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PHAR123 > Acute Kidney Disease > Flashcards

Acute Kidney Disease Flashcards

1
Q

Describe the anatomy of the kidney.

A

we have two
back, below rib cage, behind peritoneum on both sides of the spine (T12-L3)
4-5 inches long (slightly larger than a fist)

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2
Q

Which structure of the kidney contains arteries, veins, and some nerves?

A

renal hilum
contains the renal vein, renal artery, and renal nerve

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3
Q

What are the major functions of the kidneys?

A

filter blood/excrete toxins (major function)
metabolize compounds
secrete hormones (endocrine functions)
maintain pH (HCO3) and electrolyte balance

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4
Q

What is a likely reason that kidney disease is usually silent until advanced?

A

no pain receptors in the kidney

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5
Q

What is an example of a rare occasion where kidney pain would be present without being in advanced stage of kidney disease?

A

kidney stones
-scratching the walls of the ureter

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6
Q

Describe blood flow through the kidney.

A
  1. renal artery (segmental artery, interlobar artery, arcuate
    artery, interlobular artery)
  2. afferent arteriole
  3. glomerulus
  4. efferent arteriole
  5. peritubular capillaries
  6. renal vein (interlobular vein, arcuate vein, interlobar vein)
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7
Q

What is the normal GFR?

A

100-120ml/min filtered into tubules

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8
Q

How long does it take to filter all of the blood in the body?

A

40-50 minutes (5L of blood)
kidneys are constantly working to remove waste

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9
Q

What size of molecules are filtered at the glomerulus?

A

small molecules (<70 kDa)
-glucose, ions, amino acids, proteins

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10
Q

Describe reabsorption at the proximal tubule.

A

substantial reabsorption of filtered material
60-70% of filtered Na+
almost all K+
almost all glucose
water reabsorbed passively along Na+ osmotic gradient

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11
Q

Describe reabsorption at the Loop of Henle.

A

30ml/min of filtrate delivered to the Loop
substantial Na+ and H20 reabsorption:
-Descending Limb: H20
-Ascending Limb: Na+

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12
Q

Describe reabsorption at the distal and collecting tubules.

A

water channels under control of vasopressin
-stimulates H20 reabsorption without Na+
target for aldosterone
-K+ excretion, Na+ reabsorption

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13
Q

Which part of the nephron plays a role in regulation of pH? How does it regulate pH?

A

distal and collecting tubules
respond toward acidosis by increasing H+ secretion and HCO3- generation

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14
Q

How much filtrate reaches the ureters?

A

1-2ml/min
thus, the reabsorption rate is ~99% (we started with 100-120ml/min)

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15
Q

Where does secretion occur in the nephron?

A

proximal tubule
-many transporters in the proximal tubule
-the transporters are uni or multi directional

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16
Q

Which transporters are involved in drug resistance?

A

ABC transporters

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17
Q

What is NCC?

A

thiazide-sensitive NaCl cotransporter

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18
Q

What is ENac?

A

amiloride-sensitive epithelial sodium channels
Na+ reabsorption at distal tubule

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19
Q

What is one of the most commonly used markers of kidney function/estimating GFR?

A

serum level of creatinine

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20
Q

What are normal serum creatinine levels?

A

0.9-1.3mg/dL

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21
Q

Describe creatinine.

A

produced daily by muscles as part of normal metabolism
easily filtered (levels dont rise unless GFR is reduced)

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22
Q

What would happen to serum creatinine levels as GFR decreases?

A

less creatinine is excreted
production by muscles continues
=serum creatinine rises

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23
Q

What is the issue of using serum creatinine as a measure of kidney function?

A

people with low muscle mass will generate less creatinine
thus, creatinine levels will appear normal when GFR is decreased

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24
Q

What is the equation which generates the creatinine clearance (CrCl) to estimate GFR?

A

Cockroft-Gault equation
CrCl= (140-age) x Ideal Body Weight (kg)/0.814 x Serum Creatinine (ug)
x 0.85 if female

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25
Q

What is the important concept of the Cockroft-Gault equation?

A

it converts serum creatinine level to an estimated GFR

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26
Q

How do we estimate ideal body weight?

A

For a 5’0’’ tall person:
-50kg for men
-45kg for women
add 2.3kg for every 1” taller than 5’0”

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27
Q

What is the MDRD equation?

A

modification of diet in renal disease
can be used to estimate GFR
GFR (ml/min/1.73m²)=175 x (Scr)-1.154 x (Age)-0.203 x (0.742 if female) x (1.212 if African American

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28
Q

What are the consequences of not performing necessary dosing adjustments if renal function is less than optimal?

A

regular doses will be excreted more slowly, leading to accumulation of drug in the body and risk for adverse drug reactions

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29
Q

What are the major factors determining whether drugs are renally-excreted?

A

water solubility
-highly soluble=exist freely in the bloodstream, fit through the
glomerulus easier
protein binding
-bound to plasma protein=less likely to be filtered
tubular secretion
-some drugs are concentrated in the urine by active secretion
rather than filtration

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30
Q

What are some drugs that are concentrated in the urine by active secretion rather than filtration?

A

metformin
furosemide
digoxin

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31
Q

What is the estimated GFR of each stage of CKD?

A

Stage 1 (kidney damage with normal or GFR): >90
Stage 2 (kidney damage with mild GFR): 89-60
Stage 3A (mild to moderate GFR): 59-45
Stage 3B (moderate GFR): 45-30
Stage 4 (severe GFR): 30-15
Stage 5 (kidney failure): <15 or dialysis

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32
Q

What is proteinuria?

A

protein in the urine
sign of kidney damage

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33
Q

What is a very common marker of dysfunction in patients with CKD?

A

proteinuria

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34
Q

True or false: proteinuria can ONLY be elevated with reduced GFR

A

false
can also be elevated without reduced GFR (damaged glomerulus)

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35
Q

What is a early marker of kidney disease?

A

low level of albumin in the urine

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36
Q

What are the levels for microalbuminuria? What about macroalbuminuria?

A

microalbuminuria: 30-300 mg/day
macroalbuminuria: >300 mg/day

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37
Q

What is the advantage of the albumin/creatinine ratio?

A

a simple spot urine test that accurately predicts microalbuminuria (more convenient than collecting urine for 24hrs)

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38
Q

True or false: albuminuria is a more sensitive marker than total protein

A

true

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39
Q

What are the ways to measure proteinuria?

A

urinalysis (most common)
X-ray
MRI
CT
ultrasounds
biopsy

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40
Q

What are the four components of urinalysis closely associated with kidney damage? What are their reference ranges?

A

specific gravity:
-reference range: 1.005-1.029
protein:
-reference range: negative
epithelial cells:
-reference range: 0-3/HPF
casts:
-reference range: 0-5/HPF

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41
Q

What is AKI? List off some characteristics of this state.

A

rapid deterioration of renal function within a few hours or a few days
typically diagnosed if either of the following occur:
-rise in SCr by more than 25 uM within 48hrs OR
-decrease in urine output to <0.5 ml/kg/hr for 6hrs
rapidly rising BUN/urea and SCr
diminished urine volume is common (but not necessary)
cause a build-up of waste products in the blood

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42
Q

What are some organs that can be affected by AKI?

A

brain
heart
lungs

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43
Q

What is the mechanism for developing AKI?

A

highly complex and overlapping
many mechanisms of AKI are possible

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44
Q

What are the chances of an individual drug causing AKI?

A

<1%

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45
Q

Who is more susceptible to AKI?

A

patients with CKD

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46
Q

What are the signs and symptoms of AKI?

A

too little urine leaving the body
swelling in legs, ankles, and around eyes
fatigue/tiredness
shortness of breath
confusion
nausea
seizure or coma in severe cases
chest pain or pressure

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47
Q

What are the causes of AKI?

A

pre-renal azotemia:
-reduced glomerular pressure impairing function of tubules
intrinsic renal parenchymal disease:
-direct damage to glomerulus, tubules, or renal vessels
postrenal obstruction:
-obstruction of urine outflow

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48
Q

What are some causes of pre-renal azotemia?

A

hypovolemia
decreased CO
decreased effective circulating volume (HF, liver failure)
impaired renal autoregulation (NSAIDs, ACEI/ARB, cyclosporine)

49
Q

What are some causes of intrinsic renal parenchymal disease?

A

glomerular: acute glomerulonephritis
tubules and interstitum: ischemia, sepsis/infection, toxins
vascular: vasculitis, malignant HTN, TTP-HUS

50
Q

What are the typical causes of community acquired cases of AKI?

A

volume depletion
medication ADRs
obstruction of the urinary tract

51
Q

What are the typical causes of hospital acquired cases of AKI?

A

sepsis
major surgical procedures
critical illness involving heart or liver failure
intravenously administered contrast agents
medication ADR

52
Q

What is the definition of pre-renal azotemia?

A

rise in urea (and SCr) from reduced glomerular pressure WITHOUT signs of tubular damage

53
Q

Can pre-renal azotemia be reversed?

A

completely reversible if addressed before damage occurs

54
Q

What occurs to GFR, SCr, and BUN in the following scenarios:
afferent vasoconstriction or reduced blood flow
reduced CO
severe volume depletion
reno-vascular disease

A

afferent vasoconstriction or reduced blood flow:
-GFR: decreases
-SCr: increases
-BUN: increases
reduced CO:
-GFR: decreases
-SCr: increases
-BUN: increases
severe volume depletion:
-GFR: decreases
-SCr: increases
-BUN: increases
reno-vascular disease:
-GFR: decreases
-SCr: increases
-BUN: increases

55
Q

How can NSAIDs cause AKI?

A

reduction or renal blood flow OR
direct injury (interstitial nephritis)

56
Q

What are some locations where intra-renal damage can occur?

A

glomerulus/glomerular structures
tubules or interstitial space
vascular conditions (capillaries)

57
Q

What is chronic injury to the glomerulus often a result of?

A

longstanding glomerular pressure along with other factors
MOST commonly seen in diabetes or HTN

58
Q

True or false: glomerular damage can be reversible

A

true
depends when its caught

59
Q

Explain immune-mediated glomerular injury.

A

glomerular capillary wall is susceptible to immune-mediated injury
antigens and antibodies tend to get caught in the structure
immune system may react to parts of the glomerular apparatus directly (autoimmunity)

60
Q

How do nephrotoxic drugs lead to acute tubular necrosis?

A

they cause ER stress (protein misfolding) leading to the formation of reactive oxygen species (free radicals, peroxides) which leads to oxidative cell damage

61
Q

How does ischemia lead to acute tubular necrosis?

A

causes oxidative stress in mitochondria leading to the formation of reactive oxygen species (free radicals, peroxides) which leads to oxidative cell damage

62
Q

How has the risk of Cisplatin-induced AKI been decreased?

A

pre-hydration to dilute the drug in the tubules

63
Q

Where does cisplatin accumulate to cause AKI?

A

proximal tubular cells

64
Q

What is rhabdomyolysis?

A

a syndrome resulting from the release of myoglobin into the bloodstream
myoglobin can precipitate in renal tubules-halting tubular flow, leading to tubular cell necrosis
presents as muscle pain/weakness, malaise, and dark urine

65
Q

What are the causes of rhabdomyolysis?

A

traumatic/crush injuries
non-traumatic muscle compression, prolonged immobility
exertional
drugs/toxins (infections, electrolyte disorders, STATINS)

66
Q

What is interstitial nephritis?

A

spaces between tubules become inflamed
inflammation generally spreads to tubules but spares glomeruli
often called “hypersensitivity” reactions because no injury appears to take place before the reaction

67
Q

How much CO do healthy kidneys receive? How much of resting O2 consumption do healthy kidneys account for/

A

20-25%
10%

68
Q

Under what conditions does the medulla operate?

A

hypoxic conditions

69
Q

What is an important cause of CKD as a result of chronic renal ischemia?

A

atherosclerotic vascular disease
reduced blood flow in large vessels

70
Q

True or false: AKI due to intrinsic causes will have very different clinical presentations

A

false

71
Q

What is usually the only way to confirm a diagnosis of intrinsic AKI?

A

renal biopsy

72
Q

What is the treatment of intrinsic AKI?

A

options are limited other than discontinuing the offending agent

73
Q

What is the usual cause of kidney stones?

A

idiopathic hypercalciuria
alterations in the solubility of various substances in the urine

74
Q

Kidney stone formation in the kidneys is painless, what can occur in the absence of pain?

A

renal damage and hematuria

75
Q

What is the cause of the pain from kidney stones?

A

distention of the ureters, renal pelvis or renal capsule

76
Q

What are the risk factors for kidney stones?

A

dehydration
protein intake
high Na intake
calcium intake may NOT play a big role

77
Q

True or false: the pain, hematuria, and ureteral obstruction from kidney stones are usually self-limiting

A

true

78
Q

Complications of kidney stones are rare but can happen. How can complications occur?

A

damage from complete blockage of urine and back-up of toxins and pressure
infection or abscess
repeated stones may cause accumulated damage

79
Q

How are smaller kidney stones managed?

A

passage only requires fluids, bed rest, and analgesia

80
Q

What is RIFLE?

A

classification system for acute kidney injury:
-Risk of renal dysfunction
-Injury to the kidney
-Failure of kidney function
-Loss of kidney function
-End-stage renal disease

81
Q

What is the GFR criteria and urine output criteria for each portion of RIFLE?

A

Risk:
-GFR: increase in SCr >1.5x baseline or decrease of GFR >25%
-urine: UO < 0.5ml/kg/h x 6h
Injury:
-GFR: increase in SCr >2.0x baseline or decrease of GFR >50%
-urine: UO < 0.5ml/kg/h x 12h
Failure:
-GFR: increase in SCr >3.0x baseline or decrease of GFR >75%
or SCr >4mg/dL
-urine: UO <0.3ml/kg/h x 24h or anuria x 12h
Loss:
-persistent ARF=complete loss of renal function <4wks
ESRD:
-end-stage renal disease

82
Q

What are the strengths and limitations of RIFLE?

A

strengths:
-broadly validated in incidence identification
-good prognostic accuracy
-correlated with length of hospital stay, renal replacement
therapy requirements
limitations:
-baseline SCr is required, its normally unknown
-MDRD equation was validated only for CKD patients
-only using SCr could decrease diagnostic sensitivity of AKI

83
Q

What is the GFR criteria and urine output criteria in each stage of the AKIN criteria?

A

Stage 1:
-GFR: increase in SCr >1.5-2x baseline or increase in SCr
>0.3mg/dl within 48h
-urine: UO < 0.5ml/kg/h x 6h
Stage 2:
-GFR: increase in SCr >2-3x baseline
-urine: UO < 0.5ml/kg/h x 12h
Stage 3:
-GFR: increase in SCr > 3.0x baseline or SCr >4mg/dl or dialysis
-urine: UO < 0.3ml/kg/h x 24h or anuria x 12h

84
Q

What are the strengths and limitations of AKIN?

A

strengths:
-added etiological information
-solely based on SCr change, not on GFR change
limitations:
-does not provide AKI classification if increase of SCr occurs in
more than 48h
-stage 3 requires criteria on SCr, UO, and RRT requirement

85
Q

How is AKI diagnosed?

A

urine output test
urinalysis
blood test
imaging test: X-ray, CT, MRI, ultrasounds
kidney biopsy (renal needle biopsy and open kidney biopsy)
-renal needle biopsy used for glomerulonephritis

86
Q

What are the potential complications of AKI?

A

pulmonary edema–>respiratory failure
anemia
chest pain (pericarditis)
muscle weakness (due to unbalance of fluids and electrolytes)
hyperkalemia
metabolic acidosis
permanent kidney damage
death

87
Q

Explain how pulmonary edema occurs in AKI.

A

pulmonary epithelial Na, K-ATPase, ENaC and aquaporin 5 are downregulated in AKI
-downregulation of Na, K-ATPase and ENac=decrease the
transport of fluids out of alveoli
-downregulation of aquaporin 5: may reduce pulmonary
secretion
pulmonary inflammation

88
Q

Explain how hyperkalemia occurs in AKI.

A

common complication for AKI with injuries to distal tubule and collecting duct
distal tubule and collecting duct are the target for aldosterone

89
Q

Explain how metabolic acidosis occurs in AKI.

A

due to the loss of bicarbonate, most likely due to damage at the proximal tubule
can cause nausea, vomiting, shortness of breath, etc

90
Q

What are the risk factors for AKI?

A

hospitalization: ICU
aging
CV diseases
hypertension
diabetes
kidney diseases
liver diseases
certain cancers and cancer treatments

91
Q

How can the risk of AKI be reduced?

A

living a healthy lifestyle
managing kidney and other chronic conditions
paying attention to drug labels, especially OTCs
develop preventive strategies for high risk patients

92
Q

What are the preventive strategies for patients at high AKI risk?

A

cancer chemotherapy:
-pre-hydration and allopurinol a few days before
chemotherapy
exposure to nephrotoxic drugs:
-avoid nephrotoxic drugs if possible, measure and follow drug
levels, adjust doses and intervals
exposure to radiographic contrast agents:
-avoid IV contrast media, and use iso- or low-osmolar contrast
agents at lowest volume
hemodynamic instability:
-optimal fluid resuscitation
liver failure:
-avoid hypotension and GI bleeding
rhabdomyolysis:
-maintain adequate hydration
undergoing surgery:
-adequate volume of resuscitation, and prevention of
hypotension

93
Q

List off the many ways in which AKI is treated.

A

patients should be hospitalized
management of AKI is primarily supportive
requiring collaboration among primary physicians, nephrologists, hospitalists, and other specialists in care team
key to treatment: maintaining adequate renal perfusion and avoiding hypovolemia
treat underlying causes
treat complications until kidney recovers

94
Q

Explain how the complications of AKI are treated.

A

balance body fluid level:
-less body fluid–>IV fluids
-extra body fluid–>diuretics
control blood potassium level:
-high blood potassium–>arrhythmias
-prescribe calcium, glucose or sodium polystyrene sulfonate
restore blood calcium level:
-low blood calcium–>IV infusion of calcium gluconate
remove toxins via dialysis

95
Q

What is kidney dialysis?

A

treatment of kidney failure
perform the normal function of kidney
remove toxins, wastes, and extra fluids from the blood

96
Q

What are the two types of kidney dialysis?

A

hemodialysis
peritoneal dialysis

97
Q

What is hemodialysis?

A

most common type of dialysis
uses a hemodialyzer
blood is removed from the body and filtered by the hemodialyzer and then filtered blood is returned to the body
vascular access:
-arteriovenous (AV) fistula (preferred)
-AV graft
-vascular access catheter

98
Q

What is the difference between AV fistula and AV graft? Provide some advantages and disadvantages of both.

A

AV fistula:
-need a small surgery to bring artery and vein together
-blood doesnt go through capillaries, goes directly to vein
-advantages: less likely to get infected or clot, permanent
-disadvantages: 2 week recovery after surgery, only for certain
people (not small veins), need mature time
AV graft:
-tube to connect artery to vein
-advantages: not hard to get tube in there, better for people
with small veins, quicker
-disadvantages: 2-3 week recovery after surgery, higher
chance of infection and clot, needs
replacement

99
Q

What is the vascular access catheter? Provide some advantages and disadvantages.

A

catheter inserted into vein around arm, neck, or chest
advantages: easy to find vein, faster (no surgery), no wait (can
get dialysis immediately)
disadvantages: clotting, easily infected, not permanent, needs
to be clean

100
Q

What is peritoneal dialysis?

A

removes wastes and toxins from the blood when kidneys are no longer functional
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 wastes and extra fluid
after several hours, the solution, along with its wastes, is drained out into an empty bag

101
Q

What are the two types of peritoneal dialysis?

A

continuous ambulatory peritoneal dialysis (CAPD)
automated peritoneal dialysis

102
Q

True or false: there is clear cut evidence showing diuretics help in treatment of AKI

A

false
diuretics may even increase in-hospital mortality and nonrecovery of renal function

103
Q

How are diuretics classified?

A

site of action and mechanism

104
Q

What are the classes of diuretics and the drugs in each class?

A

thiazides: chlorthalidone, hydrochlorothiazide, indapamide,
metolazone
loops: furosemide, torsemide, bumetanide, ethacrynic acid
potassium-sparing;
-ENaC blockers: amiloride, triamterene
-aldosterone receptor antagonists: spironolactone,
eplerenone
osmotic: mannitol, urea, glycerin, isosorbide

105
Q

What are the uses of diuretics?

A

hypertension
heart failure
edema
hepatic cirrhosis
renal insufficiency

106
Q

Describe thiazide diuretics.

A

working site: distal convoluted tubules
block thiazide-sensitive NaCl cotransporter
primary use: HTN

107
Q

What are the adverse effects of thiazide diuretics?

A

hypovolemia–>orthostatic hypotension, dizziness
hyperglycemia–>caution in diabetes
tinnitus
photosensitivity
GI disturbance

108
Q

Describe loop diuretics.

A

working site: ascending limb of loop of Henle
block luminal Na/K/2Cl cotransporter (NKCC2)
more potent than thiazides
primary use: acute pulmonary edema, congestive HF

109
Q

What are the adverse effects of loop diuretics?

A

electrolyte losses: Na+, K+, Cl-
hypotension
ototoxicity
hyperuricemia
hyperglycemia
increased serum TGs
increased LDL
muscle cramps

110
Q

Describe potassium-sparing diuretics.

A

working site: collecting duct
primary use: people at risk of low K+ levels
do not reduce blood pressure

111
Q

What are the adverse effects of potassium-sparing diuretics?

A

hyperkalemia–>arrhythmias; watch dietary K+ intake
spironolactone: diarrhea, cramping, gastritis, abnormal liver
function, androgenic effects, gynecomastia in
males
amiloride: abdominal pain, loss of appetite, rash
muscle cramps

112
Q

Which osmotic diuretic is most commonly used?

A

mannitol

113
Q

Describe osmotic diuretics.

A

working site: proximal tubule, descending limb of loop of
Henle, and collecting duct
freely filtered at glomerulus
limited reabsorption in the renal tubules
produce osmotic gradient and retain water in the tubules

114
Q

What are the adverse effects of osmotic diuretics?

A

electrolyte depletion
could worsen CHF or pulmonary edema due to increase in extracellular fluid volume upon initiation of therapy
headache
nausea/vomiting
blurred vision
dizziness

115
Q

What is a very common complication of cancer?

A

AKI
one-year risk of AKI is up to 60% for certain cancers

116
Q

What are the cancers with high risk of AKI?

A

kidney cancer
multiple myeloma
liver cancer
bladder cancer
leukemia

117
Q

Give examples of cancer caused by anticancer therapeutics.

A

chemotherapy:
-cisplatin, gemcitabine, methotrexate, ifosfamide
targeted therapy:
-ipilimumab/nivolumab combo, bevacizumab, sorafenib
immunotherapy:
-CAR-T therapy, PD-1 and PD-L1 inhibitors

118
Q

True or false: the prognosis of patient with cancer and AKI is very poor

A

true

119
Q

How do we treat/manage patients with cancer and AKI?

A

aggressive care is beneficial for patients survival
treatment plan, such as initiation of dialysis, is complex and requires input from whole care team
identify underlying cause of AKI and carefully designate the treatment plan

PHAR123 (15 decks)

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