Nephro final

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What is the urine output rate for an anuric patient

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1
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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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3
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What is the urine output rate for a non oliguric patient

500 ml/day

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4
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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: <1%)

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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

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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

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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 stabilityFluid 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)

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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

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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

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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 (
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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

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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

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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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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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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

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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 therapyOR ---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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