Pharmacotherapy of AKI Flashcards
Define anuria
Less than 100 mL/d
Define oliguria
100-400 mL/d
Define non-oliguria
> 400 mL/d
Goals of therapy are
Prevention of AKI Avoid or minimize renal insults Survive the acute insult Provide supportive measures Regain life-sustaining renal function
High risk patients are:
preexisting renal prob CHF Cirrhosis DM Advancing age Dehydration Nephrotoxic drugs IV contrast dye
Nephrotoxic agents include
AG, amp B, cisplatin
IV contrast
Agents that have impact on renal blood flow:
NSAIDs
ACE-i
cyclosporine
tacrolimus
Benefits of volume expansion
Maintain renal perfusion
Flush out toxins
Decreased RAAS activation
Minimize the decreases in NO and prostacycline (dilators)
Goal of therapy of volume expansion
> 150 mL/hr
In a patient who is critically ill what volume expansion would you use:
isotonic crystalloids
Volume expansion for contrast dye administration
NS (0.9% NaCl)
Sodium bicarbonate
NS dose
1.0-1.5 mL/kg/hr for 3-12 hours before and 6-12 hours after
Sodium bicarbonate
3 mL/kg/hr for 1 hour prior to dye administration, then 1 mL/kg/hr for 6 hours after
Aminoglycosides
Use only when necessary
QD dosing in appropriate pts
Monitor levels and adjust accordingly
Amp B
Use only when necessary
Lipid formulation preferred
N-acetylcystein (Mucomyst) oral
Adjunct to isotonic crystalloids
Inexpensive, few side effects, well tolerated
MOA: scavengers free oxygen radicals
N-acetylcystein (Mucomyst) oral dose
600-1200 mg BID before and after contrast
Drugs that are not recommended
Theophylline
Ascorbic Acid
Statins
Fenoldopam
Define oliguria
100-400 mL/d
Define non-oliguria
> 400 mL/d
Goals of therapy are
Prevention of AKI Avoid or minimize renal insults Survive the acute insult Provide supportive measures Regain life-sustaining renal function
High risk patients are:
preexisting renal prob CHF Cirrhosis DM Advancing age Dehydration Nephrotoxic drugs IV contrast dye
Nephrotoxic agents include
AG, amp B, cisplatin
IV contrast
Benefits of volume expansion
Maintain renal perfusion
Flush out toxins
Decreased RAAS activation
Minimize the decreases in NO and prostacycline (dilators)
Goal of therapy of volume expansion
> 150 mL/hr
In a patient who is critically ill what volume expansion would you use:
isotonic crystalloids
Volume expansion for contrast dye administration
NS (0.9% NaCl)
Sodium bicarbonate
NS dose
1.0-1.5 mL/kg/hr for 3-12 hours before and 6-12 hours after
Sodium bicarbonate
3 mL/kg/hr for 1 hour prior to dye administration, then 1 mL/kg/hr for 6 hours after
Aminoglycosides
Use only when necessary
QD dosing in appropriate pts
Monitor levels and adjust accordingly
Amp B
Use only when necessary
Lipid formulation preferred
N-acetylcystein (Mucomyst) oral
Adjunct to isotonic crystalloids
Inexpensive, few side effects, well tolerated
MOA: scavengers free oxygen radicals
N-acetylcystein (Mucomyst) oral dose
600-1200 mg BID before and after contrast
Drugs that are not recommended:
Theophylline Ascorbic Acid Statins Fenoldopam Dopamine Diuretics
Goals of therapy for AKI
Remove offending agent
Treat underlying cause
Limit exposure to subsequent nephrotoxic events
Speed up recovery of renal function
Treatment of Postrenal AKI
Removal of obstruction
Electrolyte management
Fluid management
Treatment of Prerenal, intrinsic AKI
Electrolyte management (Na/K) Maintain blood pressure and CO Carefully anuric and oliguric
Treatment of Prerenal, intrinsic AKI
Electrolyte management (Na/K) Maintain blood pressure and CO Carefully anuric and oliguric
Hypovolemic Treatment
250-500 mL over 15-20 minutes, then reassess
Hypervolemic treatment
Reduce IV fluids to keep vein open
Concentration of IV meds and tube feeds
Diuretics
Reserved for hypervolemic patients who make adequate urine in response to diuretics
What are the loop diuretics
Furosemide (lasix)
Torsemide (demadex)
Bumetanide (bumex)
Ethacrynic acid (edecrin)
Furosemide dose
40-80 mg IV/PO, increase 20-40 mg/dose Q6-8 hrs
Torsemide dose
10-20 mg IV/PO, double dose Q2 hours if necessary
Torsemide dose
10-20 mg IV/PO, double dose Q2 hours if necessary
Loop diuretic resistance MOA
They increase delivery of sodium to distal tubule and collecting ducts and in time the kidney gets used to this and increases the reabsorption there
Causes of diuretic resistance
Excessive sodium intake Inadequate dose or drug regimen Reduced bioavailability Nephrotic syndrome Reduced renal blood flow Increased Na reabsorption
Thiazides work where?
Distal convoluted tubule
Where do loops work?
Thick ascending limb
Metolazone (zaroxoxlyn) is good when
CrCl is
Renal Replacement Therapy
Acid-base abnormalities Electrolyte imbalance Intoxication Fluid overload Uremia
Pre-renal cause
Decreased blood flow to the kidney or issue getting blood to the kidney
Intrinsic cause
damage to the kidney itself
Postrenal cause
obstruction that keeps blood from flowing from the kidney
