Acute Kidney Injury Flashcards
What is AKI?
rapid reduction of GFR → increased nitrogenous waste products
- +/- Decreased urine output
- 5-7% of hospitalizations results in AKI
- 5-10x as many as community AKI
- critically ill patients may end up with CKD → mortality rate > 50% with AKI
- 5-10x as many as community AKI
Staging System for AKI
-
Stage 1:
- absolute serum creatinine increase
- ≥ 0.3mg/dL or 150-200% increase from baseline
- Urine Output: less than 0.5ml/kg/hour for 6+ hours
- absolute serum creatinine increase
-
Stage 2:
- absolute serum creatinine increase (unavailable) or 200-300% increase from baseline
- Urine Output: less than 0.5ml/kg/hr for 12+ hours
-
Stage 3:
- absolute serum creatinine increase ≥ 4mg/dL with an acute increase of ≥ 0.5mg/dL or 300% or greater increase from baseline
- Urine Output: urine output less than 0.3ml/kg/hr for 24 hours or anuria for 12 hours
- → need renal replacement therapy
RIFLE Criteria and AKI
- RIFLE: Risk, Injury, Failure, Loss, ESKD
- GFR criteria
- Risk: increase SCr x 1.5 or GFR decrease greater than 25%
- Injury: increase SCR x 2 or GFR decrease greater than 50%
- Failure: increase SCr x 3 or GFR decrease greater than 75%
- OR SCr greater than 4mg/dL, acute ≥ 0.5mg/dL
- Urine Output Criteria
- Risk: UO <0.5mL/kg/hour x 6 hours
- Injury: UO <0.5 mL/kg/hour x 12 hours
- Failure: UO <0.3mL/kg/hour x 24 hours, or anuria x 12 hours
- LOSS: persistent AKI - complete loss of kidney function > 4 weeks
- ESKD: loss of kidney function > 3 months
Cockcroft-Gault Equation For Adults
Meds that can cause AKI
- high risk pts should avoid these meds
- aminoglycosides
- amphotericin B
- radiocontrast Dye
- Cyclosporine and Tacrolimus
- ACE and ARB
- NSAIDs
- MTX etc
Diuretics and AKI
they may increase urine output but do not decrease mortality
- should only be used for hypervolemic states
- should NOT be used to make oliguric patients nonoliguric in AKI, nor increase urine output when pt is NOT hypervolemic
Loop Diuretics and dosage
40mg furosemide = 20 mg torsemide = 1 mg bumetanide
- torsemide and bumetanide have a greater bioavailability and duration than furosemide
- 40mg furosemide IV → response in 30min - 1 hour (output ≥ 1mL/kg/hr)
- can double dose if AKI pt with fluid overload is not initially responsive → if still not responsive then add thiazide
Dopamine & Fenoldopam and AKI
- Dopamine = improves urine output but does not have any clinical benefit
- fenoldopam = low dose reduces SCr but did not improve mortality or lower the need for dialysis
Fenoldopam (Corlopam)
Stimulates dopamine D1-like and Alpha-2 (mild-mod affinity) receptors → causes rapid vasodilation
- R-isomer = responsible for biological response
-
INDICATIONS: severe HTN
- contrast induced nephropathy (off-label)
-
SEs:
- ≥ 5%: flushing, hypotension, headache, nausea
- <5%: angina, bradycardia,, chestpain, MI, orthostatic hypotension
- anxiety, dizziness
- hyperglycemia, hypokalemia
- abdominal pain, N/V/D Constipation
- UTIs
- bleeding, leukocytosis
- IOP increased
- BUN and creatinine increase
- DDI: antihypertensive meds → increases hypotension
Preventing Contrast-Induced Nephropathy
-
NS or NAHCO<u>3</u> IV infusion → decreases incidence of nephropathy
- give 1mL/kg/hr NS IV 12 hours before and 12 hours after procedure
- if pt high risk for volume overload: CHF with EF <40% → use 3 amps NaHCO3 + 1L D5W
-
N-acetylcysteine:
-
PO at 1200mg Q12 hours
- for high-risk pts the before contrast and day of procedure
- AVOID: diuretics, NSAIDs, ACEI, Metform 24-48 hours prior
-
PO at 1200mg Q12 hours
-
Statins:
- use before coronary angiography → reduces contrast induced AKI
- high intensity
Rule of Thumb for Fluid Replacement in adults
30-40mL/kg/day + normal insensible losses (lungs: 400mL/day, Skin 400mL/day, Feces 100mL/day)
Drugs that cause HyperK
K-sparing diuretics
K-supplements
Abx with K salts
ACE-I
ARBs
NSAIDs
Hypokalemia Tx
When to tx? <3.5 mEq/L and/or pt is symptomatic
- treatment:
- oral: K-chloride, KPO4, K-acetate, K-citrate, k-gluconate
- IV: if >10 mEq/L should be monitored via telemetry
- other: diuretic induced (spironolactone- K+ sparing diuretic)
- correct hypomagnesemia
- ****low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently*****
- correct acid-base imbalance
- correct hypomagnesemia
- oral: K-chloride, KPO4, K-acetate, K-citrate, k-gluconate
Hyperkalemia Tx
-
Symptomatic (urgent/emergent)
- IV calcium to stabilize the heart membrane
- insulin +/- glucose/dextrose to temporarily push K+ back into the cell
- albuterol to also temporarily push K+ back into the cell
- Sodium bicarb to be considered to tx acidosis
- Eliminate Source: IV, total parenteral nutrition (TPN), tube feeds, oral supplements, K sparing diuretics
-
Symptomatic:
- sodium polystyrene sulfonate (Kayexelate) → binds potassium, slower onset, but duration of 4-6 hours (constipation though…)
- Loop diuretics (lasix)
-
Asymptomatic;
- eliminate source
- kayexelate (sodium polystyrene sulfonate) → binds potassium
- loop diuretics
Serum and Ionized/Free Calcium Levels
- Normal Total Serum Ca2+: 8.5-10.5mg/dL
- >13 or <6 = critical values
- Normal Ionized/Free Ca2+: 1.18-1.30mmol/L
- critical values= <0.9 or >1.6
Roles of Calcium and interaction with albumin
- Roles: bone health, nerve transmission, muscle contraction
- 50% bound to albumin
- → alkalosis increases binding to albumin
Parathyroid Hormone and Ca2+ Regulation
- increased PTH → efflux of calcium from the bones
- decreased loss of calcium in urine
- increased release of vitamin D from the kidney
- → enhanced absorption of calcium from the intestine
Hypocalcemia S/Sxs and Causes
- S/sxs: tetany, paresthesia of fingers/toes, cramping, spasms, confusion, hairloss, psoriasis
- causes: malabsorption
- vitamin D deficiency
- deficient PTH
- hypomagnesia
- renal failure
- inadequate hydroxylation of 25-hydroxy vitamin D
- Drugs: furosemide, Biphosphonates, Phenobarbital → increases metab of vitamin D
- Phenytoin → increases metab of vitamin D
Hypocalcemia and Tx
When to tx: corrected serum Ca2+<8.5mg/dL and/or s/sxs and/or Ca2+ x PO4 <55
- tx underlying condition
- IV calcium gluconate/calcium chloride
- Ca-gluconate: 9% elemental Ca2+
- Ca-Cl: 27% elemental Ca2+
- Oral Calcium/Vitamin D supplement
- <18yo → 1200-1500mg/day
- 18-50 → 1000mg/day
- >50 yo → 1200-1500 mg/day
Phosphorus Normal Levels
Normal Serum levels: 2.7-4.6mg/dL
mostly intracellular
70-90% absorbed in jejunum
Hyperphosphatemia S/sxs and Causes
- S/sxs: related to development of hypocalcemia secondary to calcium precipitation
- Causes:
- ARF/CRF
- exogenous admmin
- HypoPTH (decreased Ca2+)
- Rhabdomyolysis
- DKA
Hyperphosphatemia Tx
when to tx: PO4 >9mg/dL and/or Ca2+ x PO4 product ? 55
- tx: IV calcium
- dietary restriction
- calcium salts (Ca-ACE), aluminum salts (AlOH), magnesium salts (MgOH)
- sevelamer (Renagel) TID with food
-
Lanthanum Carbonate (Fosrenal)
- cationic polymer
-
sucroferric oxyhydroxide (Velphoro)
- cationic polymer
-
Ferric Citrate (Auryxia)
- 1 gm ferric citrate = 210mg ferric iron
- PO with food
When do d/c ACEI in AKI?
if AKI is more severe: SCr 1-2 or GFr < 30
ACE-I
captopril, lisinopril, benzapril, etc. “-pril”
not for GFR <30
good for reducing proteinuria in CKD pts with HTN
ARBs
losartan, candesartan, valsartan, etc “-sartan”
good for reducing proteinuria in CKD pts with HTN
Potassium sparing Diuretics
Spironolactone, Triamterene, Amiloride
