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
2
Q
Why is kidney disease typically silent until advanced?
A
No pain receptors in the kidneys so pain is not usually present
3
Q
What is one instance where you may feel kidney pain?
A
Kidney stones
Not kidney pain however; ureter pain
4
Q
What part of the kidney collects the filtrate?
A
Bowman’s capsule – drains into urine
5
Q
What part of the kidney collects reabsorbed nutrients?
A
arteries – goes into the veins
6
Q
What is a normal GFR?
A
100-120 mL/min
7
Q
What size of molecules can be filtered at the glomerulus
A
small molecules < 70 kDa
8
Q
What happens to larger molecules at the glomerulus?
A
cannot be filtered and therefore go back into the blood
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
10
Q
How much nutrients are reabsorbed at the proximal tubule?
A
60-70% of Na+, almost all K+ and glucose
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)
12
Q
How much filtrate is delivered to the loop of Henle?
A
30 mL/min
13
Q
What occurs at the descending loop of Henle?
A
permeable for water and therefore water is reabsorbed
14
Q
What occurs at the ascending loop of Henle?
A
not permeable for water and therefore Na+ is reabsorbed
15
Q
How much filtrate is delivered to the collecting duct?
A
5-10 mL/min (about 5-10%)
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+
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
18
Q
What regulates K+ excretion
A
K+ levels in the blood
low levels = less excretion of K+ to maintain levels
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
20
Q
Approximately how much filtrate (urine) enters the ureters and into bladder?
A
1-2 mL/min
98-99% reabsorption rate
21
Q
Where are drugs and toxins secreted from in the kidney?
A
Proximal tubule
22
Q
4 types of transporters in the renal proximal tubule
A
anionic
cationic
peptide/hormone
ABC
23
Q
Which type of transporter is responsible for conferring drug resistance?
A
ABC transporter
24
Q
What channel do thiazide diuretics inhibit?
A
NCCs
25
What channel do potassium sparing diuretics inhibit?
ENaCs
26
What is the most commonly used marker of kidney function?
serum creatinine
27
What is normal serum creatinine?
0.9-1.3 mg/dL
28
What is the normal cycle of creatinine?
Produced daily by muscles as a part of metabolism
easily filtered so level does not typically change
29
If GFR decreases, how does this affect serum creatinine and why?
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
30
What may be the problem with using serum creatinine in someone with a low muscle mass
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
31
What factors does the Cockroft-Gault equation take into account?
age, ideal body weight, gender
serum creatinine
32
What factors does the MDRD equation take into account?
age, gender, race
serum creatinine
33
How do we estimate ideal body weight?
5'0" man = 50 kg; 5'0" woman = 45 kg
add 2.3 kg for every inch above 5'0"
34
Why do some drugs need to be adjusted based on renal function?
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
35
What 3 factors influence whether drugs are renally excreted?
Water solubility
Protein binding
Tubular secretion (excretion)
36
How is water solubility a factor in determining if a drug is renally excreted?
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
37
How is protein binding a factor in determining if a drug is renally excreted?
drugs that are highly bound to plasma proteins are less likely to be filtered therefore more will stay in the blood
38
How is tubular secretion a factor in determining if a drug is renally excreted?
tubular secretion = excretion
some drugs are concentrated in the urine by active secretion rather than filtration
39
What does stage 1 kidney disease mean and what GFR is needed for a diagnosis?
kidney damage with a normal GFR
≥ 90
40
What does stage 2 kidney disease mean and what GFR is needed for a diagnosis?
kidney damage with mild GFR
89-60
41
What does stage 3a kidney disease mean and what GFR is needed for a diagnosis?
mild to moderate GFR
59-45
42
What does stage 3b kidney disease mean and what GFR is needed for a diagnosis?
moderate GFR
45-30
43
What does stage 4 kidney disease mean and what GFR is needed for a diagnosis?
severe GFR
30-15
44
What does stage 5 kidney disease mean and what GFR is needed for a diagnosis?
kidney failure
< 15 or dialysis
45
TRUE OR FALSE
proteinuria can be elevated even without a decrease in GFR
TRUE
46
what is albuminuria?
Albumin in the urine
more sensitive marker for kidney disease than total protein
47
what is considered microalbuminuria?
30-300 mg/d
48
what is considered macroalbuminuria?
>300 mg/d
49
What is eGFR based on?
serum creatinine
50
What is ACR based on?
creatinine in the urine
51
what is ACR?
albumin/creatinine ratio
simple spot urine test that accurately predicts microalbuminuria
52
what is A1 and what are the numbers?
normal to mildly increased albuminuria
< 30 mg/g
53
what is A2 and what are the numbers?
moderately increased albuminuria
30-300 mg/g (microalbuminuria)
54
what is A3 and what are the numbers?
severely increased albuminuria
> 300 mg/g
55
According to the ACR/eGFR chart:
what is considered "green" and what does this mean?
G1/A1 or G2/A1
everything is okay -- no dose adjustment is needed
56
According to the ACR/eGFR chart:
what is considered "yellow" and what does this mean?
G1/A2, G2/A2 or G3a/A1
dose adjustment is needed
57
According to the ACR/eGFR chart:
what is considered "orange" and what does this mean?
G1/A3, G2/A3, G3a/A2 or G3b/A1
dose adjustment is needed
58
According to the ACR/eGFR chart:
what is considered "red" and what does this mean?
G3a/A3, G3b/A2-A3 or anything G4 or G5
we cannot do anything here -- patient should be in the hospital
59
what can urinalysis tell us about kidney function?
can only tell us that something is wrong somewhere
60
what tests confirm kidney damage?
imaging
x-ray, CT, MRI, ultrasound
61
when is a biopsy done in AKI?
once damage has been confirmed by imaging
62
what 4 factors in a urinalysis test are associated with kidney damage?
specific gravity
protein
epithelial cells
casts
63
what is required in order to be diagnosed with AKI?
rise in SCr by >25uM within 48h
AND/OR
decrease in urine output to <0.5 mL/kg/h for at last 6h
64
what is azotemia?
rapidly rising BUN
BUN = blood urea nitrogen
65
TRUE OR FALSE
CKD patients are more susceptible to AKI
true
66
Signs and symptoms of AKI
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
67
What are the most common causes of community-acquired AKI?
volume depletion (N,D)
medication ADRs
kidney stress
68
What are the most common causes of hospital-acquired AKI?
sepsis
major surgery
critical illness involving heart or liver failure
IV contrast agents
medication ADRs
69
What is pre-renal azotemia?
Damage causing AKI happens before the kidneys
decrease in glomerular pressure impairs function of tubules causing accumulation of waste in the blood (azotemia)
70
What are some causes of pre-renal azotemia?
reduced cardiac output
severe volume depletion
reno-vascular disease
medication ADRs
71
How does reduced cardiac output cause AKI?
need pressure to cross the glomerulus --> when flow rate decreases, pressure decreases and therefore GFR decreases if something were to happen
72
How does severe volume depletion cause AKI?
decrease blood to glomerulus and therefore decrease GFR
73
How does renal artery stenosis lead to AKI?
blocks the flow of blood to the kidneys and therefore decreased GFR
74
What 3 markers are used to determine AKI?
decreased GFR
increased BUN
increased SCr
75
how do medications cause AKI and what is an example?
NSAIDs
2 mechanisms: decrease renal blood flow OR direct injury (interstitial nephritis) therefore causing apoptosis and necrosis
76
What is intra-renal damage defined as?
direct damage to glomerulus, tubules, or renal vessels
77
What is the most common cause of chronic injury to the glomerulus?
longstanding glomerular pressure
often seen in HTN and DM
78
What is immune mediated glomerular injury?
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)
79
How does Cisplatin cause AKI?
how do you lower the risk of AKI with this drug?
accumulates in proximal tubules causing direct toxicity
pre-hydration (to dilute drug in tubules) decreases the risk of AKI
80
What is rhabdomyolysis
a syndrome resulting from the release of myoglobin from muscles into the bloodstream
81
How can rhabdomyolysis cause AKI?
myoglobin can precipitate in renal tubules which halts tubular flow (blocks tubules) leading to tubular cell necrosis
82
What are some symptoms of rhabdomyolysis
muscle pain/weakness, malaise, dark urine
myoglobin concentration very high
83
What can cause rhabdomyolysis?
traumatic/crush injuries
non-traumatic muscle compression, prolonged immobility
exertional (esp in untrained people and hyperthermia)
drugs/toxins (statins)
84
What is interstitial nephritis
drug related
occurs when spaces between tubules become inflamed --> spreads to tubules but spares the glomeruli
often called "hypersensitivity" reactions
85
How does ASCVD cause AKI?
decrease blood flow in large vessels due to plaques means decrease GFR
86
TRUE OR FALSE
AKI always causes CKD?
false
can be reversible if treated soon enough
87
What are the 2 main causes of kidney stones
hypercalciuria (calcium rich stones)
hyperuricosuria (uric acid stones)
88
what group of people are more likely to get uric acid stones over calcium stones?
patients with a history of gout
89
How can kidney stones cause damage to the kidneys?
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
90
what causes kidney stones?
caused from alterations in the solubility of various substances in the urine
91
symptoms of kidney stones
stone formation is typically painless but renal damage and hematuria can occur
pain is due to distension of ureter as stone travels down
92
what are some risk factors for developing kidney stones?
dehydration
protein intake
increased Na+ intake
93
how does high protein intake lead to formation of kidney stones?
increases blood and urine acidity leading to Ca or uric acid stones
94
TRUE OR FALSE
increased Ca intake is likely to cause kidney stones
false
no evidence to show that high Ca in the diet causes kidney stones
95
what is the treatment for small kidney stones?
fluids, bed rest, and analgesia
96
what do the different letters mean in the RIFLE classification (just the description)
Risk of renal dysfunction
Injury to the kidneys
Failure of kidney function
Loss of kidney function
End-stage renal disease (ESRD)
97
What is the GFR and UO criteria for risk in RIFLE?
increase in SCr >1.5x baseline OR decrease of GFR >50%
UO <0.5mL/kg/h x 6h
98
What is the GFR and UO criteria for injury in RIFLE?
increase in SCr >2.0x baseline OR decrease of GFR >50%
UO <0.5mL/kg/h x 12h
99
What is the GFR and UO criteria for failure in RIFLE?
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
What is the criteria for loss in RIFLE?
persistent ARF = complete loss of renal function for more than 4 weeks
101
What are some strengths of RIFLE?
broadly validated in incidence identification
provided good prognostic accuracy
strongly correlated with length of hospitalisation stay, RRT requirement, etc.
102
what are some weaknesses of RIFLE?
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
What are the AKIN criteria stages RIFLE equivalents?
stage 1 = R
stage 2 = I & F
stage 3 = L & E
104
What is the GFR and UO criteria for Stage 1 in AKIN criteria?
increase SCr >1.5-2.0x baseline or increase SCr ≥ 0.3 mg/dL within 48h
UO < 0.5mL/kg/h x 6h
105
What is the GFR and UO criteria for Stage 2 in AKIN criteria?
increase SCr >2.0-3.0x baseline
UO < 0.5mL/kg/h x 12h
106
What is the GFR and UO criteria for Stage 3 in AKIN criteria?
increase SCr >3.0x baseline or SCr ≥4mg/dL or dialysis
UO < 0.3 mL/kg/h x 24h or anuria x 12h
107
What are strengths of AKIN critera?
added etiological information
solely based on SCr changes, not GFR
108
What are some limitations of AKIN criteria?
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
what is required in order to be eligible for a renal needle biopsy?
1) blood in urine
2) protein in urine
3) increase level of toxins in the blood
110
what can be used to diagnose AKI?
urine output test
urinalysis
blood test
imaging (x-ray, CT, MRI, ultrasounds)
biopsy
111
What is the advantage and disadvantage of open kidney biospy?
advantage: better in diagnosing
disadvantage: more invasive
112
What are some complications of AKI?
pulmonary edema
anemia
chest pain
muscle weakness
hyperkalemia
metabolic acidosis
permanent kidney damage
death
113
How does AKI cause pulmonary edema?
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
how is pulmonary edema different in kidney injury versus in kidney failure?
in kidney injury: non-hydrostatic pulmonary edema
in kidney failure: hydrostatic pulmonary edema
115
why can AKI cause anemia?
The kidneys make erythropoietin --> loss of function = less erythropoietin
116
why can AKI cause hyperkalemia?
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
why can AKI cause metabolic acidosis
proximal tubule can get damaged meaning it can no longer produce bicarbonate to maintain pH balance
118
What are some risk factors of AKI?
hospitalisation
aging
CV disease
HTN
diabetes
kidney diseases
certain cancers and cancer treatments
drugs
119
what is the preventative strategy put in place to prevent AKI in patients undergoing chemotherapy?
pre-hydration and allopurinol a few days before chemo
120
what is the main treatment of AKI?
supportive -- maintain fluid and electrolyte levels
121
What is the key to therapy of AKI?
maintaining adequate renal perfusion and avoiding hypervolemia
122
how can we treat the complications of AKI before the kidneys are able to recover?
balance body fluid levels
control K levels
restore blood Ca level
remove toxins via dialysis
123
how is hyper and hypovolemia treated
hypervolemia -- diuretics
hypovolemia -- IV fluids
124
why is it important to prevent hyperkalemia? how can we prevent it?
can cause arrhythmias
Ca2+ wont reduce K level but will reduce risk of arrhythmias
glucose and sodium polystyrene sulfonate
125
what is dialysis?
performs the normal function of the kidney: removes toxins, waste and extra fluid from the blood
126
what are the 2 kinds of dialysis?
hemodialysis and peritoneal dialysis
127
what is hemodialysis
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
what are the 3 kinds of hemodialysis? which one is preferred?
AV fistula -- preferred
AV graft
vascular access catheter
129
what is an AV fistula for dialysis?
connect artery and vein together via surgery
130
what is an AV graft for dialysis?
a tube is surgically put in to connect your artery and vein
131
what is vascular access catheter for dialysis?
a catheter is placed into the vein -- not permanent
132
what are the advantages and disadvantages of AV fistula?
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
what are some advantages and disadvantages of AV graft?
advantages: less recovery time and good for people with small weak veins
disadvantages: increase risk for infection and clot and have to replace
134
what are some advantages and disadvantages of vascular access catheter?
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
what is peritoneal dialysis?
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
when is peritoneal dialysis used?
when the kidneys are no longer functional at all
137
what are the 2 kinds of peritoneal dialysis and what is the difference?
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
what class of drug is chlorothiazide?
thiazide diuretic
139
what class of drug is hydrochlorothiazide?
thiazide diuretic
140
what class of drug is chlorothalidone?
thiazide diuretic
141
what class of drug is indapamide?
thiazide diuretic
142
what class of drug is furosemide?
loop diuretic
143
what class of drug is torsemide?
loop diuretic
144
what class of drug is bumetanide?
loop diuretic
145
what class of drug is ethacrynic acid?
loop diuretic
146
what class of drug is amiloride?
ENaC blocking K-sparing diuretic
147
what class of drug is triamterene?
ENaC blocking K-sparing diuretic
148
what class of drug is spironolactone?
aldosterone receptor antagonizing K-sparing diuretic
149
what class of drug is eplerenone?
aldosterone receptor antagonizing K-sparing diuretic
150
what class of drug is mannitol?
osmotic diuretic
151
what class of drug is isosorbide?
osmotic diuretic
152
what class of drug is urea?
osmotic diuretic
153
when are diuretics used in kidney disease?
when kidneys are still functional -- not in ESRD
154
what is the mechanism of action of thiazide diuretics?
inhibit thiazide sensitive NaCl cotransporters
155
where do thiazide diuretics work?
distal convoluted tubule
156
what are some side effects of thiazide diuretics
hypovolemia (orthostatic hypertension, dizziness)
hyperglycemia
tinnitus
photosensitivity
GI disturbances
157
what is the primary use of thiazide diuretics?
hypertension
158
what is the MOA of loop diuretics?
blocks luminal Na/K/2Cl cotransporter
159
where do loop diuretics work?
ascending loop of Henle (not descending)
160
what are the primary uses of loop diuretics?
acute pulmonary edema, congestive heart failure, AKI
161
what are some side effects of loop diuretics?
electrolyte imbalances
hypotension
ototoxicity
hyperuricemia (gout)
hyperglycemia
increase serum TG
increase LDL-cholesterol
muscle cramps
162
where do K-sparing diuretics work?
collecting duct
163
what is the MOA of ENaC blocking K-sparing diuretics?
block amiloride-sensitive ENaC epithelial Na channels
164
what is the MOA if aldosterone receptor antagonizing diuretics?
antagonizes aldosterone receptor blocking Na reabsorption and K+ excretion
165
what is the primary use of K sparing diuretics>
for people at risk of low K levels
166
what are some side effects of K-sparing diuretics?
hyperkalemia
muscle cramps
spironolactone: diarrhea, cramping, gastritis, abnormal liver function, androgenic effects, gynecomastia in males
amiloride: abdominal pain, loss of appetite, rash
167
what is the MOA of osmotic diuretics?
produce osmotic gradient and retain water in the tubules which is then freely filtered at glomerulus
limited reabsorption in renal tubules
168
where do osmotic diuretics work?
proximal tubules, descending loop of Henle, and collecting duct
169
what are some side effects of osmotic diuretics?
electrolyte depletion
headache
nausea/vomiting
blurred vision
dizziness
may worsen CHF or pulmonary edema initially but improves
170
what are the cancers with the highest risk of AKI?
kidney, multiple myeloma, liver, bladder and leukemia
171
what is the treatment plan for patients with cancer and AKI?
prognosis very poor
initiation of dialysis
identifying underlying cause of AKI
172
What is CKD defined as?
abnormalities in kidney structure or function (death of nephrons) present for 3 months or longer and with implications for health
173
what is classification of CKD based off of?
GFR and albuminuria (proteinuria)
174
What are some risk factors of CKD?
diabetes
HTN
heart and blood vessel disease
obesity
family history of kidney disease
abnormal kidney structure
older age
smoking
175
When can CKD be diagnosed without signs of kidney damage (proteinuria)?
if GFR < 60 mL/min for at least 3 months
176
When can CKD be diagnosed with evidence of kidney damage (proteinuria)?
if GFR ≥60 mL/min and proteinuria is present for at least 3 months
177
what are the signs and symptoms of stage G1-G3a CKD?
no symptoms are observed
178
What is the treatment of stage G1/G2 CKD?
try to identify cause and try to reverse it
monitor albumin and GFR
179
what is the treatment of stage G3a CKD?
monitor albumin and GFR, BP, general health and well being
try to stop or slow down the worsening of kidney function
180
what are the signs and symptoms of stage G3b CKD?
early symptoms may occur but not necessarily
tiredness, poor appetite and itching
181
what is the treatment for stage G3b CKD?
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
what are the signs and symptoms of stage G4 CKD?
tiredness, poor appetite, itching may get worse
183
what is the treatment for stage G4 CKD?
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
what are the signs and symptoms of kidney failure?
severe fatigue, nausea, difficulty breathing and itchiness
185
what is the treatment of kidney failure?
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
What is the normal rate of decline in kidney function?
1 mL/min every year after 20
187
what is the average GFR of a 20 year old?
120 mL/min
188
what does the progression of CKD depend on?
the cause of CKD
GFR at time of diagnosis
degree of albuminuria
presence of comorbid conditions
189
what percent of nephrons can be lost without any symptoms?
50% (why you can live with 1 kidney)
if 80% are lost some azotemia occurs but could still be asymptomatic
190
what are the 2 markers of waste accumulation in CKD?
creatinine and urea
many other toxins and wastes are also present but arent tested for
191
what are some signs and symptoms of toxin accumulation in CKD?
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
why can CKD cause hypertension?
retention of Na and therefore increase in BP
193
when do thiazide diuretics lose their effectiveness and why?
if GFR < 30 mL/min
distal tubules no longer present
194
why can loop diuretics cause ototoxicity?
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
what can you see on a renal ultrasound in ESRD?
can see structure changes i.e. dont see tubules
196
what are the 2 main causes of ERSD?
diabetes and HTN
197
what is glomerulonephritis?
kidney issue that causes death of kidney cells
198
what is cystic kidney?
genetic condition that causes cyst build up on kidneys
199
when is a kidney transplant the most effective?
stage 4
best to transplant before ERSD -- lower risk of rejection and avoidance of dialysis
200
why does HTN cause CKD?
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
what are first line treatment in HTN with CKD?
ACEI and ARBS
202
How does diabetes lead to CKD?
glycated products (sugar coated molecules) damage kidney structure directly
203
What changes are make in the glomerulus structure in diabetes?
foot processes are gone
more mesangial cells present
distortion in structure of the capillary loop
glomerular basement membrane is thicker
204
what is the leading cause of death in CKD patients?
cardiovascular disease
205
what 2 trials proved the efficacy of ACEI and ARBS in CKD?
RENAAL and IDNT
206
At what point of CKD are ACEI and ARBS considered effective?
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
when does hyperkalemia become a serious problem in CKD?
when GFR falls below 5 mL/min
208
how does sodium polystyrene sulfonate treat hyperkalemia? (MOA)
binds K in GIT (exchanges for Na+)
209
when is sodium/calcium polystyrene sulfonate used?
NOT IN EMERGENCY SITUATIONS
takes days for onset of action so used for low level and unserious hyperkalemia
210
how does calcium polystyrene sulfonate treat hyperkalemia? (MOA)
binds K in GIT (exchanges for Ca2+)
211
what is the difference between calcium polystyrene sulfonate and sodium polystyrene sulfonate?
one replaces K with Ca and other replaces with Na
1 Ca exchanges for 2 K versus 1 Na or for 1 K
212
what is used to treat emergency hyperkalemia?
dialysis
213
what is the majority of the acid produced through metabolism?
CO2
214
what does anaerobic glycolysis produce?
lactic acid
215
how is lactic acid eliminated from the body?
either via kindeys or can be reconverted to pyruvate
216
what does fatty acid oxidation produce?
ketones
217
how are ketones eliminated from the body?
via kidneys
218
what are the 2 ways that H+ is eliminated?
1. secretion of H+ ions into lumen directly
2. combines with ammonia (NH3) from protein metabolism to form ammonium (NH4+)
219
how is urea formed?
circulating NH3 molecules are combined with CO2 in the liver
makes ammonia less toxic
220
what is the major excreted N waste source?
urea
221
what is the pH, PaCO2, and HCO3 in respiratory acidosis?
pH decreased
PaCO2 increased
HCO3 normal
222
what is the pH, PaCO2, and HCO3 in respiratory alkalosis?
pH increased
PaCO2 decreased
HCO3 normal
223
what is the pH, PaCO2, and HCO3 in metabolic acidosis?
pH decreased
PaCO2 normal
HCO3 decreased
224
what is the pH, PaCO2, and HCO3 in metabolic alkalosis?
pH increased
PaCO2 normal
HCO3 increased
225
what is the main cause of metabolic alkalosis?
antacid overuse
226
when is metabolic acidosis considered a problem in CKD?
when GFR < 20 mL/min
227
at is used to treat metabolic acidosis?
bicarbonate (antacids, sodium bicarbonate)
228
what is the main risk associated with treatment of metabolic acidosis in CKD?
sodium load
229
what is the active form of vitamin D and where is it made?
Calcitriol (1,25 dihydroxy vitamin D)
kidney
230
what is the connection between CKD and vitamin D?
vitamin D is converted to tis active form in the kidney
therefore if kidney function decreases, so does vitamin D level
231
in addition to low serum calcium, what does the kidneys also fail to excrete in CKD?
phosphate
232
management strategies for Ca/phosphate disorders in CKD?
decrease phosphorous in diet
phosphate binding agents such as Sevelamer
Calcitriol
233
if Ca2+ levels fall in the body, what happens?
parathyroid gland secretes PTH
234
what are the effects of PTH in the kidney?
promote renal tubular calcium reabsorption
promote phosphate excretion
stimulates production of calcitriol
235
what are the effects of PTH in the bones?
promotes catabolism of bone to release calcium and phosphorous in bloodstream
236
what happens to bones in CKD?
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
what is the treatment for CKD caused anemia?
exogenous EPO
238
what does EPO do?
stimulates the bone marrow to produce more RBC
239
when does anemia typically begin in CKD?
when GFR falls below 30-45 mL/min (stage 3b)
seen in virtually all ERSD patients
240
what are the two EPO replacements?
Epoetin alfa (Eprex)
Darbepoetin alfa (Aranesp)
241
what is the difference between Epoetin alpha and Darbepoetin alpha?
Epoetin is lab produced APO
Darbepoetin amino acids have been modified so that it has a longer duration of action
242
what are some adverse events that can occur with increasing RBC production?
hypertension or thrombosis
