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Year 4 - Toxicology > Kidney > Flashcards

Kidney Flashcards

1
Q

What is the kidney responsible for?

A
  • synthesis of renin
  • acid-base balance
  • reabsorption of electrolytes
  • regulation of extracellular fluids
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2
Q

Where is angiotensin released?

A

the liver

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3
Q

how much do kidneys make up of total body mass

A

0.5%

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4
Q

how much of the resting cardiac output do the kidneys receive?

A

20-25%

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5
Q

what are risk factors for acute kidney injury?

A
  • dehydration
  • advanced age
  • cirrhosis
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6
Q

List some nephrotoxic NSAIDs (i think all of them are?)

A
  • ibuprofen
  • celecoxib
  • aspirin
  • naproxen
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7
Q

how much does the kidney reabsorb?

A

bulk reabsorption: up to 80% of solute and water

controls urine concentration, up to 25% of water & solute are reabsorbed

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8
Q

What are some functions of the kidney?

A
  • Excretion of wastes in the form of urine
  • Regulation of extracellular fluid volume, electrolyte composition, acid/base balance
  • Synthesis and release of hormones
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9
Q

What hormones are synthesized and released from the kidneys?

A
  • 1,25 dihydroxyvitamin D
  • renin
  • EPO (erythropoietin) - stimulates production of RBC
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10
Q

What does the 20-25% of CO mean?

A

so 20-25% of any drug in the blood stream ends up in the kidneys, so that’s why kidneys are so susceptible to drug toxicity due to high exposure

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11
Q

Where are concentrate toxicants ?

A

in tubular fluid

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12
Q

Why are the kidneys susceptible to toxicity?

A
  • 20-25% of CO, 0.5% of body mass
  • concentrate toxicants in tubular fluid
  • kidneys are responsible for metabolism of xenobiotics
  • glomeruli and insterstitium are susceptible to attack by the immune system
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13
Q

Describe what will happen in an AKI (acute kidney injury)

A

Abrupt decline in GFR
-SCr increase >0.3mg/dL within 48 hours
OR
-SCr to > 1.5 times baseline within 7 days
OR
-urine volume < 0.5 mL/kg/hr for 6 hours

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14
Q

AKI is ___% secondary to medications

A

30

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15
Q

Describe a pre-renal AKI

A
  • will cause impaired renal perfusion

- 55-60% of AKI’s are pre-renal

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16
Q

_____ can cause pre-renal AKI

A

NSAIDs

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17
Q

what causes volume depletion

A

diuretics, cathartics (purgative drug?), emetics

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18
Q

what causes bleeding

A

anticoagulants

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19
Q

what drugs cause cardiac dysfunction

A

B blockers, cardio toxins (such as doxorubicin)

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20
Q

what drugs cause vasoconstriction

A 
NSAIDs
calcineurin inhibitors (cyclosporin)
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21
Q

describe a renal AKI

A
  • intrinsic damage to the kidney (glomerulus or vascular damage)
  • 35-40% of AKI patients
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22
Q

what drugs cause vascular damage (thrombotic thrombocytopenia purpura)

A

cyclosporine, tacrolimus, quinine, clopidogrel

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23
Q

What is thrombotic thrombocytopenia purpura?

A
  • blood clots form in the vessels, can lead to oxygen depletion
  • uses up all the platelets and can lead to bleeding elsewhere
  • shows up as red spots all over the skin
24
Q

what drugs affect the glomerulus

A
  • ACEi cause vasodilation of efferent arteriole

- NSAIDs cause vasoconstriction of afferent arteriole

25
Q

what drugs can cause acute-tubular necrosis?

A
  • acetaminophen
  • aminoglycosides
  • antifungals
  • chemotherapeutic agents
  • iodinated contrast media
26
Q

what drugs can cause acute interstitial nephritis (hypersensitivity)?

A
  • antimicrobials
  • NSAIDs
  • diuretics
  • antihistamines
  • PPI
27
Q

Describe post-renal AKI

A
  • obstruction of urine flow
  • nothing wrong with kidney itself, problem with urethra or bladder
  • <5% of AKI patients
  • kidneys fail rapidly
28
Q

what drugs cause bladder dysfunction

A
  • anticholinergics

- antipsychotics

29
Q

what drugs can cause crystal formation

A
  • acyclovir
  • ciprofloxacin
  • methotrexate
  • sulfonamides
30
Q

what drugs can cause retroperitoneal fibrosis

A
  • B blockers
  • bromocriptine
  • hydralazine
  • methyldopa
31
Q

What are some patient risk factors for developing an AKI?

A
  • Pre-existing renal impairment
  • Dehydration (diuresis, vomiting, diarrhea, hemorrhage)
  • Medical conditions such as cirrhosis, HF, DM
  • Multiple nephrotoxic agents
  • Seriously ill: septic shock, hypotension
  • Advanced age
32
Q

Need to measure ___ as baseline before any nephrotoxic agent

33
Q

What is chronic kidney disease?

A

Progressive deterioration of renal function

  • usually caused by DM, HTN
  • secondary pathophysiologic processes triggered by AKI
  • long-term exposure to nephrotoxic chemicals

Chronic interstitial nephritis

34
Q

Which class of NSAIDs cause AKI? (non-selective or cox-2 selective)

35
Q

how many AKI do NSAIDs make up

A

7% of all AKI

36% of drug-induced AKI

36
Q

NSAIDs cause _______ AKI

A

pre-renal

by decreasing vasodilatory PGs, causing vasoconstriction and reducing blood flow

37
Q

NSAIDs can also cause acute ____ _____

A

interstitial nephritis

38
Q

how do NSAIDs affect glomerular filtration rate

A

reduced blood flow to afferent arteriole means reduced GFR

39
Q

What are the clinical manifestations with the use of NSAIDs?

A
  • increased plasma creatinine
  • decreased renal blood flow and GFR
  • oliguria (decreased urine output)
40
Q

How can we prevent AKI caused by NSAIDs?

A
  • avoid NSAIDs in high-risk patients
  • creatinine should be monitored closely
  • avoiding NSAIDs prior to procedures involving radiocontrast dye
41
Q

Aminoglycosides make up ___% of drug-induced AKI in hospitals

42
Q

How do aminoglycosides affect the kidney?

A

Proximal tubular necrosis:

  • freely filtered, accumulate in the proximal tubule
  • bind to phospholipids within the plasma membrane

Interstitial nephritis

43
Q

What are clinical manifestations of aminoglycosides?

A
  • increase plasma creatinine
  • increase in BUN
  • non-oliguric
  • electrolyte abnormalities (infrequent)
44
Q

What are some drug-related risk factors for aminoglycoside nephrotoxicity?

A
  • elevated plasma drug concentrations
  • prolonged duration of therapy
  • type of aminoglycosides: gentamicin > tobramycin > amikacin
  • frequency of dosing: once daily vs traditional dosing (i.e. EID better for renal fcn)
45
Q

How can we prevent renal impairment with aminoglycosides?

A
  • avoiding in patients with risk factors
  • adjust the dose for renal function
  • correct hypokalemia and hypomagnesemia
  • limiting the duration of therapy to 7-10 days
  • minimizing concomitant nephrotoxic medications
  • choosing an aminoglycoside with less nephrotoxicity
  • pharmacokinetically monitoring aminoglycoside therapy
  • utilizing a once-daily dosing regimen
46
Q

What is the AKI incidence of iodinated contrast media?

A

<1% (no risk factors) - 50% (high risk patients)

47
Q

how does iodinated contrast media cause AKI

A

high osmolality can lead to:

  • acute tubular necrosis
  • vasoconstriction
48
Q

Describe the first generation of iodinated contrast media

A
  • Ionic monomers
  • Highly hyperosmolal
  • 1400 - 1800 mosm/kg

*these ones are related to highest risk of toxicity because of the highly hyperosmolal

49
Q

Describe the second generation of iodinated contrast media

A
  • Nonionic monomers
  • Lower osmolality
  • 500-850 mosm/kg
50
Q

Describe the newest iodinated contrast media

A
  • Nonionic
  • Dimers
  • iso-osmolal
  • 290 mosm/kg
51
Q

Clinical manifestations of iodinated contrast media

A
  • within 24-48 hours after exposure
  • mild increase in serum creatinine (nothing too severe)
  • usually non-oliguric
  • hyperkalemia, acidosis, hyperphosphatemia
52
Q

is kidney damage reversible with iodinated contrast media

A

yes - kidney function will be restored in 5-7 days

53
Q

What are risk factors for AKI with iodinated contrast media?

A
  • dose of contrast agent
  • type of contrast agent
  • specific procedure (intra-arterial versus IV and interval vs diagnostic angiography)
54
Q

What patients are at risk for AKI with iodinated contrast media?

A
  • GFR < 60 mL/min + significant proteinuria (>500mg/day)
  • GFR < 60 mL/min + comorbidities (DM, HF, liver failure, or multiple myeloma)
  • GFR < 45 mL/min
  • GFR < 30 mL/min (highest risk)
55
Q

Prevention of AKI with iodinated contrast media?

A
  • Avoid volume depletion
  • Withhold NSAIDs for 24-48 hours prior to the procedure
  • Dose and type of contrast agent (smallest dose, avoid high osmolality agents, use iso-osmolal agent or nonionic low-osmolal agents)
  • Hydration: IV isotonic saline
  • Premedication: acetylcysteine

Year 4 - Toxicology (24 decks)

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