Nephro final

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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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What is the urine output rate for a non oliguric patient
> 500 ml/day
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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
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What are some causes of prerenal AKI
Volume Depletion
Decreased Cardiac Output
Functional (NSAIDS, ACEI)
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What are some factors that may lead to pre-renal AKI caused by dehydration?
Hemorrhage
Decreased effective perfusion volume (nephrotic syndrome, cirrhosis, edema)
Vasodilation (sepsis)
Diuretics
Thirst, hypotension, tachycardia
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What are some factors that may lead to pre-renal AKI caused by decreased cardiac output?
Congestive heart failure
Myocardial infarction
Cardiac surgery
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Desribe the lab values that would indicate pre-renal AKI
Urine sodium < 20
Urine osmolality : serum osmolality > 1.5
BUN : Scr > 20
Low fractional excretion of sodium (FeNa) (Pre-renal failure:
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What is the treatment goal for prerenal AKI management
restore renal blood flow by increasing intravascular volume
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what is the treatment for prerenal AKI when it is caused by hemorrhage
Packed red blood cells
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what is the treatment for pre renal AKI when it is caused by plasma losses (burns) or volume loss
Crystalloids or colloids solutions
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what is the treatment for pre renal AKI when it is caused by decreased cardiac output
Positive inotropes, Vasopressors, intra-aortic balloon pump
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What is the cause of the majority of cases intrinsic AKI
acute tubular necrosis
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Fill in the blank: Tubules highly susceptible to _______ damage
Ischemic
16
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What are some nephrotoxins that may cause ATN
Antibiotics
Chemotherapy
Contrast
Many more
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What can cause renal hypoperfusion?
Hypovolemic states
Low cardiac output
Sepsis
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What are some causes of ATN
nephrotoxins, renal hypoperfusion
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What are the four phases of ATN
1) Initiation
--Renal tubular epithelial cell injury (vasoconstriction and ischemia)
--Lead to GFR reduction
2)Extension
--Continued cell injury and inflammatory response
3)Maintenance
--GFR reaches lowest point
--Initial recovery of kidneys
4)Recovery
--New tubule cells are regenerated
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What are some lab results that indicate ATN
Color and appearance: muddy brown (RBC and WBC Casts)
Granular or epithelial cell casts
Urine : serum osmolality < 1.3
BUN : Scr ≈ 15
FeNa >2%
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Hhow do you manage ATN
Improve urine output
Restore kidney function
Improve survival
22
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What are some causes of post renal AKI
Bladder Outlet obstruction (BPH, cancer, surgery)
Ureteral obstruction (Nephrolithiasis)
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What are some lab results that indicate post renal AKI
Urine sodium> 40
BUN : Scr ratio ≈ 15
Some cellular debris in urine
Urine : serum osmolality < 1.5
FeNa: Variable
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How do you manage post renal AKI
Removal of obstruction
Pharmacological: alpha1 blockers for BPH
Catheterization
Percutaneous nephrostomy
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What are some complications of AKI
Volume overload and edema
Electrolyte imbalance
Acid Base disorder
Malnutrition
Drug dosage adjustment
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What does the in general management of AKI look like?
Supportive care
Maintaining hemodynamic stability
Fluid and electrolyte management
Maintain renal perfusion
Eliminate nephrotoxins (if feasible), drug dosing
Renal Replacement Therapy (RRT)
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What are the two forms of renal replacement therapy
intermittent hemodialysis (IHD)
continuous renal replacement therapy (CRRT)
28
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describe intermittent hemodialysis
Short treatment session (3 to 4 hours)
Rapid removal of volume and small solutes
Can cause hypotension
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Describe continuous renal replacement therapy
Reserved for unstable patients
More solute removal
Less hypotension risk
30
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Describe the clinical presentation of volume overload
peripheral and pulmonary edema
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Describe the management of volume overload
Fluid Restriction/Limit sodium intake
Loop Diuretics (Careful in AKI, increased mortality..Diuretic resistance)
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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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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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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
NSAIDS
ACEI/ARB
SGLT-2s inhibitors
Diuretics
Cyclosporine
Tacrolimus
37
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Describe the presentation of ACEI/ARB Nephropathy
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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Describe the management of ACEI/ARB Nephropathy
Scr threshold for discontinuation not in guidelines
Scr increase (
40
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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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Relafen generic
Nabumatone
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Sulindac brand
Clinoril
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Clinoril generic
Sulindac
52
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Describe the presentation of tacrolimus nephropathy
Occurs within days of initiation
Rise in Scr
HTN
Hyperkalemia
Sodium retention
Renal tubular acidosis
Hypomagnesemia
53
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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
54
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Describe the prevention of tacrolimus nephropathy
PD and PK monitoring
Decreased doses when used with other non-nephrotoxic immunosuppressants
55
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Describe the prevention of cyclosporine nephropathy
PD and PK monitoring
Decreased doses when used with other non-nephrotoxic immunosuppressants
56
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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
57
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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
58
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Which SGLT 2 inhibitors have some evidence to show that they can induce acute kidney injury
Canagliflozin and dapagliflozin
59
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What is the incidence of SGLT 2 inhibitor nephropathy
over 100 cases reported to the FDA
60
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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
63
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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
64
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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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What is the incidence of radiographic contrast-media-induced nephrotoxicity
10 to 13%
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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
76
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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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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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describe the prevention for drug induced acute interstitial nephritis
you can't
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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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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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How do you find total body water for males
.6 x weight
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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)