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PHAR255 > Kidney Disorders 2 > Flashcards

Kidney Disorders 2 Flashcards

CKD

1
Q

Briefly describe the epidemiology of CKD.

A

1/10 Canadians live with CKD
diabetes is the leading cause of CKD
ESRD increased 35% since 2009
95% of patients managed in primary care

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2
Q

What is chronic kidney disease?

A

progressive loss of function occurring over several months to years
characterized by gradual replacement of normal kidney architecture with fibrosis
can progress to the need for dialysis or transplant

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3
Q

Why is CKD one of the leading causes of morbidity and mortality in North America?

A

progressive loss of kidney function leads to:
-complications
-may require RRT
cardiovascular disease
-leading cause of mortality*

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4
Q

What are the two main causes of CKD?

A

diabetes and HTN
diabetes being the leading cause

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5
Q

Which populations are at higher risk for CKD?

A

hypertension
diabetes
cardiovascular disease
first degree relative with CKD
Indigenous

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6
Q

What are the two definitions of CKD?

A

kidney function:
-GFR < 60ml/min/1.73m2 for 3 months or more with or without kidney damage
kidney structure:
-kidney damage for > 3 months, with or without decreased GFR, as evidence by pathological abnormalities, abnormalities in blood or urine or as seen by imaging

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7
Q

What are the markers for kidney damage?

A

albuminuria (ACR > 3mg/mmol)
urine sediment abnormalities (ex: RBC casts)
electrolyte abnormalities
abnormalities detected by histology
structural abnormalities
history of kidney transplant

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8
Q

Describe the screening process for CKD.

A

measure eGFR and ACR
-if eGFR < 60ml/min re-measure in 3 months or sooner
-if ACR > 3 re-measure 1-2 times over next 3 months
confirm CKD diagnosis after 3 months
-eGFR > 60ml/min and ACR < 3=person doesnt have CKD
-eGFR 30-59ml/min and/or ACR 3-60=person has CKD but can be managed in primary care
-eGFR < 30ml/min and/or ACR > 60=person has CKD but refer to nephrologist

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9
Q

Describe the decline in GFR due to age.

A

GFR decreases by ~ 1ml/min/1.73m2/year beginning in the 4th decade of life
GFR will decrease to < 60ml/min in 5-25% of otherwise healthy adults due to aging alone

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10
Q

What is the concern with reduced GFR due to age alone?

A

there are still risks associated:
-higher risk of AKI
-medication accumulation with reduced GFR
-reduced reserves in the event other comorbidities develop over time

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11
Q

Describe the staging of CKD based on GFR.

A

G1 (normal or high): > 90ml/min
G2 (mildly decreased): 60-89ml/min
G3a (mild-moderately decreased): 45-59ml/min
G3b (moderate-severely decreased): 30-44ml/min
G4 (severely decreased): 15-29ml/min
G5 (kidney failure): < 15ml/min
G3a and lower can be classified as CKD

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12
Q

Describe the staging of CKD based on albuminuria.

A

note: using ACR
A1 (normal-mildly increased): < 3mg/mmol
A2 (moderately increased): 3-30mg/mmol
A3 (severely increased): > 30mg/mmol

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13
Q

To determine GFR category, what equation would you use to estimate the GFR?

A

CKD-EPI

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14
Q

Are albuminuria and GFR dependent on each other in the context of CKD?

A

no, they are independent
-GFR could be fine but ACR could be high leading to a poor prognosis and vice versa
-worst possibility is a combo of both being bad

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15
Q

What is the clinical presentation of CKD?

A

often asymptomatic
-symptoms minimal in stages 1-2
higher incidence of symptoms in stages 3-4
-low energy, fatigue, confusion
-foaming, tea-coloured, bloody or cloudy urine
-edema
-shortness of breath
-pruritis

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16
Q

Provide a very brief overview of care for CKD based on GFR.

A

eGFR 30-59ml/min (3a-3b): usually managed in primary care
eGFR < 30ml/min (4-5): usually with nephrologist
delay progression
reduce CV risk
treat complications

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17
Q

Describe the progression of CKD.

A

once CKD develops, it generally progresses over time
-autoimmune CKD may undergo remission
rate of GFR decline highly variable between individuals
-lower GFR and greater albuminuria=faster progression
rate of progression is related to etiology
-quick: diabetic nephropathy, glomerular dx, polycystic kidney disease, transplant
-slow: hypertensive, tubulointerstitial disease

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18
Q

What are the non-modifiable factors associated with faster progression of CKD?

A

African American
male
advanced age
family history

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19
Q

What are the modifiable factors associated with faster progression of CKD?

A

uncontrolled HTN
poor blood glucose control
proteinuria
smoking
obesity

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20
Q

What are the interventions to delay the progression of CKD?

A

blood pressure control
RAAS blockade
-ACEI/ARB
-non steroidal MRAs
blood glucose control in people with DM
-SGLT2 inhibitors
-GLP 1 agonists?
smoking cessation
avoidance of nephrotoxins

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21
Q

Describe blood pressure control in the context of CKD.

A

HTN can be both a cause and a consequence of CKD
associated with faster progression of CKD and CVD
strict bp control delays progression of CKD

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22
Q

What are the blood pressure targets according to Hypertension Canada?

A

<130/80 for patient with diabetic CKD
SBP < 110 for adults with polycystic kidney disease
SBP < 120 for “high risk” patients
SBP < 140 for “all other patients”

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23
Q

What are the blood pressure targets according to KDIGO?

A

SBP < 120 for patients with high bp and CKD when tolerated
<130/80 for kidney transplant recipients

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24
Q

What are the indications defining high-risk patients for intensive blood pressure management?

A

AARF
age > 75
atherosclerosis
renal (eGFR < 60ml/min/1.73m2 or proteinuria < 1g/d)
Framingham risk score > 15%

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25
Q

What are cautions and contraindications for pushing SBP to < 120?

A

heart failure
institutionalized elderly individuals
diabetes
previous stroke
eGFR < 20 (includes dialysis and transplant)
patient unwilling/unable to adhere to multiple meds
standing SBP < 110
inability to measure SBP accurately

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26
Q

What are the results from the SPRINT trial in regards to SBP <120 and CKD progression?

A

did not slow CKD progression

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27
Q

Describe proper BP measurement.

A

sitting position
back supported
arm bare and supported
middle of cuff at heart level
do not talk or move before or during
legs uncrossed
feet flat on floor

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28
Q

What are the lifestyle recommendations from Hypertension Canada for blood pressure control?

A

salt restriction
-reduce sodium intake towards < 2000mg (5g of salt)/day
exercise
-30 to 60 minutes moderate intensity 4-7 days/week
weight reduction in overweight/obese patients
-BMI 18.5-25kg/m2
limit alcohol consumption
-1 to 2 drinks/day

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29
Q

How many drugs are often required to control blood pressure with CKD?

A

3-4

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30
Q

What are the first-line options for blood pressure control and CKD?

A

ACEI/ARB
diuretics
long acting CCB
consider comorbidities, stage of CKD, degree of albuminuria, type of CKD

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31
Q

What is the first line treatment for HTN if a patient has proteinuria?

A

ACEI/ARB
-diabetic kidney disease: ACR > 3mg/mmol
-nondiabetic proteinuric CKD: ACR > 30mg/mmol

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32
Q

What is the benefit of ACEI/ARBs in the context of CKD?

A

reduce BP and glomerular capillary pressure
-by selectively vasodilating the efferent arteriole
reduce proteinuria
improvement in kidney outcomes (failure, doubling of SCr, GFR decline, progression of albuminuria) and CV outcomes

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33
Q

Which antihypertensive reduces proteinuria more than any other?

A

ACEI/ARB

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34
Q

Which ACEI/ARB is used for RAAS blockade in CKD?

A

used interchangeably

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35
Q

What are the contraindications to ACEI/ARBs?

A

pregnancy
angioedema
bilateral renal artery stenosis

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36
Q

What are the precautions to ACEI/ARBs?

A

intravascular fluid depletion
-reduce/hold dose if severe vomiting, diarrhea, fluid loss
eGFR < 30ml/min/m2
hypotension (caution if BP < 110/70)
hyperkalemia (K+ > 5.5mmol/L)

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37
Q

What are the monitoring parameters for ACEI/ARB therapy?

A

2-4 weeks following initiation or any dose increase
-SCr (increase > 30% from baseline may warrant dc)
-K+ (if high: restrict dietary K+, add diuretic)
-blood pressure
-urinary ACR

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38
Q

What are the strategies that can be done to reduce potassium if hyperkalemia occurs to a patient with CKD on an ACEI/ARB?

A

moderate potassium intake
review concurrent drugs
consider:
-diuretics
-sodium bicarbonate
-potassium binders
ACEI/ARB are so important that we want to do as much as we can to keep them on board

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39
Q

What is the dosing of ACEI/ARBs for CKD?

A

start at a low dose and titrate to maximum tolerated dose (or highest approved dose)
-dose dependent reduction in albuminuria lowering effect

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40
Q

What was the old recommendation for combo ACEI+ARB therapy?

A

CKD with refractive proteinuria

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41
Q

What is the recommendation today for combo ACEI/ARB therapy?

A

avoid ACEI/ARB combination
-superior for reducing proteinuria and BP but actually worsened renal outcomes

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42
Q

Which drug is a direct renin inhibitor?

A

aliskiren

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43
Q

What is the use of aliskiren for CKD?

A

no longer used
-does more harm than good

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44
Q

What did the Cochrane review from 2014 find regarding MRAs and CKD?

A

reduced proteinuria 30-40%
improved bp
possible slowing of CKD progression
no CV/ESRD outcomes
doubled risk of hyperkalemia
5 fold risk of gynecomastia

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45
Q

What are the steroidal aldosterone antagonists?

A

spironolactone and eplerenone
non-selective

46
Q

What is the non-steroidal aldosterone antagonist?

A

finerenone
higher specificity for MR vs glucocorticoid/androgen receptor

47
Q

What is the benefit of finerenone?

A

reduction in albuminuria while having less side effects

48
Q

What are the KDIGO recommendations regarding finerenone in CKD with diabetes?

A

use with proven kidney or CV benefit for patients with T2DM, an eGFR > 25ml/min, normal K+ levels (<4.8), and albuminuria (ACR > 3) despite maximum tolerated dose of a RAASi

49
Q

What are the KDIGO guidelines regarding MRAs for hypertension?

A

possible use in refractory HTN (uncontrolled on 3 other drugs including a diuretic) with GFR > 45ml/min
steroidal or non-steroidal MRA

50
Q

What are the limitations of finerenone?

A

not currently covered by SK formulary or NIHB
less evidence available in patients also taking a SGLT2i
not to use in combo with steroidal MRAs in patients with HF

51
Q

Why are diuretics frequently used for hypertension in CKD?

A

fluid retention is an important contributor to HTN in CKD
most patients require diuretic therapy

52
Q

Which diuretic should you initiate with for hypertension treatment in CKD?

A

thiazide
-may switch to or combine with loops for volume control or if BP becomes resistant to therapy
-may prefer combo with metolazone, chlorthalidone, or indapamide (effective diuresis at GFR < 30ml/min)

53
Q

Which diuretics should be avoided in stage 3-5 CKD?

A

potassium sparing diuretics

54
Q

Describe DHP CCBs for hypertension control in CKD.

A

preferred to thiazides in combo with ACEI/ARB in patients with diabetes (CV benefits)
no evidence for slowing CKD progression
may cause fluid retention and edema (nuisance effect in CKD)

55
Q

Describe non-DHP CCBs for hypertension control in CKD.

A

shown to decrease proteinuria but not same extent as ACEIs
not preferentially used for reducing proteinuria but may provide benefit when added to ACEI/ARB
-no evidence for slowing CKD progression
tolerability and safety:
-constipation and bradyarrhythmia
-lots of drug interactions and contraindications

56
Q

Which beta-blockers are renally eliminated and require dosage adjustment once CrCl approaches 30ml/min?

A

atenolol
bisoprolol

57
Q

What is the use of beta-blockers for hypertension control in CKD?

A

only used if compelling indications (not used as stand alone)
-ex: HF, post-MI, angina
-inconsistent evidence for CV benefits in CKD

58
Q

What are the common side effects of beta-blockers?

A

fatigue
limited exercise tolerance

59
Q

What is the use of alpha-2 agonists for hypertension control in CKD?

A

adjunctive therapy for HTN because no drug interactions with commonly used bp meds

60
Q

What are the side effects of alpha-2 agonists?

A

CNS (caution in the elderly)
rebound HTN if abruptly stopped

61
Q

What is the use of alpha-1 blockers for hypertension control in CKD?

A

adjunctive treatment for elevated bp
-might consider in patients with BPH

62
Q

What are the common side effects of alpha-1 blockers?

A

dizziness
orthostatic hypotension

63
Q

What is the use of direct vasodilators for hypertension control in CKD?

A

adjunct treatment
-use is limited by side effects (headache, fluid retention)
-hydralazine has no renal dose adjustment=positive

64
Q

What is the role of SGLT2 inhibitors for hypertension control in CKD?

A

bp reduction is a side advantage
-not the main reason they are used

65
Q

Describe proteinuria.

A

linked with progression of diabetic and non-diabetic CKD
high risk of progressing to kidney failure
indicator of subclinical CVD
>150 mg protein lost in urine per day (albumin or others)

66
Q

What is microalbuminuria a predictor of?

A

loss of kidney function

67
Q

Why do we want to identify microalbuminuria early?

A

so that we can institute appropriate therapy (ACEI/ARB) to slow progression

68
Q

Differentiate between mild proteinuria, moderate proteinuria, and nephrotic range.

A

mild: 150-500mg (A2)
moderate: > 500mg (A3)
nephrotic range: more than 3g or albumin excretion > 2200mg/24h

69
Q

What are the symptoms of nephrotic syndrome?

A

hyperlipidemia
hypoalbuminemia
edema
thromboembolic risk
foamy urine

70
Q

Why do we treat patients with CKD that have no hypertension with an ACEI/ARB?

A

reduce glomerular capillary pressure and volume
possible direct effect on podocytes to decrease proteinuria

71
Q

What is the first line therapy for kidney diseases with proteinuria?

A

ACEI/ARB (CV and kidney benefits)
-diabetic or hypertensive kidney disease with A2 or A3 albuminuria
-other kidney diseases with proteinuria

72
Q

What is the benefit of SGLT2 inhibitors for CKD?

A

renal and CV benefits
-reduces decline in GFR, progression to ESRD, death due kidney disease, all-cause and CV mortality
-regardless of diabetes or not

73
Q

What is the recommendation from CCS for SGLT2 inhibitors in CKD?

A

recommended for adults with CKD (ACR > 20mg/mmol or GFR > 25ml/min/1.73m2)
-even without diabetes

74
Q

How often should diabetics be screened for CKD?

A

at least annually in stable patients
-random urine ACR, SCr, and eGFR

75
Q

What is the importance of blood glucose control in CKD?

A

prevents and delays progression of diabetic nephropathy

76
Q

What is the target A1C in CKD?

A

< 7.0 for most patients
-< 6.5 may be appropriate in some to decrease CKD risk

77
Q

In which patients might A1C measurements be less accurate?

A

advanced CKD (G4-G5)
-particularly with dialysis

78
Q

What is the benefit of metformin for blood glucose control in CKD?

A

CV benefit
-lack of evidence for kidney protective effects

79
Q

True or false: metformin does not require renal dose adjustments

A

false
renal dose adjustments due to the concern of lactic acidosis

80
Q

What are KDIGOs recommendations regarding SGLT2 inhibitors for diabetics with CKD?

A

1st line for patients with T2DM, CKD, and eGFR > 20ml/min

81
Q

What are the complimentary actions of SGLT2 inhibitors with ACEI/ARBs?

A

ACEI/ARBs dilate the efferent arteriole to reduce glomerular pressure, SGLT2 inhibitors constrict the afferent arteriole to further reduce glomerular pressure and long-term renal protection

82
Q

What is the key point regarding SGLT2 inhibitors and CKD?

A

guidelines recommend them to improve renal and CV outcomes regardless of the patients A1C (even if targets are met)

83
Q

What are the guidelines for SGLT2 inhibitors and dialysis?

A

not to be initiated if eGFR < 20ml/min but may be continued until dialysis

84
Q

What is the early decline in eGFR with SGLT2 inhibitors that we are willing to accept and continue with?

A

< 30%

85
Q

What are the adverse effects of SGLT2 inhibitors?

A

thirst
urinary frequency (take in AM)
genital mycotic infections
hypovolemia
dizziness/orthostatic hypotension
DKA

86
Q

What are the benefits of GLP-1 agonists?

A

evidence for CV benefits and favorable kidney benefits
-FLOW trial in 2024 to provide more info on renal benefits

87
Q

What are the KDIGO recommendations for GLP-1 agonists in CKD?

A

use if A1C targets not achieved with metformin/SGLT2 inhibitors

88
Q

How does smoking increase the progression of CKD?

A

increased BP and HR
decreased renal blood flow (constriction)
vascular injury
also a risk factor for CV events

89
Q

What are some examples of nephrotoxic drugs?

A

NSAIDs, COX-2 inhibitors
lithium
aminoglycosides
amphotericin B
calcineurin inhibitors
cisplatin
avoid combinations, especially like ACEI/ARB, NSAID, diuretic

90
Q

Describe sick day management in CKD.

A

when patients with CKD become acutely ill and are unable to maintain adequate fluid intake, recommend to hold potentially nephrotoxic or renally excreted drugs
-SAD MANS
=sulfonylureas, ACEI, diuretics, metformin, ARB, NSAID, SGLT2i

91
Q

What is the leading cause of death in patients with CKD?

A

cardiovascular disease
-most patients with CKD will die from CVD before RRT

92
Q

What are the common CV risk factors that patients with CKD should be screened for?

A

DM
HTN
dyslipidemia
smoking
obesity
LVH

93
Q

What are the statin indicated conditions?

A

ASCVD
most diabetics
CHRONIC KIDNEY DISEASE
-most guidelines recommend a statin regardless of LDL

94
Q

What are the KDIGO guidelines for the treatment of dyslipidemia in CKD?

A

> 50 yrs old with eGFR < 60 and not on dialysis
-low dose statin or statin/ezetimibe
50 yrs old with CKD and eGFR > 60
-tx with statin
18-49 yrs old with CKD
-tx with statin if estimated CV risk is > 10%
if on dialysis: do not initiate therapy
-continue therapy if already on it
kidney transplant
-tx with statin (in some cases)

95
Q

What is the difference in recommendations for statins in CKD between KDIGO and the dyslipidemia guidelines?

A

KDIGO:
-stick with low dose statin (fire and forget)
-limitation: studies were only done in dialysis patients
dyslipidemia guidelines:
-high intensity statin therapy (atorv 80, rosuv 40)

96
Q

What is the benefit of the “fire and forget” strategy for statins in CKD?

A

CV risk reduction and mortality
-no benefits to slowing CKD progression

97
Q

What is the role of antiplatelet therapy in CKD?

A

no role in primary CV prevention in CKD
used in secondary prevention

98
Q

What are the forms of renal replacement therapy?

A

dialysis
-hemodialysis
-peritoneal dialysis
-continuous renal replacement therapy
kidney transplant
-preferred option for eligible patients (better mortality)
-subject to organ availability

99
Q

When is renal replacement therapy initiated in CKD?

A

no set GFR at which RRT is required
-based on clinical status of the patient
-most require at GFR ~ 10ml/min
signs and symptoms indicated need for RRT:
-serositis, acid-base or elyte abnormalities, pruritis
-inability to control volume status or BP
-malnutrition refractory to dietary intervention
-cognitive impairment

100
Q

Describe hemodialysis.

A

most common RRT modality
patients blood is passed through an external filter to remove wastes and fluid
-solutes move from the blood across the filter into the dialysis solution down their concentration gradient
-filtered blood is returned to the body
-requires chronic vascular access that can withstand high blood-flow rates
can be done at home or in a dialysis clinic
3-5x/week at the clinic (3-5hrs per visit)

101
Q

What are the types of hemodialysis?

A

AV fistula
-preferred method, requires months to heal before start
synthetic AV graft
-susceptible to infection
catheter in neck
-highest complication risk

102
Q

Which systemic therapy is given during hemodialysis and why?

A

anticoagulation
-prevents blood clot in the machine

103
Q

What are the common adverse effects of hemodialysis?

A

fatigue
hypotension (massive fluid shifts)
hypertension
cramps
N/V

104
Q

What are the vascular access problems associated with hemodialysis?

A

infection
clotting
bleeding

105
Q

Which micronutrients are removed from the body during dialysis?

A

water soluble vitamins (B and C)
-all dialysis patients require Replative (1 tab po OD)
-avoid multivitamins containing minerals, vit A or D

106
Q

Which micronutrients require monitoring in dialysis patients?

A

serum folate and B12 q6-12mo

107
Q

Describe peritoneal dialysis.

A

relies on patients own peritoneal membrane to act as a filter for fluid and waste
-2-3L of dialysate is instilled in the peritoneal cavity through an indwelling catheter in the abdominal wall
-wastes and fluid diffuse across the peritoneal membranes down their concentration gradient
-dialysate is drained and replaced with fresh solution
preferred in pts continuing to work, travel, etc BUT requires patients to be diligent

108
Q

What are the two types of peritoneal dialysis?

A

continuous ambulatory peritoneal dialysis (CAPD)
-manual exchange, 4-5x/day
-each exchange takes 30-45min
automated peritoneal dialysis
-automated using a machine while sleeping
-takes 8-10hrs

109
Q

What is the most frequent complication of peritoneal dialysis?

A

peritonitis
-treated with local or systemic antibiotics

110
Q

Describe continuous renal replacement therapy.

A

used in acute settings
-not suitable for chronic RRT
for patients who cannot tolerate abrupt fluid shifts with HD
-hemodynamically unstable patients requiring RRT for AKI

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