Pharm - AKI and CKD Flashcards
overview of the general management of a pt w/ AKI
management of life-threatening fluid and electrolyte abnormalities d/t AKI should be started immediately
indication for correction of fluid status
- pt w/ clinical hx of fluid loss (v/d)
- PE consistent w/ hypovolemia (hypotension and tachy)
- and/or oliguria
what type of IV fluids are preferred?
- crystalloid
- ex: isotonic saline
what is the overall goal of fluid therapy ?
increase CO and improve tissue oxygenation in pts who are preload dependent or volume responsive
what are fluids targeted at?
- physiological endpoints such as:
- mean arterial pressure
- urine output
- CO
what does the total amount of administered volume depend on?
- degree of volume depletion
- ongoing losses
what indications during fluid treatment would lead you to think pre-renal vs. AKI?
- pre-renal: restoration of adequate urine flow and improvement of renal fxn w/ fluid resuscitation
- ADK: don’t respond to administered volume w/ increase urine output or have decrease Cr
what is the preferred method to treating volume overload?
diuretics
monitoring hypervolemia when using diuretics
- pts should be regularly checked to see if urine output responds
- if no increase, dyalsis should be considered
preferred diuretic
- loop diuretic
- provides greater natriuretic effect than thiazides
starting dose and agent for fluid overload
- IV furosemide
- 40-80 mg
- dose can be titrated up if needed
what is the approach to management of hyperkalemia?
in general, all pts w/ AKI and hyperkalemia that’s refractory to medical therapy should be dialyzed unless the cause is easily reversed
if it is hyperkalemic emergency, what is the treatment?
- IV calcium
- IV insulin
- therapy to remove excess K from body:
- diuretic
- GI cation exchanger (Kayelexate)
- and/or dialysis
when would immediate therapy to correct hyperkalemia while waiting on dialysis be warranted?
- EKG changes
- peripheral neuromuscular abnormalities
specific tx of hyperkalemia is directed at what?
antagonizing the membrane effects of K, driving extracellular K into the cells, or removing excess K from the body
What is the general approach to management of metabolic acidosis?
- dialysis
- bicarb administration
- the choice of therapy depends on absence/presence of vol. overload and the underlying cause and severity of acidosis
in a patient with metabolic acidosis that is also volume overloaded, what is the preferred tx?
- dialysis
- bicarb could contribute to vol. overload
what is the goal for pts w/ metabolic acidosis d/t bicarb loss from diarrhea who are treated w/ bicarb?
- 20-22 mEq/L serum bicarb
- pH > 7.2
what is the relationship b/w hypocalcemia and AKI?
- hypocalcemia is common among AKI pts
- related to increases in serum phosphorus levels cause by reduced GFR
what to measure to monitor hypocalcemia in AKI pts
- serum ionized Ca (metabolically active)
- total serum Ca
tx of hypocalcemia when the pt is asymptomatic and hyperphosphatemia is present
- initial therapy is the correction of the hyperphosphatemia
- tx w/ oral phosphate binders
tx of symptomatic pts w/ hypocalcemia
- more aggressive
- IV Calcium
- caution: if pt is severely hyperphosphatemic, this may result in the deposition of Ca phosphate into vasculature and organs
tx of all AKI pts w/ moderately to severely elevated serum phosphate (>6mg/dL)
- dietary phosphate binders
- selection of the binder depends on level of serum ionized Ca
if the serum ionized Ca concentration is low in a pt w/ hyperphosphatemia, what is the preferred tx?
calcium-containing phosphate binders
- calcium acetate
- calcium carbonate
if the serum ionized Ca concentration is high in a pt w/ hyperphosphatemia, what is the perferred tx?
non-calcium phosphate binders
- lanthanum carbonate
- sevelamer
- Al(OH)3
if a pt has nephrotoxic effects from an aminoglycoside, when would the ATN occur?
5-10 days after therapy is initiated
lab findings in nephrotoxicity d/t aminoglycosides
- gradual progressive rise in serum creatinine (.5-1.0 mg/dL) and BUN
- decrease in CrCl
- OR:
- 50% increase in plasma creatinine concentration from baseline
other:
- mild proteinuria
- hyaline and granular casts
- FE(Na) > 1%
what are the preventative action that can be taken to decrease the chance of nephrotoxicity when taking an aminoglycoside?
- select other abx
- avoid volume depletion
- monitor aminoglycoside serum levels
- monitor renal fxn
if nephrotoxicity d/t aminoglycoside occurs, when does SCr return to nl?
after 3 weeks
what are the risk factors for vancomycin nephrotoxicity?
- coadmin of vanc and aminoglycoside
- total daily dose of vanc > 4g
- duration of therapy
- presence of underlying renal dysfunction
- critical illness
clinical manifestations d/y radiographic contrast dye
- nonoliguria kidney injury w/i 24-48 hrs after admin
- SCr peak at 3-4 days after exposure
- muddy brown granular and epithelial casts
- epithelial cells
- low FE(Na)
- low/absent proteinuria
what preventative actions can be taken to prevent radiographic contrast dye toxicity?
- minimize dose
- use noniodinated contrast studies
- avoid nephrotoxic drugs
- IV fluids
- n-acetylcysteine before and after
what is the timeframe of ACE/ARB nephrotoxicity?
- within 3-5 days of starting therapy
- stabilizes 1-2 weeks and is reversible when drug is stopped
what is the mechanism by which ACE/ARB cause nephrotoxicity?
- angiotensin II synthesis decreases –> dilation of the efferent arteriole –>
- reduced outflow resistance from glomerulus –> decrease hydrostatic pressure in glomeruluar capillaries
- decreased GFR
given a pt w/ nephrotoxicity d/t ACE or ARB, when do you dc therapy?
- when hyperkalemia can’t be controlled
- when serum Cr increases > 30% above baseline w/i 6-8 weeks when BP is reduced
presentation of NSAID induced nephrotoxicity
- c/o diminished urine output
- weight gain
- edema
- urine Na concentration <20
- elevated BUN, Scr, K, and BP
what is the mechanism of NSAID and COX-2 inhibitors in causing nephrotoxicity
- disruption of nl intraglomerular autoregulation
- PG inhibition results in renal ischemia and reduced GFR
risk factors for NSAID and COX-2 inhibitor nephrotoxicity
- > 60 yo
- preexisting kidney dz
- hepatic dz w/ acites
- HF
- dehydration
- SLE
- concurrent tx w/ ACE/ARB or diuretics
prevention of NSAID and COX-2 inhibitor nephrotoxicity
- avoid in high risk pts
- lowest effective dose
- use for shortest possible time
- avoid dehydration
- avoid hypotensive and nephrotoxic agents
- optimal management of predisposing medical probs
CrCl equation
(140-age)(weight in kg) / (72 x SCr)
x .85 if female
what is the goal of iron therapy for pts w/ CKD?
to correct absolute iron deficiency and/or increase Hgb level
What is needed before ESA (EPO-stimulating agents) therapy in CKD?
- iron assessment
- correction of anemia (if needed)
- correction of BP
what is the goal of ESA tx in dialysis pts?
- avoid transfusions
- minimize or avoid anemia sx
indication for ESA therapy in the tx of anemia in dialysis pts
hemoglobin level <10 g/dL
what is the hgb goal to attain in ESA therapy?
11-12 g/dL
ESA agents
- epoetin alfa (Epogen, Procrit)
- darbepoetin alfa (Aranesp)
MoA of ESAs
- induces erythropoesis by stimulating the division and differentialtion of committed erythroid progenitor cells
- induces the release of reticulocytes from the bone marrow into the blood stream where they mature
- reticulocytes increase followed by a rise in hct and hgb
what is nl serum phosphate?
2.5 - 4.5 mg/dL
what is the therapy goal for serum phosphorus in non-dialysis pts?
<4.5 in nl range
what is the therapy goal for serum phosphorus in dialysis pts?
between 3.5 - 5.5 mg/dL
Ca-containing phosphate binders
- calcium carbonate (tums)
- calcium acetate (phoslo)
ADRs of ca-containing phosphate binders
- hypercalcemia
- extraskeletal Ca phosphate deposition
- increase risk of vascular and tissue calcification
non-calcium containing phosphate binders
- sevelamer HCl (renagel)
- sevelamer carbonate (renvela)
iron based binder products
- sucroferric oxyhydroxide (velphoro)
- ferric citrate (auryxia)
pt status: hypocalcemic
-what product to use?
ca-containing binder
pt status: normocalcemic
-what product to use?
- pts w/o vascular calcification or adynamic bone dz: Ca-containing binder
- pts taking vit. D: non-Ca containing binder
pt status: hypercalcemic
-what product to use?
non-Ca containing binder
pt status: adynamic bone dz
-what product to use?
non-Ca containing binder
pt status: vascular calcification
-what product to use?
non-Ca containing binder
the amount of elemental Ca contained in the phosphate binder should not exceed ____ ?
1500 mg per day
tx parameters for the use of ergocalciferol in CKD
- check 25,hydroxy vit. D level
- deficiency = calcidiol < 30 ng/mL
- replace w/ vit. D2 if low
be able to . . .
- use CrCl equation
- use the calculated CrCl to select appropriate drug dose
