PREVENTION OF ACUTE KIDNEY INJURY Flashcards

1
Q

Decreased GFR, increased SCr within 1-2 weeks by >30%

A

ACEIs and ARBs

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2
Q

• 20%-25% of hospitalized patients with CHF develop AKI

A

ACEIs and ARBs

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3
Q

Dilating the efferent arteriole by blocking the effect of

angio II

A

ACEIs and ARBs

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4
Q

Prevention of ACEIDIKD

3

A

– Start with low doses of a short-acting ACEI (e.g., captopril
6.25 mg to 12.5 mg), then titrate
– Monitor kidney function with treatment
– Avoid using drugs that affect renal hemodynamic

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5
Q

Management ACEI DIKD

A

Treat hyperkalemia if developed
– Slight reductions in kidney function (maintenance of a Scr
concentration of 2 to 3 mg/dL) may be an acceptable
trade-off

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5
Q

Management ACEI DIKD

A

Treat hyperkalemia if developed
– Slight reductions in kidney function (maintenance of a Scr
concentration of 2 to 3 mg/dL) may be an acceptable
trade-off

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6
Q

Unlikely to acutely affect kidney function in the absence of renal
ischemia or excess renal vasoconstrictor activity.

A

NSAIDS

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7
Q

presentation of NSAID DIKD

A

diminished urine output, weight gain, and/or
edema, low Na excretion, high BUN, Scr, potassium, and blood
pressure.

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8
Q

Why NSAID cauuse DIKD

A

– Decreased prostaglandin-induced afferent vasodilation

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9
Q

systemic

lupus erythematosus as a risk factor in

A

NSAIDS

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10
Q

– Recovery is usually rapid within 3-5 days

after discontinuation

A

NSAIDS

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11
Q

how to prevent NSAID AKD

A

Avoiding potent compounds such as indomethacin and using
analgesics with less prostaglandin inhibition
We can use non acetylated salicylates, aspirin, and NSAID with Less
potency possibly nabumetone”or sulindac (Short half-life )

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12
Q

• Nephrotoxicity a major dose-limiting adverse effect

A

Cyclosporine & Tacrolimus

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13
Q

Reversible AKI occurred frequently in transplant recipients

during

A

the first 6 months of cyclosporine therapy

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14
Q

The 5-year risk of CKD after transplantation ranges from

A

7% to

21%

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15
Q

Presentation in Cyclosporine & Tacrolimus

A

Rise in SCr, hypertension, hyperkalemia, sodium retention,

oliguria, renal tubular acidosis, and hypomagnesemia

16
Q
  • Increase in vasoconstrictors and a reduction in the vasodilators
A

Cyclosporine & Tacrolimus

17
Q

ncrease in potent vasoconstrictors including thromboxane A2 and
endothelin, activation of the renin–angiotensin and sympathetic nervous
systems, as well as a reduction in the vasodilators nitric oxide,
prostacyclin, and prostaglandin E2”

A

Cyclosporine & Tacrolimus

18
Q

risk factors of cyclosprine and tacrolimus

A

age, higher dose, concomitant therapy with
nephrotoxic and interacting drugs (CYP3A4 inhibitors), salt
depletion, diuretic use, and polymorphic expression of Pglycoprotein

19
Q

Prevention of Cyclosporine & Tacrolimus

A

Decrease dose (rejection may occur)
– Calcium channel blockers may antagonize the vasoconstrictor
effect of cyclosporine by dilating glomerular afferent
arterioles

20
Q

– CKD is usually irreversible in

A

Cyclosporine & Tacrolimus

20
Q

– CKD is usually irreversible in

A

Cyclosporine & Tacrolimus