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Chronic Kidney Disease Flashcards

1
Q

What is the definition of CKD?

A

abnormalities in kidney structure of function, present for 3 months or longer, and with implications for health

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2
Q

Which population is CKD more prevalent in?

A

the eldery

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3
Q

What is the classification system for CKD based mainly on?

A

GFR
albuminuria

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4
Q

What is the final stage of CKD?

A

end stage renal disease
-defined as GFR<15ml/min
-need dialysis or kidney transplant to live

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5
Q

What are the risk factors for CKD?

A

diabetes
high blood pressure
cardiovascular disease
obesity
family history of kidney disease
abnormal kidney structure
older age
smoking

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6
Q

What are the signs and symptoms of CKD?

A

signs and symptoms develop over time if kidney damage progresses slowly
nonspecific:
-nausea; vomiting; loss of appetite; fatigue and weakness;
sleep problems; changes in UO, decreased mental sharpness;
muscle twitches and cramps; swelling of ankles and feet;
persistent itching
-chest pain if fluid builds up around lining of heart
(pericarditis)
-shortness of breath if fluid builds up in lungs (pulmonary
edema)
-hypertension
ALL RELATED TO FLUID+WASTE BUILDUP

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7
Q

What are the classifications of CKD based on GFR?

A

G1 (normal-high): >90
G2 (mildly decreased): 60-89
G3A (mild-moderately decreased): 45-59
G3B (moderately-severely decreased): 30-44
G4 (severely decreased): 15-30
G5 (kidney failure): <15

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8
Q

What are the classifications of CKD based on albuminuria?

A

A1 (normal-mildly increased): <30
A2 (moderately increased): 30-300
A3 (severely increased): >300

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9
Q

What happens to prognosis of CKD as albuminuria and GFR get worse?

A

prognosis gets worse

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10
Q

True or false: CKD can be diagnosed without signs of kidney damage such as proteinuria

A

true
CKD can be diagnosed if:
GFR<60ml/min for at least 3 months (even without signs of kidney damage)
OR
if evidence of kidney damage such as proteinuria for at least 3 months (even if GFR>60ml/min)

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11
Q

Describe the kidney function for “normal”, the symptoms, and treatment options.

A

normal:
-kidney function: >60%
-symptoms: no symptoms observed
-tx options: identify cause and try to reverse it,
monitor albumin and GFR

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12
Q

Describe the kidney function for “mild”, the symptoms, and treatment options.

A

mild:
-kidney function: 45-59%
-symptoms: no symptoms observed
-tx options: monitor albumin and GFR, blood pressure, general
health and well-being, try to stop or slow down
the worsening of kidney function

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13
Q

Describe the kidney function for “moderate”, the symptoms, and treatment options.

A

moderate:
-kidney function: 30-44%
-symptoms: early symptoms may occur and could include
tiredness, poor appetite, and itching
-tx options: monitor albumin and GFR, and continue to try and
stop or slow down the worsening of kidney
function, learn more about CKD and tx options

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14
Q

Describe the kidney function for “severe”, the symptoms, and treatment options.

A

severe:
-kidney function: 15-29%
-symptoms: tiredness, poor appetite and itching may get
worse
-tx options: monitor albumin and GFR, and continue to try to
stop or slow down the worsening of kidney
function. Discuss and plan treatment choice:
dialysis access, assessment for transplant, or
information on non-dialysis supportive care

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15
Q

Describe the kidney function for “kidney failure”, the symptoms, and treatment options.

A

kidney failure:
-kidney function: <15%
-symptoms: severe fatigue, nausea, difficulty breathing, and
itchiness
-tx options: monitor albumin and GFR, and continue to try to
stop or slow down the worsening of kidney
function. Continue with non-dialysis supportive
care, plan for transplant or start dialysis

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16
Q

What are the potential underlying causes of CKD?

A

glomerular diseases
tubulointerstitial diseases
vascular diseases
cystic and congenital diseases

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17
Q

What are examples of systemic diseases that cause glomerular diseases?

A

diabetes
systemic autoimmune diseases
systemic infections
drugs
neoplasia

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18
Q

What are examples of systemic diseases that cause tubulointerstitial diseases?

A

systemic infections
autoimmune
sarcoidoisis
drugs
urate
environmental toxins (lead, aristolochic acid)
neoplasia (myeloma)

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19
Q

What are examples of systemic diseases that cause vascular diseases?

A

atherosclerosis
hypertension
ischemia
cholesterol emboli
systemic vasculitis
thrombotic microangiopathy
systemic sclerosis

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20
Q

What are examples of systemic diseases that cause cystic and congenital diseases?

A

polycystic kidney disease
Alports syndrome
Fabrys disease

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21
Q

How easy is it to identify CKD?

A

very difficult

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22
Q

Which stages of CKD are asymptomatic?

A

1 and 2

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23
Q

At what rate does GFR decline after the age of 20?

A

declines by 1ml/min/year in healthy people after the age of 20

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24
Q

What does the progression of CKD depend on?

A

depends on:
-cause of kidney disease
-GFR at time of diagnosis
-degree of albuminuria
-presence of comorbid conditions such as:
–>hypertension
–>diabetes
–>congestive heart failure
–>ischemic heart disease
–>COPD

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25
What is CKD a result of?
CKD is a result of irreversible injury-nephrons are lost
26
What do the healthy nephrons in someone with CKD have to do?
remaining nephrons take on more filtrate to accommodate for the loss in nephrons
27
What is the result of healthy nephrons taking on more filtrate in someone with CKD?
damaging the remaining nephrons hyperfiltration effect
28
What % of nephrons can be lost without clinical signs?
50% thats why you can donate one kidney
29
What happens when 80% of nephron loss occurs?
some degree of azotemia occurs but may still be asymptomatic
30
What are the clinical manifestations of CKD?
accumulation of toxins (e.g., protein metabolite) consequences of non-excretory functions (fluid/electrolytes, hormones) progressive inflammation
31
What is uremia?
caused by numerous toxins hundreds of toxins have been implicated
32
As loss of renal function progresses, what might be needed?
routine dialysis or kidney transplant
33
What is the clinical presentation of toxin accumulation?
symptoms: fatigue, weakness, shortness of breath, mental confusion, nausea and vomiting, bleeding, loss of appetite, itching, cold intolerance, and peripheral neuropathies signs: edema, weight gain (from accumulation of fluid), changes in urine output (volume consistency), "foaming" of urine (indicative of proteinuria), and abdominal distension
34
What is the excretion of Na and water based on in healthy kidneys?
adjustments of Na and water excretion are based on intake
35
What are the fluid and electrolyte problems in CKD?
in CKD, adjustments are lost so intake of Na and water exceeds excretion results in Na retention and ECFV expansion (edema or HTN)
36
How do the fluid symptoms associated with CKD progress?
initially, asymptomatic eventually, can become very difficult to manage, contributing to heart failure, hypertension, edema, and weight gain
37
What is the use of diuretics in CKD?
reduce blood pressure and treat swelling (edema)
38
At what GFR do thiazide diuretics often lose their effectiveness?
GFR below 30ml/min
39
Which diuretics are preferred in CKD?
loop diuretics preferred but higher doses are often needed
40
What is the drug combination for diuretic resistance?
loop diuretic + thiazide diuretic (metolazone)
41
What is required for untreatable edema and HTN?
dialysis
42
What is ESRD?
end stage renal disease kidneys permanently fail to work
43
How is ESRD diagnosed?
blood tests-blood cell counts, electrolyte levels, kidney function urine tests sonography (renal ultrasound) CT scan kidney biopsy
44
What are the treatment options for ESRD?
dialysis: not cure -peritoneal dialysis -hemodialysis kidney transplantation -deceased/living donor kidney transplant -pre-emptive kidney transplant (~20% of kidney transplants)
45
What are advantages of pre-emptive kidney transplants?
lower risk of rejection improved survival rates improved quality of life lower treatment costs avoidance of dialysis
46
What is the link between hypertension and CKD?
increased glomerular pressure chronic glomerular hypertension can lead to hypertrophy of tissues and loss of nephrons altogether elevated ANG II may promote tissue remodelling over time
47
What is first line for HTN and CKD?
ACEI and ARBs (along with diuretics depending on volume issues)
48
As CKD progresses, proteinuria will exceed ___.
1g/24hrs
49
What is the implication of proteinuria on the kidneys?
promote additional loss of nephrons through direct cellular damage proteins are toxic to tubular cells caused increased production of inflammatory cytokines (attracting inflammatory cells) damage leads to scarring, structural changes, and progressives loss of renal function
50
How is proteinuria identified?
ACR (albumin to creatinine ratio) protein dipstick blood levels can decline in severe proteinuria
51
What is the correlation between diabetes and CKD?
diabetes is associated with glomerular mesangial matrix expansion and renal vascular damage often associated with HTN glycated products (sugar coated molecules) somehow damage kidney structures directly
52
What is a benefit to the kidneys on controlling glucose in people with diabetes?
slows the progression of CKD
53
True or false: CVD and CKD are closely interrelated
true
54
What are the risk factors in a CKD patient for atherosclerosis and heart failure?
hypertension lipid sympathetic nervous system tone
55
What are non-traditional risk factors that appear to accelerate atherosclerotic cardiovascular disease?
anemia high phosphate, high parathyroid hormone generalized inflammation
56
What is the bottom line with ACEI/ARBs in CKD?
benefit to kidney increases in people with more severe disease in lower risk people other drugs appear to provide similar protection some BP-independent benefits on kidneys are likely in higher risk situations ACEI/ARBs are first line in patients with diabetes+nephropathy
57
Which hormone serves to excrete K+?
aldosterone
58
What causes hyperkalemia in CKD?
as tubules are lost, the ability to excrete K+ becomes more problematic -distal tubules are the target for aldosterone
59
At what GFR is hyperkalemia a serious problem?
<5ml/min
60
What are the drug options for hyperkalemia?
K-wasting diuretics minimization of K-sparing medications potassium-binding resins -sodium polystyrene sulfonate -calcium polystyrene sulfonate
61
Describe sodium polystyrene sulfonate.
used for hyperkalemia bind potassium in GIT (in exchange for Na+) supplied as powder, suspension, or rectal suspension *not absorbed* onset of effect is slow (days) -should not be used as an emergency treatment for life- threatening hyperkalemia
62
Describe calcium polystyrene sulfonate.
used for hyperkalemia binds potassium in exchange for Ca not absorbed dispensed as powder
63
True or false: both calcium/sodium polystyrene sulfonate have the potential to bind to other orally administered medications
true
64
What is normal arterial blood pH?
7.35-7.45
65
What is the reaction that serves as a very important regulator of pH?
H + HCO3 <--> H2CO3 <--> CO2 + H2O
66
Which organ maintains bicarbonate concentration?
the kidney at the proximal tubule
67
How much bicarbonate is re-absorbed at the proximal tubule?
85-90%
68
True or false: metabolic acidosis is common in advanced CKD
true
69
Why is metabolic acidosis common in advanced CKD?
diminished capacity to excrete acid and generate base day to day cellular metabolism produces large quantities of acid (much of which is CO2, as CO2 increases so does H)
70
What are some acids that cannot be eliminated by respiration?
lactic acid (produced by anaerobic glycolysis) ketones (fatty acid oxidation) *kidneys must eliminate these acids*
71
What are the two ways that H+ is eliminated?
secretion of H+ ions -secreted into lumen directly -combines with NH3 already circulating secretion of NH4+ ions -within tubular cells and secretion into tubular lumen
72
What does circulating NH3 combine with?
circulating NH3 combines with CO2 in the liver to form urea
73
Describe urea.
odorless and colourless highly soluble in water easily excreted by kidney
74
Which foods contain nitrogen?
meats fish potatoes milk eggs cereals legumes
75
What is metabolic acidosis characterized by?
decreased pH decrease in HCO3 PaCO2 is normal
76
Metabolic acidosis is normally mild in CKD until GFR ___.
<20ml/min
77
How does the kidney play a role in calcium homeostasis?
activation of vitamin D in addition to low serum calcium, the kidneys fail to excrete phosphate
78
What are the management strategies for Ca/phosphate disorders in CKD?
decrease phosphorus in diet phosphate binding agents such as Sevelamer calcitriol
79
How is PTH secreted?
parathyroid gland senses level of calcium in blood if Ca 2+ falls, the gland secretes PTH
80
What are the effects of PTH?
kidney -promotes renal tubular calcium reabsorption -promotes phosphate excretion -production of 1, 25-dihydroxyvitamin D bones -promotes catabolism of bone to release calcium and phosphorus
81
What are some common vitamin D products?
alfacalcidol -requires conversion to calcitriol in liver calcitriol -active cholecalciferol -synthesized in skin, requires 2 step activation -fatty fish, fish oils ergocalciferol -occurs in nature (wild mushrooms) -similar to D3 as it requires 2 step activation
82
How are the kidneys involved in regulation of RBC production?
contain specialized cells that detect low oxygen levels -hypoxia-induced erythropoietin production -act as a critimer to maintain hematocrit
83
What is the hematocrit?
ratio of volume of red blood cells to the total volume of blood -men 47 +/-5% -women: 42 +/- 5%
84
What is erythropoietin?
naturally occurring hormone that stimulates the bone marrow to produce more RBC
85
At what GFR does anemia often begin?
<30-45ml/min present in virtually all patient with ESRD
86
What are some erythropoiesis-stimulating agents?
epoetin alfa (recombinant EPO with same amino acid sequence) darbepoetin alfa (modified amino acids for longer duration of action)
87
What are some adverse effects of increasing RBC production?
hypertension or thrombosis
88
Approximately half of patients with GFR ___ are at risk for ___.
<60ml/min ADRs
89
What are some PK and PD considerations in CKD?
increased Vd in moderate to severe CKD metabolite accumulation non-renal clearance loading dose maintenance dose serum drug monitoring
90
What are the risk factors for CKD patients and ADRs?
Age ACEI/ARB usage Diabetes Advanced CKD

PHAR123 (15 decks)

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