What is the urine output rate for an anuric patient
less than 50 milliliters per day
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What is the urine output rate for an oliguric patient
< 500 milliliters per day
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3
What is the urine output rate for a non oliguric patient
> 500 ml/day
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4
What are some limitations in staging AKI?
Biomarkers of Scr and urine output have limitations Scr ----Lag in SCr rise (48-72 hours from time of injury) ----Baseline SCr must be known Urine Output ----Non-specific marker ----Depends on volume, diuretic use and cause of AKI
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What are some risk factors for AKI
Age volume status Comorbid conditions (CKD, DM, HTN, CAD, CHF, Liver) Proteinuria Medication and nephrotoxic exposure Surgery Sepsis
Why is there diuretic resistance in volume overload
Bioavailability reduced
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What are some methods to improve diuretics efficacy when dealing with diuretic resistance in volume overload
Continuous instead of intermittent (More consistent concentration) Combination therapy (use loops with another diuretic that works at distal tubule)
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34
What are some important considerations when dosing in AKI
Pharmacokinetic alterations Estimate of renal function Vd (drug’s normal Vd and patient’s volume status) Type of RRT Drug monitoring/Therapeutic window Individualized approach
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35
What are some risk factors for drug induced kidney disease
Advanced age (>70) Male Gender African American Race Pre-existing renal disease Diabetes Heart Failure Presence of other nephrotoxic drugs Sepsis Volume depletion Cirrhosis Surgery Shock Acidosis Dose, duration, & frequency of toxins
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What are some drugs that can cause prerenal acute renal failure
Acutely reduce GFR Moderate rise in Scr up to 30% common after initiation Scr stabilizes within 1 to 2 weeks
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What are some methods to prevent ACEI/ARB Nephropathy
Recognize risk factors Initiate at low doses and gradually titrate (every 2 to 4 weeks) Monitor Scr and potassium frequently Avoiding other nephrotoxic drugs if possible
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39
Describe the management of ACEI/ARB Nephropathy
Scr threshold for discontinuation not in guidelines Scr increase (
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40
What is the incidence of NSAID nephropathy
500,000 to 2.5 million people annually
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Describe the mechanism of NSAID nephropathy
Ischemic kidney damage Decreased synthesis of renal vasodilator Afferent vasoconstriction Result in reduced renal perfusion and pressure
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What are some risk factors for NSAID nephropathy
Age > 60 Pre-existing kidney disease Hepatic disease CHF Volume depletion Lupus Concurrent treatment with ACEI/ARB or diuretics –avoid in high risk
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Describe the clinical presentation of NSAID nephropathy
Occur within 2 to 7 days after initiation Diminished urine output, weight gain, edema Elevated Scr, potassium and BP
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Describe the prevention of NSAID nephropathy
Avoiding use in high-risk patients (If necessary, minimal effective dose for shortest duration) Maintain adequate hydration
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Describe the treatment of NSAID nephropathy
Discontinuation of offending agent and other nephrotoxic drugs Reversible, recovery within 3 to 5 days Rare cases of chronic renal failure
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Etodolac brand
Lodine
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Lodine generic
Etodolac
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Nabumatone brand
Relafen
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49
Relafen generic
Nabumatone
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50
Sulindac brand
Clinoril
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51
Clinoril generic
Sulindac
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52
Describe the presentation of tacrolimus nephropathy
Occurs within days of initiation Rise in Scr HTN Hyperkalemia Sodium retention Renal tubular acidosis Hypomagnesemia
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escribe the presentation of cyclosporine nephropathy
Occurs within days of initiation Rise in Scr HTN Hyperkalemia Sodium retention Renal tubular acidosis Hypomagnesemia
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Describe the prevention of tacrolimus nephropathy
PD and PK monitoring Decreased doses when used with other non-nephrotoxic immunosuppressants
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Describe the prevention of cyclosporine nephropathy
PD and PK monitoring Decreased doses when used with other non-nephrotoxic immunosuppressants
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Describe the treatment of tacrolimus nephropathy
Acute injury: dose related and improves with dose reduction or discontinuation of interacting meds Chronic kidney injury: not dose related and irreversible
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Describe the treatment of Cyclosporine nephropathy
Acute injury: dose related and improves with dose reduction or discontinuation of interacting meds Chronic kidney injury: not dose related and irreversible
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58
Which SGLT 2 inhibitors have some evidence to show that they can induce acute kidney injury
Canagliflozin and dapagliflozin
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What is the incidence of SGLT 2 inhibitor nephropathy
over 100 cases reported to the FDA
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describe the mechanism of SGLT 2 inhibitor nephropathy
Osmotic diuresis that leads to volume depletion Delivery of sodium chloride vasoconstricts afferent arterioles and reduce GFR
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What are some risk factors for SGLT 2 inhibitor nephropathy
Older age Concomitant nephrotoxic medication (ACEI/ARB, diuretics, NSAIDS) Volume depletion
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Describe the prevention of SGLT 2 inhibitor nephropathy
Close follow-up in patients taking ACEI/ARB and diuretics Avoiding nephrotoxins
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Describe the management of SGLT 2 inhibitor nephropathy
Discontinuing SGLT-2 allows kidney recovery If volume depletion – IV fluids If ATN develops – supportive care (RRT) SGLT-2s can be restarted when kidney recovers
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64
Rank the aminoglycosides in order from most to least likely to cause nephrotoxicity
Neomycin>gentamicin>tobramycin>amikacin
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Describe why some aminoglycosides are more nephrotoxic than others
Toxicity related to cationic charge of the drug. The more cationic, the more likely to create reactive oxygen species
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what are some risk factors for aminoglycoside nephrotoxicity
aggressiveness dosing, synergistic toxicity from combination, and pre-existing clinical conditions
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Describe the prevention of aminoglycoside nephrotoxicity
selection of patient, alternative agents when possible, avoid volume depletion, limit total dose, avoid concomitant therapy, PK monitoring, once daily dosing
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Describe the treatment of aminoglycoside nephrotoxicity
discontinue the agent and other nephrotoxic drugs if possible, maintain hydration, supportive case Typically reversible, although short term renal replacement may be necessary
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69
What is the incidence of radiographic contrast-media-induced nephrotoxicity
10 to 13%
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70
describe the presentation of radiographic contrast-media-induced nephrotoxicity
presents within first 24 to 48 hours after admission serum creatinine peaks between three and four days after exposure recovery after 7 to 10 days irreversible AKI has been reported
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Describe the mechanism of radiographic contrast-media-induced nephrotoxicity
Renal Ischemia (systemic hypotension and acute vasoconstriction) Direct cellular toxicity
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Describe the risk factors for radiographic contrast-media-induced nephrotoxicity
Pre-existing kidney disease (most important) Decreased renal flow (CHF, volume depletion, hypotension) Diabetes Concurrent use of nephrotoxins
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Describe the prevention of radiographic contrast-media-induced nephrotoxicity
Assess patient for risk factors Use alternative imaging in high-risk patient (ultrasound, MRI) Contrast: use noniodinated contrast, minimize contrast volume/dose, use low contrast agents Avoid nephrotoxic drugs Hydration: Isotonic saline infusion (3 to 12 hours prior and continue 6-24 hours after exposure) at rate of 1-1.5 mL/kg/hr to maintain urine rate of 150 mL/hr Urgent cases: 0.9%NaCl at 3mL/kg/hr beginning at 1 hour prior and continue for 6 hours after
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How should you manage hydration in the prevention of radiographic contrast-media-induced nephrotoxicity
Isotonic saline infusion (3 to 12 hours prior and continue 6-24 hours after exposure) at rate of 1-1.5 mL/kg/hr to maintain urine rate of 150 mL/hr Urgent cases: 0.9%NaCl at 3mL/kg/hr beginning at 1 hour prior and continue for 6 hours after
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Describe the treatment of radiographic contrast-media-induced nephrotoxicity
no specific therapy supportive care: discontinue other nephrotoxic drugs, delay subsequent contrast studies
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Describe the incidence of amphotericin B nephrotoxicity
Variable rates Dose-dependent
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Describe the presentation of amphotericin B nephrotoxicity
Non-oliguria, rise in Scr and BUN Renal tubular potassium, sodium and magnesium wasting Distal renal tubular acidosis Onset: few days to weeks Tubular dysfunction 1-2 weeks after initiation
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Describe the mechanism of amphotericin B nephrotoxicity
Direct tubular epithelial cell toxicity --Necrosis of proximal tubular cells Afferent arteriolar vasoconstriction --Reduction in renal blood GFR
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What are some risk factors for amphotericin B nephrotoxicity
Pre-existing kidney disease Large individual and cumulative doses Short infusion time Volume depletion Hypokalemia Increased age Concomitant administrations of diuretics and nephrotoxin
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Describe the prevention of amphotericin B nephrotoxicity
Liposomal formulation Limiting cumulative doses Increasing infusion time Avoiding other nephrotoxic meds Hydrating patient ---1L of 0.9% NaCl IV daily during therapy OR ---10 – 15 mL/kg prior to amphotericin B Use other antifungals
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81
describe the treatment of amphotericin B nephrotoxicity
Discontinue therapy and substitute with alternative antifungal Tubular damage will improve gradually but may be irreversible in some patients Monitor Scr and BUN daily Monitor K, Mg and correct as needed
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Describe the mechanism of toxicity of drug induced acute interstitial nephritis
Systemic manifestation of hypersensitivity reaction Caused by medications, infections or connective tissue disease
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Describe the presentation of drug induced acute interstitial nephritis
Presents days to weeks (usually 14 days) after drug exposure Fever, rash, arthralgia, eosinophilia
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Describe the risk factors for drug induced acute interstitial nephritis
there are none
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85
describe the prevention for drug induced acute interstitial nephritis
you can't
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86
is drug induced acute interstitial nephritis reversible
yes
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what are some drugs that can cause drug induced acute interstitial nephritis
Penicillin Cephalosporin NSAIDs Diuretics PPI
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Describe the treatment of drug induced acute interstitial nephritis
Discontinue offending medication If renal failure > 7 days, steroids (High dose prednisone 1mg/kg/day for 4 to 6 weeks with taper over 4 weeks can be considered)
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Describe the dose of steroids that may be used if the patient develops renal failure from drug induced acute interstitial nephritis
High dose prednisone 1mg/kg/day for 4 to 6 weeks with taper over 4 weeks can be considered
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90
Describe it the mechanism of toxicity for drug induced post renal acute renal failure
Obstruction of urine flow from crystal formation or retroperitoneal fibrosis
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What are some risk factors for drug induced post renal acute renal failure
Severe volume depletion Underlying renal insufficiency Bolus drug administration Metabolic acidosis or alkalosis
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What are some drugs that can cause drug induced postrenal acute renal failure
Acyclovir Sulfonamides Methotrexate High dose vitamin C Indinavir, atazanavir
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Describe the prevention of drug induced post renal acute renal failure
urine alkalinization
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describe the treatment of drug induced post renal acute renal failure
stop the offending agent, replace volume, alkalinize urine
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95
How do you find total body water for males
.6 x weight
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96
how do you find total body water for females
.5 x weight
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how do you find the intracellular fluid volume
2/3 of total body water
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how do you find the extracellular fluid volume
1/3 of total body water
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how do you find the volume of water that is in the interstitial space
3/4 of extracellular fluid (extracellular fluid is 1/3 of body water)
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how do you find the volume of plasma
1/4 of extracellular fluid (extracellular fluid is 1/3 of body water)
Studied by 6 people
Note 
Flashcard (95)