss
Treatment of OSA (if present)
Low sodium diet - 2300 mg/day

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43
Q

pharm tx for HTN - CKD

A
  1. ACE inhibitors or ARBs
    - Check sCr and K+ in 7-14 d - starting or ￪ dose
    - Hyperkalemia or >30% Cr increase - reduce or stop
  2. Diuretics nearly always needed
    - Thiazides - early CKD
    - Loop - more effective in later CKD (GFR < 30)
    - Overdiuresis or low vascular volume → AKI
  3. Other anti-HTN rx - CCBs, BBs
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44
Q

primary finding + other labs of hyperlipidemia - CKD

A

Hypertriglyceridemia
Total cholesterol concentration - usually normal
Lower HDL and increased lipoprotein (a) also common

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45
Q

what CAD/hyperlipidemia condition is accelerated especially in ESRD?

A

atherosclerosis

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46
Q

tx for CAD / Hyperlipidemia - CKD

A
  1. Lifestyle changes
  2. Statins - recommended for most patients with CKD due to CV risk
  3. PSK9 inhibitors and ezetimibe - may be used as adjunct to statin therapy
  4. Fibrates - increased rhabdomyolysis risk when paired with statins in CKD pts
    - Not shown to reduce risk of mortality
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47
Q

Increased cardiac workload in CKD can lead to what CV complication?

A

HF

48
Q

HF from CKD is due to ?

A

HTN, volume overload, anemia, atherosclerosis

49
Q

HF - CKD can lead to what dysfunction

A

LVH and diastolic dysfunction
Systolic dysfunction may also develop

50
Q

what HF medication is higher risk for toxicity than non-CKD pts

A

digoxin
Due to electrolyte disturbances common in CKD

51
Q

tx for HF - CKD

A

Diuretics, ACE/ARB, fluid and salt restriction
- Thiazides - early CKD
- Loop - later CKD (GFR <30)
- ACE/ARB - can help with progression of HF
Monitor closely for hyperkalemia

52
Q

Disproportionately high rates of what irregular heart rhythm in late-stage and end-stage CKD? tx?

A

atrial fibrillation
Stage 1-4 CKD patients - treated similarly to general population
Stage 5/ESRD patients - higher bleeding risk with anticoag

53
Q

Rare CV complication, but may develop in uremic patients
Always an indication for hospitalization and initiation of hemodialysis

A

Pericarditis

54
Q

CKD is experiencing retrosternal chest pain, friction rub
what could they be experincing?

A

pericarditis
Uremic pericardial effusion - pulsus paradoxus, enlarged cardiac silhouette, low voltage QRS
Cardiac tamponade may develop

55
Q

uremic pericardial effusions are generally ____, therefore you must avoid these medications

A

hemorrhagic
anticoags

56
Q

MC mineral metabolism complication patterns

A

Abnormal calcium, phosphorus, PTH, active vitamin D
1. Hyperphosphatemia
- Decreased excretion by kidney
2. Hypovitaminosis D
- Decreased production by kidney
3. Hypocalcemia
- Phosphorus complexes with Ca
— soft tissue deposits
- ￬ gut Ca absorption due to ￬ vitamin D
4. Secondary hyperparathyroidism
- Due to ￪ phosphate, ￬ calcium

57
Q

mineral metabolism complicatoin commonly leads to what? how to diagnose it?

A

Renal Osteodystrophy
bone bx

58
Q

which renal osteodystrophy is Due to hyperparathyroidism → osteoclast stimulation
High rates of bone turnover
Bone pain, proximal muscle weakness

A

Osteitis fibrosa cystica

59
Q

types of renal osteodystrophy

A
  1. Osteitis fibrosa cystica MC
  2. Adynamic bone disease
  3. Osteomalacia

All increase the risk of fracture

60
Q

which renal osteodystrophy is d/t - low bone turnover
Suppression of PTH or low endogenous PTH

A

adynamic bone disease

61
Q

which renal osteodystrophy is d/t lack of bone mineralization. what were the MC causes in the past and now?

A

Osteomalacia
In the past → aluminum toxicity
Currently → due to hypovitaminosis D, bisphosphonates

62
Q

first step tx for mineral metabolism

A

control hyperphosphatemia (≥ 4.5 mg/dL or ≥ 5.5 mg/dL in ESRD)
1. Initially - dietary phosphorus restriction
- Meats (especially processed), Colas, Baked, goods/mixes, Fast food, Frozen premade foods
2. Later - Oral phosphorus binders
- Calcium carbonate or calcium acetate
— Block absorption of phosphorus in GI tract; dosed TID w/ meals
- Non-calcium-based - first-line therapy - Sevelamer or Lanthanum
- Aluminum hydroxide - highly effective, but limited d/t SE
- Iron-based agents - ferric citrate, sucroferric oxyhydroxide - Limited evidence

63
Q

which oral phosphorus binder may cause increased vascular calcification, hypercalcemia?

A

Calcium carbonate or calcium acetate

64
Q

which oral phosphorous binder is Safe to combine either with a calcium-based phosphate binder

A

non-calcium-based - Sevelamer or Lanthanum

65
Q

what are the potential SE of aluminum hydroxide as a oral phosphorus binder?

A

Osteomalacia, neurologic complications
May use if severe hyperphosphatemia (>7 mg/dL) or short periods (< 3 weeks)

66
Q

overall tx plan for mineral metabolism

A
  1. control hyperphosphatemia
  2. manage PTH
67
Q

After phosphorus levels are controlled, what is the next step of tx for mineral metabolism complication? how?

A

manage PTH:
1. Vitamin D3 (calcitriol)
* 0.25 or 0.5 mcg orally daily or every other day
* For secondary hyperparathyroidism in stage 3-5 CKD
* Measure and normalize vitamin D before using to tx elevated PTH
* Will increase serum Ca and phosphorus - Routine labs to monitor required
2. Cinacalcet (Sensipar) 30-90 mg orally once daily
* Targets calcium-sensing receptors of parathyroid gland
* Good option if ￪ phosphorus or Ca prohibit use of calcitriol
* May cause hypocalcemia

68
Q

Goal PTH levels in late CKD are ? why?

A

higher - To avoid adynamic bone disease

69
Q

anemia primarly due to ?

Hematologic Complications - CKD

A

decreased erythropoietin
Often becomes significant during stage 3 CKD

70
Q

Prior to tx with erythropoiesis-stimulating agents for anemia (CKD), what must we do beforehand?

A

must rule out other anemia causes

71
Q

many CKD pts have what type of anemia? why?

A

iron deficiency
Hepcidin - blocks GI iron absorption and mobilization
of iron from body stores - Elevated in CKD patients

72
Q

what is necessary before erythropoiesis - stimulating rx
what ranges make someone iron deficient?

anemia - CKD

A

Adequate iron stores
Goal of higher iron stores in CKD patients
Ferritin < 100-200 ng/mL OR iron saturation < 20% = iron deficiency

73
Q

iron deficiency tx for anemia complication from CKD

A
  1. Oral therapy preferred for pre-ESRD CKD
    * Ferrous sulfate, ferrous gluconate, or ferrous fumarate
    * Auryxia (ferric citrate) - FDA-approved
  2. If oral iron isn’t tolerated OR has poor response → parenteral iron
  3. Do not give iron supplementation if ferritin
    >500-800 ng/mL - Even if iron saturation <20%
74
Q

Erythropoietin Tx for anemia complication from CKD

A

Goal Hb of 10-11 g/dL
* Higher Hb goal → increased risk of CV events
* Hb should rise at most 1 g/dL every 3-4 weeks
* Likely no benefit to starting tx if Hb > 9 g/dL

  1. epoetin - given 1-2x/week
  2. darbepoetin - given every 2-4 weeks
    * Both may be given IV (hemodialysis) or SC
    * SC dosing - 30% more effective
75
Q

potention Se of erythropoietin tx for anemia complication

CKD

A

HTN

76
Q

what Coagulopathy is mainly d/t platelet dysfunction?
How would they present?

CKD

A

Hypocoagulability
Prolonged bleeding time, petechiae, purpura

77
Q

management for coagulopathy

A
  1. Tx only indicated if symptomatic
    * Raising Hb to 9-10 g/dL can reduce risk
    * Desmopressin 25 mcg IV every 8-12 hrs x 2 doses
    — Short-lived; mainly used in preparation for surgery
    * Dialysis - improves bleeding time
    * Other Tx - conjugated estrogens, cryoprecipitate - rarely used
78
Q

If severe proteinuria you may see what coagulopathy complication?

CKD

A

hypercoagulability

79
Q

what complication Usually manifests in stages 4-5
Can occur earlier in high potassium diet, DM pts, hemolysis, rhabdomyolysis, medications

CKD

A

Hyperkalemia

80
Q

what medicatoins can lead CKD ito hyperkalemia?

A
  1. Decrease K+ secretion - triamterene, spironolactone, NSAIDs, ACE, ARB
  2. Block K+ uptake by cells - BBs
81
Q

tx for chronic hyperkalemia

A
  1. Dietary K+ restriction
  2. Reduce or stop medications that affect K+ metabolism
  3. Loop diuretics (if not volume-depleted)
82
Q

Loss of ability to excrete acid in the urine would lead to what acid-base complication?

CKD

A

metabolic acidosis

83
Q

Loss of ability to excrete acid in the urine is primarily due to what?

A
  1. loss of renal mass
  2. Distal tubules may be unable to help excrete
  3. May lead to chronic metabolic acidosis
84
Q

metabolic acidosis can contribute to what other CKD complication?

A

renal osteodystrophy
Calcium pulled from bones to help buffer acidosis

85
Q

tx for metabolic acidosis

CKD

A

Maintain serum bicarbonate at > 21 mEq/L
Oral sodium bicarbonate - given BID

86
Q

this CKD complicatoin is Due to aggregation of uremic toxins

A

Uremic Encephalopathy

87
Q

s/s of Uremic Encephalopathy

A

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

88
Q

tx for uremic encephalopathy

A

Dialysis

89
Q

Distal, symmetrical, mixed peripheral neuropathy
what is this CKD complication

A

Uremic Neuropathy
Indication to start dialysis
Can occur in some pts already on dialysis

90
Q

s/s of Uremic Neuropathy

A

Sensory precedes motor
1. Initial - loss of position and vibration sense in toes, decreased DTRs
2. Sensory - paresthesias, burning, pain, RLS
3. Motor - may lead to muscle atrophy, myoclonus, eventual paralysis

91
Q

diagnostic test for uremic neuropathy?

A

electrophysiologic studies

92
Q

tx for uremic neurpathy

A
  1. dialysis - Less improvement if sx present for a long time prior to dialysis
  2. Symptomatic tx for neuropathic pain - TCAs, anticonvulsants
  3. RLS - may improve with tx of anemia, iron deficiency
93
Q

how does CKD affect renal clearance of insulin?

A

CKD → decreased renal clearance of insulin
Increased risk of hypoglycemia
May need dose adjustment of oral medication, exogenous insulin

94
Q

management for hypoglycemia complication from CKD

A

Metformin - discontinue after serum Cr > 1.4-1.5 or GFR < 30
Increased risk of lactic acidosis

95
Q

reproductive changes in CKD complication

A
  1. Decreased libido and ED are common
    * Men - decreased testosterone
    * Women - often anovulatory
  2. Pregnancy - if serum Cr >1.4, CKD may progress faster
    * Fetal mortality almost 50% in female ESRD pts
    * Surviving infants are often premature
96
Q

Best odds for healthy pregnancy for CKD pts

A

transplant

97
Q

dietary changes in CKD

A
  1. Protein restriction - Avoid if cachectic, low albumin
  2. Sodium restriction - 2 g/d
    * > 3-4 g/d → HTN, volume overload
    * < 1 g/d → hypotension, volume depletion
  3. Water restriction - 2 L/d (if volume overload)
  4. Potassium restriction - If GFR < 10-20 mL/min OR hyperkalemia
  5. Phosphorus restriction
    If GFR < 20-30 mL/min - phosphate binders
98
Q

medication changes in CKD

A
  1. Renally excreted drugs - insulin, BBs, abx, etc.
    - Adjust dose based on pt’s GFR and clinical presentation
  2. AVOID
    * Magnesium-containing drugs - laxatives, antacids, etc.
    * Phosphorus-containing drugs - e.g., cathartic laxatives
    * Nephrotoxic drugs - NSAIDs, IV contrast, etc.
    * Morphine - metabolites can accumulate in late CKD - Not seen with other opioids
99
Q

indications for dialysis in CKD

A
  1. GFR <10
  2. Uremic symptoms
  3. metabolic disturbances
  4. Fluid overload unresponsive to diuretics
100
Q

Ideal method of renal replacement therapy

A

Renal Transplantation
No standardized criteria for recipients; 2-6 yr wait for transplant

101
Q

most renal transplants are ?

A

deceased
2/3 transplants

102
Q

which type of renal transplant has a better survival rate

A

living donors

103
Q

factors determining renal transplant match

A
  • ABO blood groups and major histocompatibility
  • Age and race of recipient, age of donor
  • Comorbidities (hyperlipidemia, HTN, CMV)
  • Length of time spent on dialysis
104
Q

what is the management for renal transplants afterward?

A

immunosuppressive regimens
* Must balance between avoiding rejection of graft and risk of side effects
* Cancer, infection, new-onset DM
* Transplant nephrologist usually also will follow the patient to manage medical regimen

105
Q

which dialysis Requires a constant flow of blood along one side of a semipermeable membrane

A

hemodialysis
Diffusion and convection → removal of unwanted substances in blood and replacement of needed substances
MC modality for ESRD

106
Q

types of hemodialysis

A
  1. Arteriovenous fistula (preferred)
    * Lasts longest
    * Requires 6-8 wks for maturation after
    * surgical construction
  2. Prosthetic graft
    * Shorter duration, but only needs 2 wks to mature
    * Higher risk of infection, thrombosis, aneurysm than fistulas
  3. Indwelling vascular catheter
    * Very high risk of infection
    * Temporary only
107
Q

where can hemodialysis be done?

A
  1. hemodialysis center
    * 3x/wk for 3-5 hrs at a time
  2. home with assistance
    * 3-6x/wk for shorter sessions
108
Q

how does the peritoneal dialysis work?

A

Peritoneal membrane acts as “dialyzer”
* Dialysate put in peritoneal cavity via indwelling catheter
* Water and solutes move across capillary bed in peritoneum between blood and dialysate
* Dialysate is periodically drained and new dialysate instilled

109
Q

what are the types of peritoneal dialysis

A
  • Continuous Ambulatory Peritoneal Dialysis (CAPD) - patient manually exchanges dialysate 4-6x/day
  • Continuous Cyclic Peritoneal Dialysis (CCPD) - cycler machine automatically exchanges dialysate at night
110
Q

pros vs cons of peritoneal dialysis

A

Benefits:
* Increased patient autonomy
* Continuous - less symptomatic volume and electrolyte shifts
* Poorly dialyzable compounds are better cleared → less diet restrictions
* May be better for pts with limited transport
* Allows pt to stay in their home

Risks:
* Removes 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

111
Q

MC complication of peritoneal dialysis

A

Peritonitis

112
Q

pt on peritoneal dialysis is now experincing N/V/D/C, abd pain, fever, cloudy dialysate
their Peritoneal fluid >100 WBC/mcL, 51% PMNs
what are they experiencing?

A

peritonitis

112
Q

MC pathogen to cause peritonitis

A

staphylococcus aureus
Gram negative rods, strep also common
May do culture for organism
Tx - abx for appropriate organism

112
Q

prognosis for ESRD and dialysis

A

Higher mortality > renal transplant pts
* Little difference in survival for PD vs. HD
* Overall 5-year survival - 39%
* Estimated life expectancy - 3-5 years

113
Q

MCC death of ESRD

A

cardiac disease (>50%)
Poor prognostic indicators - DM, advanced age, hypoalbuminemia, low socioeconomic status, inadequate dialysis, high fibroblast growth factor

GU: Clin Med IIA (13 decks)

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