PREVENTION OF ACUTE KIDNEY INJURY Flashcards
Decreased GFR, increased SCr within 1-2 weeks by >30%
ACEIs and ARBs
• 20%-25% of hospitalized patients with CHF develop AKI
ACEIs and ARBs
Dilating the efferent arteriole by blocking the effect of
angio II
ACEIs and ARBs
Prevention of ACEIDIKD
3
– 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
Management ACEI DIKD
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
Management ACEI DIKD
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
Unlikely to acutely affect kidney function in the absence of renal
ischemia or excess renal vasoconstrictor activity.
NSAIDS
presentation of NSAID DIKD
diminished urine output, weight gain, and/or
edema, low Na excretion, high BUN, Scr, potassium, and blood
pressure.
Why NSAID cauuse DIKD
– Decreased prostaglandin-induced afferent vasodilation
systemic
lupus erythematosus as a risk factor in
NSAIDS
– Recovery is usually rapid within 3-5 days
after discontinuation
NSAIDS
how to prevent NSAID AKD
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 )
• Nephrotoxicity a major dose-limiting adverse effect
Cyclosporine & Tacrolimus
Reversible AKI occurred frequently in transplant recipients
during
the first 6 months of cyclosporine therapy
The 5-year risk of CKD after transplantation ranges from
7% to
21%
Presentation in Cyclosporine & Tacrolimus
Rise in SCr, hypertension, hyperkalemia, sodium retention,
oliguria, renal tubular acidosis, and hypomagnesemia
- Increase in vasoconstrictors and a reduction in the vasodilators
Cyclosporine & Tacrolimus
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”
Cyclosporine & Tacrolimus
risk factors of cyclosprine and tacrolimus
age, higher dose, concomitant therapy with
nephrotoxic and interacting drugs (CYP3A4 inhibitors), salt
depletion, diuretic use, and polymorphic expression of Pglycoprotein
Prevention of Cyclosporine & Tacrolimus
Decrease dose (rejection may occur)
– Calcium channel blockers may antagonize the vasoconstrictor
effect of cyclosporine by dilating glomerular afferent
arterioles
– CKD is usually irreversible in
Cyclosporine & Tacrolimus
– CKD is usually irreversible in
Cyclosporine & Tacrolimus
