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PHAR 123 > Renal > Flashcards

Renal Flashcards

1
Q

What are the functions of the kidney?

A

filter blood/excrete toxins
metabolise compounds
secrete hormones
maintain pH (acid-base) and electrolyte balance – produce bicarb

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2
Q

Why is kidney disease typically silent until advanced?

A

No pain receptors in the kidneys so pain is not usually present

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3
Q

What is one instance where you may feel kidney pain?

A

Kidney stones
Not kidney pain however; ureter pain

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4
Q

What part of the kidney collects the filtrate?

A

Bowman’s capsule – drains into urine

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5
Q

What part of the kidney collects reabsorbed nutrients?

A

arteries – goes into the veins

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6
Q

What is a normal GFR?

A

100-120 mL/min

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7
Q

What size of molecules can be filtered at the glomerulus

A

small molecules < 70 kDa

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8
Q

What happens to larger molecules at the glomerulus?

A

cannot be filtered and therefore go back into the blood

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9
Q

What happens if proteins get stuck on the surface of the glomerulus and Bowman’s capsule?

A

become a target for the immune system therefore causing inflammation and damage to the nephrons

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10
Q

How much nutrients are reabsorbed at the proximal tubule?

A

60-70% of Na+, almost all K+ and glucose

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11
Q

How is water reabsorbed at the proximal tubule

A

passively along osmotic gradients of Na+ (high conc. in tubule and low conc. outside = gradient)

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12
Q

How much filtrate is delivered to the loop of Henle?

A

30 mL/min

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13
Q

What occurs at the descending loop of Henle?

A

permeable for water and therefore water is reabsorbed

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14
Q

What occurs at the ascending loop of Henle?

A

not permeable for water and therefore Na+ is reabsorbed

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15
Q

How much filtrate is delivered to the collecting duct?

A

5-10 mL/min (about 5-10%)

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16
Q

What are the water channels in the collecting duct under control of and what does this mean for water reabsorption?

A

vasopressin – antidiuretic hormone
stimulates water reabsorption alone without Na+

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17
Q

What steroid is the distal tubule/collecting duct a target for and what action does this hormone cause?

A

Aldosterone
causes Na+ reabsorption and K+ excretion

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18
Q

What regulates K+ excretion

A

K+ levels in the blood
low levels = less excretion of K+ to maintain levels

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19
Q

How does the kidney help maintain acid-base balance in the body, and what part of the kidney is responsible for this?

A

Distal tubule/collecting duct produces bicarbonate

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20
Q

Approximately how much filtrate (urine) enters the ureters and into bladder?

A

1-2 mL/min
98-99% reabsorption rate

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21
Q

Where are drugs and toxins secreted from in the kidney?

A

Proximal tubule

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22
Q

4 types of transporters in the renal proximal tubule

A

anionic
cationic
peptide/hormone
ABC

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23
Q

Which type of transporter is responsible for conferring drug resistance?

A

ABC transporter

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24
Q

What channel do thiazide diuretics inhibit?

A

NCCs

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25
Q

What channel do potassium sparing diuretics inhibit?

A

ENaCs

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26
Q

What is the most commonly used marker of kidney function?

A

serum creatinine

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27
Q

What is normal serum creatinine?

A

0.9-1.3 mg/dL

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28
Q

What is the normal cycle of creatinine?

A

Produced daily by muscles as a part of metabolism
easily filtered so level does not typically change

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29
Q

If GFR decreases, how does this affect serum creatinine and why?

A

serum creatinine will be increased
decrease GFR means less creatinine being excreted and since creatinine is still being made by muscles, this means increase creatinine in the blood

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30
Q

What may be the problem with using serum creatinine in someone with a low muscle mass

A

they will have less creatinine normally, and so even if GFR is decreased, since we do not know their baseline, their serum creatinine levels may appear normal

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31
Q

What factors does the Cockroft-Gault equation take into account?

A

age, ideal body weight, gender
serum creatinine

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32
Q

What factors does the MDRD equation take into account?

A

age, gender, race
serum creatinine

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33
Q

How do we estimate ideal body weight?

A

5’0” man = 50 kg; 5’0” woman = 45 kg
add 2.3 kg for every inch above 5’0”

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34
Q

Why do some drugs need to be adjusted based on renal function?

A

In kidney dysfunction, regular doses will be excreted more slowly leading to accumulation of drug in the body and therefore are at risk for an adverse drug reaction
drug doses therefore must be lowered

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35
Q

What 3 factors influence whether drugs are renally excreted?

A

Water solubility
Protein binding
Tubular secretion (excretion)

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36
Q

How is water solubility a factor in determining if a drug is renally excreted?

A

Drugs that are highly soluble can exist freely in the bloodstream and therefore can fit through the glomerulus and be filtered easily
high soluble = easily excreted

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37
Q

How is protein binding a factor in determining if a drug is renally excreted?

A

drugs that are highly bound to plasma proteins are less likely to be filtered therefore more will stay in the blood

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38
Q

How is tubular secretion a factor in determining if a drug is renally excreted?

A

tubular secretion = excretion
some drugs are concentrated in the urine by active secretion rather than filtration

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39
Q

What does stage 1 kidney disease mean and what GFR is needed for a diagnosis?

A

kidney damage with a normal GFR
≥ 90

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40
Q

What does stage 2 kidney disease mean and what GFR is needed for a diagnosis?

A

kidney damage with mild GFR
89-60

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41
Q

What does stage 3a kidney disease mean and what GFR is needed for a diagnosis?

A

mild to moderate GFR
59-45

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42
Q

What does stage 3b kidney disease mean and what GFR is needed for a diagnosis?

A

moderate GFR
45-30

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43
Q

What does stage 4 kidney disease mean and what GFR is needed for a diagnosis?

A

severe GFR
30-15

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44
Q

What does stage 5 kidney disease mean and what GFR is needed for a diagnosis?

A

kidney failure
< 15 or dialysis

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45
Q

TRUE OR FALSE
proteinuria can be elevated even without a decrease in GFR

A

TRUE

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46
Q

what is albuminuria?

A

Albumin in the urine
more sensitive marker for kidney disease than total protein

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47
Q

what is considered microalbuminuria?

A

30-300 mg/d

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48
Q

what is considered macroalbuminuria?

A

> 300 mg/d

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49
Q

What is eGFR based on?

A

serum creatinine

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50
Q

What is ACR based on?

A

creatinine in the urine

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51
Q

what is ACR?

A

albumin/creatinine ratio
simple spot urine test that accurately predicts microalbuminuria

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52
Q

what is A1 and what are the numbers?

A

normal to mildly increased albuminuria
< 30 mg/g

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53
Q

what is A2 and what are the numbers?

A

moderately increased albuminuria
30-300 mg/g (microalbuminuria)

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54
Q

what is A3 and what are the numbers?

A

severely increased albuminuria
> 300 mg/g

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55
Q

According to the ACR/eGFR chart:
what is considered “green” and what does this mean?

A

G1/A1 or G2/A1
everything is okay – no dose adjustment is needed

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56
Q

According to the ACR/eGFR chart:
what is considered “yellow” and what does this mean?

A

G1/A2, G2/A2 or G3a/A1
dose adjustment is needed

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57
Q

According to the ACR/eGFR chart:
what is considered “orange” and what does this mean?

A

G1/A3, G2/A3, G3a/A2 or G3b/A1
dose adjustment is needed

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58
Q

According to the ACR/eGFR chart:
what is considered “red” and what does this mean?

A

G3a/A3, G3b/A2-A3 or anything G4 or G5
we cannot do anything here – patient should be in the hospital

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59
Q

what can urinalysis tell us about kidney function?

A

can only tell us that something is wrong somewhere

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60
Q

what tests confirm kidney damage?

A

imaging
x-ray, CT, MRI, ultrasound

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61
Q

when is a biopsy done in AKI?

A

once damage has been confirmed by imaging

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62
Q

what 4 factors in a urinalysis test are associated with kidney damage?

A

specific gravity
protein
epithelial cells
casts

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63
Q

what is required in order to be diagnosed with AKI?

A

rise in SCr by >25uM within 48h
AND/OR
decrease in urine output to <0.5 mL/kg/h for at last 6h

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64
Q

what is azotemia?

A

rapidly rising BUN
BUN = blood urea nitrogen

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65
Q

TRUE OR FALSE
CKD patients are more susceptible to AKI

A

true

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66
Q

Signs and symptoms of AKI

A

diminished urine volume
edema in legs, ankles and around the eyes
fatigue or tiredness
shortness of breath
confusion
nausea
seizures or coma in more severe cases
chest pain or pressure

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67
Q

What are the most common causes of community-acquired AKI?

A

volume depletion (N,D)
medication ADRs
kidney stress

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68
Q

What are the most common causes of hospital-acquired AKI?

A

sepsis
major surgery
critical illness involving heart or liver failure
IV contrast agents
medication ADRs

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69
Q

What is pre-renal azotemia?

A

Damage causing AKI happens before the kidneys
decrease in glomerular pressure impairs function of tubules causing accumulation of waste in the blood (azotemia)

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70
Q

What are some causes of pre-renal azotemia?

A

reduced cardiac output
severe volume depletion
reno-vascular disease
medication ADRs

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71
Q

How does reduced cardiac output cause AKI?

A

need pressure to cross the glomerulus –> when flow rate decreases, pressure decreases and therefore GFR decreases if something were to happen

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72
Q

How does severe volume depletion cause AKI?

A

decrease blood to glomerulus and therefore decrease GFR

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73
Q

How does renal artery stenosis lead to AKI?

A

blocks the flow of blood to the kidneys and therefore decreased GFR

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74
Q

What 3 markers are used to determine AKI?

A

decreased GFR
increased BUN
increased SCr

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75
Q

how do medications cause AKI and what is an example?

A

NSAIDs
2 mechanisms: decrease renal blood flow OR direct injury (interstitial nephritis) therefore causing apoptosis and necrosis

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76
Q

What is intra-renal damage defined as?

A

direct damage to glomerulus, tubules, or renal vessels

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77
Q

What is the most common cause of chronic injury to the glomerulus?

A

longstanding glomerular pressure
often seen in HTN and DM

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78
Q

What is immune mediated glomerular injury?

A

antigens and antibodies get caught in the structure (likely due to high blood flow and high pressure) and the immune system attack these Ag and Ab (autoimmunity)

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79
Q

How does Cisplatin cause AKI?
how do you lower the risk of AKI with this drug?

A

accumulates in proximal tubules causing direct toxicity
pre-hydration (to dilute drug in tubules) decreases the risk of AKI

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80
Q

What is rhabdomyolysis

A

a syndrome resulting from the release of myoglobin from muscles into the bloodstream

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81
Q

How can rhabdomyolysis cause AKI?

A

myoglobin can precipitate in renal tubules which halts tubular flow (blocks tubules) leading to tubular cell necrosis

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82
Q

What are some symptoms of rhabdomyolysis

A

muscle pain/weakness, malaise, dark urine
myoglobin concentration very high

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83
Q

What can cause rhabdomyolysis?

A

traumatic/crush injuries
non-traumatic muscle compression, prolonged immobility
exertional (esp in untrained people and hyperthermia)
drugs/toxins (statins)

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84
Q

What is interstitial nephritis

A

drug related
occurs when spaces between tubules become inflamed –> spreads to tubules but spares the glomeruli
often called “hypersensitivity” reactions

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85
Q

How does ASCVD cause AKI?

A

decrease blood flow in large vessels due to plaques means decrease GFR

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86
Q

TRUE OR FALSE
AKI always causes CKD?

A

false
can be reversible if treated soon enough

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87
Q

What are the 2 main causes of kidney stones

A

hypercalciuria (calcium rich stones)
hyperuricosuria (uric acid stones)

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88
Q

what group of people are more likely to get uric acid stones over calcium stones?

A

patients with a history of gout

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89
Q

How can kidney stones cause damage to the kidneys?

A

Bigger stones can block urine flow causing urine to flow back into the kidney (cannot get to bladder)
this causes an infection and can cause abscess

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90
Q

what causes kidney stones?

A

caused from alterations in the solubility of various substances in the urine

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91
Q

symptoms of kidney stones

A

stone formation is typically painless but renal damage and hematuria can occur
pain is due to distension of ureter as stone travels down

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92
Q

what are some risk factors for developing kidney stones?

A

dehydration
protein intake
increased Na+ intake

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93
Q

how does high protein intake lead to formation of kidney stones?

A

increases blood and urine acidity leading to Ca or uric acid stones

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94
Q

TRUE OR FALSE
increased Ca intake is likely to cause kidney stones

A

false
no evidence to show that high Ca in the diet causes kidney stones

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95
Q

what is the treatment for small kidney stones?

A

fluids, bed rest, and analgesia

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96
Q

what do the different letters mean in the RIFLE classification (just the description)

A

Risk of renal dysfunction
Injury to the kidneys
Failure of kidney function
Loss of kidney function
End-stage renal disease (ESRD)

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97
Q

What is the GFR and UO criteria for risk in RIFLE?

A

increase in SCr >1.5x baseline OR decrease of GFR >50%
UO <0.5mL/kg/h x 6h

98
Q

What is the GFR and UO criteria for injury in RIFLE?

A

increase in SCr >2.0x baseline OR decrease of GFR >50%
UO <0.5mL/kg/h x 12h

99
Q

What is the GFR and UO criteria for failure in RIFLE?

A

increase in Scr >3.0x baseline OR decrease of GFR >75% OR Scr ≥4 mg/dL
UO < 0.5 mL/kg/h x 6h

100
Q

What is the criteria for loss in RIFLE?

A

persistent ARF = complete loss of renal function for more than 4 weeks

101
Q

What are some strengths of RIFLE?

A

broadly validated in incidence identification
provided good prognostic accuracy
strongly correlated with length of hospitalisation stay, RRT requirement, etc.

102
Q

what are some weaknesses of RIFLE?

A

baseline SCr which is normally unkown is required
MDRD equation was validated only for CKD patients
only using SCr could decrease diagnostic sensitivity of AKI

103
Q

What are the AKIN criteria stages RIFLE equivalents?

A

stage 1 = R
stage 2 = I & F
stage 3 = L & E

104
Q

What is the GFR and UO criteria for Stage 1 in AKIN criteria?

A

increase SCr >1.5-2.0x baseline or increase SCr ≥ 0.3 mg/dL within 48h
UO < 0.5mL/kg/h x 6h

105
Q

What is the GFR and UO criteria for Stage 2 in AKIN criteria?

A

increase SCr >2.0-3.0x baseline
UO < 0.5mL/kg/h x 12h

106
Q

What is the GFR and UO criteria for Stage 3 in AKIN criteria?

A

increase SCr >3.0x baseline or SCr ≥4mg/dL or dialysis
UO < 0.3 mL/kg/h x 24h or anuria x 12h

107
Q

What are strengths of AKIN critera?

A

added etiological information
solely based on SCr changes, not GFR

108
Q

What are some limitations of AKIN criteria?

A

does not provide AKI classification if increase of SCr occurs in more htan 48h
stage 3 requires criteria on SCr, UO and RRI requirement
also requires baseline SCr

109
Q

what is required in order to be eligible for a renal needle biopsy?

A

1) blood in urine
2) protein in urine
3) increase level of toxins in the blood

110
Q

what can be used to diagnose AKI?

A

urine output test
urinalysis
blood test
imaging (x-ray, CT, MRI, ultrasounds)
biopsy

111
Q

What is the advantage and disadvantage of open kidney biospy?

A

advantage: better in diagnosing

disadvantage: more invasive

112
Q

What are some complications of AKI?

A

pulmonary edema
anemia
chest pain
muscle weakness
hyperkalemia
metabolic acidosis
permanent kidney damage
death

113
Q

How does AKI cause pulmonary edema?

A

pulmonary epithelial Na, K-ATPase, ENaC and aquaporin 5 are downregulated in AKI = decrease transport of fluids out of alveoli, and may decrease pulmonary secretion
can lead to pulmonary infection

114
Q

how is pulmonary edema different in kidney injury versus in kidney failure?

A

in kidney injury: non-hydrostatic pulmonary edema
in kidney failure: hydrostatic pulmonary edema

115
Q

why can AKI cause anemia?

A

The kidneys make erythropoietin –> loss of function = less erythropoietin

116
Q

why can AKI cause hyperkalemia?

A

distal tubule/collecting duct is the target for aldosterone which would normally cause Na reabsorption and K excretion
less K excretion = more K in blood

117
Q

why can AKI cause metabolic acidosis

A

proximal tubule can get damaged meaning it can no longer produce bicarbonate to maintain pH balance

118
Q

What are some risk factors of AKI?

A

hospitalisation
aging
CV disease
HTN
diabetes
kidney diseases
certain cancers and cancer treatments
drugs

119
Q

what is the preventative strategy put in place to prevent AKI in patients undergoing chemotherapy?

A

pre-hydration and allopurinol a few days before chemo

120
Q

what is the main treatment of AKI?

A

supportive – maintain fluid and electrolyte levels

121
Q

What is the key to therapy of AKI?

A

maintaining adequate renal perfusion and avoiding hypervolemia

122
Q

how can we treat the complications of AKI before the kidneys are able to recover?

A

balance body fluid levels
control K levels
restore blood Ca level
remove toxins via dialysis

123
Q

how is hyper and hypovolemia treated

A

hypervolemia – diuretics
hypovolemia – IV fluids

124
Q

why is it important to prevent hyperkalemia? how can we prevent it?

A

can cause arrhythmias
Ca2+ wont reduce K level but will reduce risk of arrhythmias
glucose and sodium polystyrene sulfonate

125
Q

what is dialysis?

A

performs the normal function of the kidney: removes toxins, waste and extra fluid from the blood

126
Q

what are the 2 kinds of dialysis?

A

hemodialysis and peritoneal dialysis

127
Q

what is hemodialysis

A

uses a hemodialyzer
blood is removed from the body and filtered by the hemodialyzer
filtered blood is then returned to the body
uses vascular access

128
Q

what are the 3 kinds of hemodialysis? which one is preferred?

A

AV fistula – preferred
AV graft
vascular access catheter

129
Q

what is an AV fistula for dialysis?

A

connect artery and vein together via surgery

130
Q

what is an AV graft for dialysis?

A

a tube is surgically put in to connect your artery and vein

131
Q

what is vascular access catheter for dialysis?

A

a catheter is placed into the vein – not permanent

132
Q

what are the advantages and disadvantages of AV fistula?

A

advantages: speeds up dialysis, and less likely to get infection or clot – also permanent

disadvantages: needs 3-4 mo. to fully mature so cannot use if needed immediately; cannot be done on small weak vessels

133
Q

what are some advantages and disadvantages of AV graft?

A

advantages: less recovery time and good for people with small weak veins

disadvantages: increase risk for infection and clot and have to replace

134
Q

what are some advantages and disadvantages of vascular access catheter?

A

advantage: faster, dont have to wait at all, can do immediately in an emergency

disadvantages: easy to get infection and clots and not permanent
if you use this method too many times you will damage the vein

135
Q

what is peritoneal dialysis?

A

dialysis fluid is flowed from a bag into the peritoneal cavity via a catheter
the lining of the peritoneum acts as a filter
the dialysis solution absorbs waste and extra fluid and after several hours, the solution with the wastes is drained into an empty bag

136
Q

when is peritoneal dialysis used?

A

when the kidneys are no longer functional at all

137
Q

what are the 2 kinds of peritoneal dialysis and what is the difference?

A

continuous ambulatory peritoneal dialysis (CAPD) and automatic peritoneal dialysis

automatic happens at night when the patient is sleeping and does not require gravity
CAPD is done 3-4x a day and requires gravity

138
Q

what class of drug is chlorothiazide?

A

thiazide diuretic

139
Q

what class of drug is hydrochlorothiazide?

A

thiazide diuretic

140
Q

what class of drug is chlorothalidone?

A

thiazide diuretic

141
Q

what class of drug is indapamide?

A

thiazide diuretic

142
Q

what class of drug is furosemide?

A

loop diuretic

143
Q

what class of drug is torsemide?

A

loop diuretic

144
Q

what class of drug is bumetanide?

A

loop diuretic

145
Q

what class of drug is ethacrynic acid?

A

loop diuretic

146
Q

what class of drug is amiloride?

A

ENaC blocking K-sparing diuretic

147
Q

what class of drug is triamterene?

A

ENaC blocking K-sparing diuretic

148
Q

what class of drug is spironolactone?

A

aldosterone receptor antagonizing K-sparing diuretic

149
Q

what class of drug is eplerenone?

A

aldosterone receptor antagonizing K-sparing diuretic

150
Q

what class of drug is mannitol?

A

osmotic diuretic

151
Q

what class of drug is isosorbide?

A

osmotic diuretic

152
Q

what class of drug is urea?

A

osmotic diuretic

153
Q

when are diuretics used in kidney disease?

A

when kidneys are still functional – not in ESRD

154
Q

what is the mechanism of action of thiazide diuretics?

A

inhibit thiazide sensitive NaCl cotransporters

155
Q

where do thiazide diuretics work?

A

distal convoluted tubule

156
Q

what are some side effects of thiazide diuretics

A

hypovolemia (orthostatic hypertension, dizziness)
hyperglycemia
tinnitus
photosensitivity
GI disturbances

157
Q

what is the primary use of thiazide diuretics?

A

hypertension

158
Q

what is the MOA of loop diuretics?

A

blocks luminal Na/K/2Cl cotransporter

159
Q

where do loop diuretics work?

A

ascending loop of Henle (not descending)

160
Q

what are the primary uses of loop diuretics?

A

acute pulmonary edema, congestive heart failure, AKI

161
Q

what are some side effects of loop diuretics?

A

electrolyte imbalances
hypotension
ototoxicity
hyperuricemia (gout)
hyperglycemia
increase serum TG
increase LDL-cholesterol
muscle cramps

162
Q

where do K-sparing diuretics work?

A

collecting duct

163
Q

what is the MOA of ENaC blocking K-sparing diuretics?

A

block amiloride-sensitive ENaC epithelial Na channels

164
Q

what is the MOA if aldosterone receptor antagonizing diuretics?

A

antagonizes aldosterone receptor blocking Na reabsorption and K+ excretion

165
Q

what is the primary use of K sparing diuretics>

A

for people at risk of low K levels

166
Q

what are some side effects of K-sparing diuretics?

A

hyperkalemia
muscle cramps

spironolactone: diarrhea, cramping, gastritis, abnormal liver function, androgenic effects, gynecomastia in males

amiloride: abdominal pain, loss of appetite, rash

167
Q

what is the MOA of osmotic diuretics?

A

produce osmotic gradient and retain water in the tubules which is then freely filtered at glomerulus
limited reabsorption in renal tubules

168
Q

where do osmotic diuretics work?

A

proximal tubules, descending loop of Henle, and collecting duct

169
Q

what are some side effects of osmotic diuretics?

A

electrolyte depletion
headache
nausea/vomiting
blurred vision
dizziness
may worsen CHF or pulmonary edema initially but improves

170
Q

what are the cancers with the highest risk of AKI?

A

kidney, multiple myeloma, liver, bladder and leukemia

171
Q

what is the treatment plan for patients with cancer and AKI?

A

prognosis very poor
initiation of dialysis
identifying underlying cause of AKI

172
Q

What is CKD defined as?

A

abnormalities in kidney structure or function (death of nephrons) present for 3 months or longer and with implications for health

173
Q

what is classification of CKD based off of?

A

GFR and albuminuria (proteinuria)

174
Q

What are some risk factors of CKD?

A

diabetes
HTN
heart and blood vessel disease
obesity
family history of kidney disease
abnormal kidney structure
older age
smoking

175
Q

When can CKD be diagnosed without signs of kidney damage (proteinuria)?

A

if GFR < 60 mL/min for at least 3 months

176
Q

When can CKD be diagnosed with evidence of kidney damage (proteinuria)?

A

if GFR ≥60 mL/min and proteinuria is present for at least 3 months

177
Q

what are the signs and symptoms of stage G1-G3a CKD?

A

no symptoms are observed

178
Q

What is the treatment of stage G1/G2 CKD?

A

try to identify cause and try to reverse it
monitor albumin and GFR

179
Q

what is the treatment of stage G3a CKD?

A

monitor albumin and GFR, BP, general health and well being
try to stop or slow down the worsening of kidney function

180
Q

what are the signs and symptoms of stage G3b CKD?

A

early symptoms may occur but not necessarily
tiredness, poor appetite and itching

181
Q

what is the treatment for stage G3b CKD?

A

monitor albumin and GFR, BP, general health and wellbeing
try to stop or slow down the worsening of kidney function
learn more about CKD and treatment options

182
Q

what are the signs and symptoms of stage G4 CKD?

A

tiredness, poor appetite, itching may get worse

183
Q

what is the treatment for stage G4 CKD?

A

monitor albumin and GFR, and continue to try to stop or slow down the worsening of kidney function
discuss and plan for treatment choice: dialysis access, assessment for transplant, or information on non-dialysis supportive care

184
Q

what are the signs and symptoms of kidney failure?

A

severe fatigue, nausea, difficulty breathing and itchiness

185
Q

what is the treatment of kidney failure?

A

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

186
Q

What is the normal rate of decline in kidney function?

A

1 mL/min every year after 20

187
Q

what is the average GFR of a 20 year old?

A

120 mL/min

188
Q

what does the progression of CKD depend on?

A

the cause of CKD
GFR at time of diagnosis
degree of albuminuria
presence of comorbid conditions

189
Q

what percent of nephrons can be lost without any symptoms?

A

50% (why you can live with 1 kidney)
if 80% are lost some azotemia occurs but could still be asymptomatic

190
Q

what are the 2 markers of waste accumulation in CKD?

A

creatinine and urea
many other toxins and wastes are also present but arent tested for

191
Q

what are some signs and symptoms of toxin accumulation in CKD?

A

symptoms: fatigue, weakness, shortness of breath, mental confusion, nausea and vomiting, bleeding, loss of appetite, itching, cold intolerance, and peripheral neuropathies

sings: edema, weight gain, changes in urine output, “foaming” of urine, and abdominal distension

192
Q

why can CKD cause hypertension?

A

retention of Na and therefore increase in BP

193
Q

when do thiazide diuretics lose their effectiveness and why?

A

if GFR < 30 mL/min

distal tubules no longer present

194
Q

why can loop diuretics cause ototoxicity?

A

2 isoforms of receptor they act at: 1 is only in the kidney, but isoform 2 is everywhere else but especially in the ear

195
Q

what can you see on a renal ultrasound in ESRD?

A

can see structure changes i.e. dont see tubules

196
Q

what are the 2 main causes of ERSD?

A

diabetes and HTN

197
Q

what is glomerulonephritis?

A

kidney issue that causes death of kidney cells

198
Q

what is cystic kidney?

A

genetic condition that causes cyst build up on kidneys

199
Q

when is a kidney transplant the most effective?

A

stage 4
best to transplant before ERSD – lower risk of rejection and avoidance of dialysis

200
Q

why does HTN cause CKD?

A

higher pressure everywhere means more pressure against the glomerulus meaning it has to work harder which eventually leads to hypertrophy
elevated angiotensin II may promote tissue remodelling over time

201
Q

what are first line treatment in HTN with CKD?

A

ACEI and ARBS

202
Q

How does diabetes lead to CKD?

A

glycated products (sugar coated molecules) damage kidney structure directly

203
Q

What changes are make in the glomerulus structure in diabetes?

A

foot processes are gone
more mesangial cells present
distortion in structure of the capillary loop
glomerular basement membrane is thicker

204
Q

what is the leading cause of death in CKD patients?

A

cardiovascular disease

205
Q

what 2 trials proved the efficacy of ACEI and ARBS in CKD?

A

RENAAL and IDNT

206
Q

At what point of CKD are ACEI and ARBS considered effective?

A

benefit increases in people with more serious disease
in lower risk people other drugs have similar protection
most beneficial when SCR and proteinuria are advances (e.g. approaching stage 5)

207
Q

when does hyperkalemia become a serious problem in CKD?

A

when GFR falls below 5 mL/min

208
Q

how does sodium polystyrene sulfonate treat hyperkalemia? (MOA)

A

binds K in GIT (exchanges for Na+)

209
Q

when is sodium/calcium polystyrene sulfonate used?

A

NOT IN EMERGENCY SITUATIONS
takes days for onset of action so used for low level and unserious hyperkalemia

210
Q

how does calcium polystyrene sulfonate treat hyperkalemia? (MOA)

A

binds K in GIT (exchanges for Ca2+)

211
Q

what is the difference between calcium polystyrene sulfonate and sodium polystyrene sulfonate?

A

one replaces K with Ca and other replaces with Na

1 Ca exchanges for 2 K versus 1 Na or for 1 K

212
Q

what is used to treat emergency hyperkalemia?

A

dialysis

213
Q

what is the majority of the acid produced through metabolism?

A

CO2

214
Q

what does anaerobic glycolysis produce?

A

lactic acid

215
Q

how is lactic acid eliminated from the body?

A

either via kindeys or can be reconverted to pyruvate

216
Q

what does fatty acid oxidation produce?

A

ketones

217
Q

how are ketones eliminated from the body?

A

via kidneys

218
Q

what are the 2 ways that H+ is eliminated?

A
  1. secretion of H+ ions into lumen directly
  2. combines with ammonia (NH3) from protein metabolism to form ammonium (NH4+)
219
Q

how is urea formed?

A

circulating NH3 molecules are combined with CO2 in the liver
makes ammonia less toxic

220
Q

what is the major excreted N waste source?

A

urea

221
Q

what is the pH, PaCO2, and HCO3 in respiratory acidosis?

A

pH decreased
PaCO2 increased
HCO3 normal

222
Q

what is the pH, PaCO2, and HCO3 in respiratory alkalosis?

A

pH increased
PaCO2 decreased
HCO3 normal

223
Q

what is the pH, PaCO2, and HCO3 in metabolic acidosis?

A

pH decreased
PaCO2 normal
HCO3 decreased

224
Q

what is the pH, PaCO2, and HCO3 in metabolic alkalosis?

A

pH increased
PaCO2 normal
HCO3 increased

225
Q

what is the main cause of metabolic alkalosis?

A

antacid overuse

226
Q

when is metabolic acidosis considered a problem in CKD?

A

when GFR < 20 mL/min

227
Q

at is used to treat metabolic acidosis?

A

bicarbonate (antacids, sodium bicarbonate)

228
Q

what is the main risk associated with treatment of metabolic acidosis in CKD?

A

sodium load

229
Q

what is the active form of vitamin D and where is it made?

A

Calcitriol (1,25 dihydroxy vitamin D)
kidney

230
Q

what is the connection between CKD and vitamin D?

A

vitamin D is converted to tis active form in the kidney
therefore if kidney function decreases, so does vitamin D level

231
Q

in addition to low serum calcium, what does the kidneys also fail to excrete in CKD?

A

phosphate

232
Q

management strategies for Ca/phosphate disorders in CKD?

A

decrease phosphorous in diet
phosphate binding agents such as Sevelamer
Calcitriol

233
Q

if Ca2+ levels fall in the body, what happens?

A

parathyroid gland secretes PTH

234
Q

what are the effects of PTH in the kidney?

A

promote renal tubular calcium reabsorption
promote phosphate excretion
stimulates production of calcitriol

235
Q

what are the effects of PTH in the bones?

A

promotes catabolism of bone to release calcium and phosphorous in bloodstream

236
Q

what happens to bones in CKD?

A

when Ca2+ levels decrease, PTH is released to promote Ca reabsorption in the kidney
if kidney nonfunctional, PTH decomposes bones to release Ca and P
= bone loss

237
Q

what is the treatment for CKD caused anemia?

A

exogenous EPO

238
Q

what does EPO do?

A

stimulates the bone marrow to produce more RBC

239
Q

when does anemia typically begin in CKD?

A

when GFR falls below 30-45 mL/min (stage 3b)
seen in virtually all ERSD patients

240
Q

what are the two EPO replacements?

A

Epoetin alfa (Eprex)
Darbepoetin alfa (Aranesp)

241
Q

what is the difference between Epoetin alpha and Darbepoetin alpha?

A

Epoetin is lab produced APO
Darbepoetin amino acids have been modified so that it has a longer duration of action

242
Q

what are some adverse events that can occur with increasing RBC production?

A

hypertension or thrombosis

PHAR 123 (2 decks)

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