PT 1: AKI (FINAL)
*KNOW* Match the following urine output values to their correct description: 1. <50 mL/day 2. <500 mL/day 3. >500 mL/day A. Anuric B. Oliguric C. Nonoliguric
1. A 2. B 3. C
*KNOW* Match the following terms with the appropriate description: 1. Azotemia 2. Uremia A. Increased BUN resulting in nitrogen accumulation in the blood B. Occurs as a result of severe CKD & is associated with signs/symptoms of nitrogenous waste accumulation
1. A 2. B *Azotemia with symptoms*
Which of the following types of injuries is most common for *community acquired*? A. Prerenal AKI B. Intrinsic AKI C. Postrenal AKI
A
Which of the following etiologies of AKI match the description below: - Volume depletion - Decrease in effective circulatory blood volume - Functional glomerular hemodynamics A. Prerenal AKI B. Intrinsic AKI C. Postrenal AKI
A *Volume issues/No damage yet = Prerenal AKI*
NSAID's result in: A. Indirect vasodilation of efferent arteriole B. Indirect vasoconstriction of afferent arteriole C. Dose-related vasoconstriction of afferent arteriole
B *We loose initial vasodilation & have an increased renal vascular resistance (vasoconstriction)*
Though rare, drug-induced glomerular disease is characterized by: A. Proteinuria B. GFR decrease C. Both A & B
C *Treated by removing offending agents & sometimes immunosuppresant therapy*
Arrange the following aminoglycosides from the MOST to the LEAST likely to cause ATN. 1. Gentamicin 2. Neomycin 3. Tobramycin 4. Amikacin
Neomycin > Gentamicin > Tobramycin > Amikacin
What are the 5 common indications for RRT (Renal Replacement Therapy)?
*AEIOU* 1. *A*cid-base abnormalities 2. *E*lectrolyte imbalance 3. *I*ntoxications 4. Fluid *o*verload 5. *U*remia
Differentiating Types of AKI table:
*Don't memorize it, know how to interpret it* *Always calculate the BUN/SCr ratio: >20 is Prerenal AKI* *Able to concentrate urine (not a large amount sodium in the urine): Prerenal AKI* *Sodium wasting: Intrinsic AKI* *RBC's & WBC's with damage to kidneys: Intrinsic AKI*
KDIGO classification staging table (based on severity):
*Don't memorize the table, know how to interpret it*
*CASE #3* You have a patient who is on furosemide 40mg IV BID but the patient appears to have diuretic resistance and is still fluid overloaded. The physician would like to switch to a more bioavailable agent. You decide you would like to switch the patient to an equivalent dose of bumetanide. What regimen of bumetanide IV would be equivalent to furosemide 40mg IV BID?
1 mg Bumetanide IV BID *In practice, you would switch and increase the dose of the equivalent*
*CASE #1* A 78 YOM comes into the hospital presenting with nausea and generalized weakness x12 hours. The physician suspects AKI. His urine is monitored for 24 hours and his total urine output is 450 mL over 24 hours. His weight is 75 kg. - What is his urine output in mL/kg/hr? - Based only on his urine output, would he be classified as having AKI? - What stage of AKI is the patient in? - Is this patient described as anuric, oliguric or nonoliguric?
1. 450 mL/75 kg = 6 mL/kg 6 mL/kg / 24 hrs = 0.25 mL/kg/hr 2. YES (urine volume <0.5 mL/kg/hr for at least 6 hrs) 3. Stage 3 (less than < 0.3 mL/kg/hr for >24 hrs) 4. Oliguric (<500 mL/day)
AKI is based on three distinct types of injury. Match the following types of injury with the correct description. 1. Prerenal 2. Intrinsic 3. Postrenal A. Sometimes referred to as "hemodynamic" & is characterized by decreased renal blood flow (perfusion & volume rather than damage) B. Structural kidney damage C. Obstruction in the urine collection system
1. A 2. B 3. C
Match the following extracellular volume depleting drugs to their mechanism of action causing reduced blood flow to the kidneys: 1. Loop diuretics 2. Negative ionotropes 3. Vasodilators A. Volume depletion B. Reduced cardiac output (ex: CCB's & BB's) C. Decreased systemic vascular resistance (ex: nitrates)
1. A 2. B 3. C *These are often NOT considered "true" drug-induced AKI since they are more of a "fluid" issue* *They all decrease BP thus reduce blood flow to the kidneys*
Biomarkers for kidney damage distinguish AKI based on functional change vs kidney damage. Match the following to their correct description below: 1. No functional change and no kidney damage 2. No functional change and kidney damage 3. Functional change and no kidney damage 4. Functional change and kidney damage A. Biomarker negative and KDIGO negative B. Biomarker positive and KDIGO negative C. Biomarker negative and KDIGO positive D. Biomarker positive and KDIGO positive
1. A 2. B 3. C 4. D *Biomarker is positive when kidney damage is present* *KDIGO is positive when functional change is present*
*Class Q* Match the following: 1. ACEI/ARB 2. NSAID's 3. Calcineurin inhibitors A. Dose-related vasoconstriction of afferent arteriole B. Indirect vasodilation of efferent arteriole C. Indirect vasoconstriction of afferent arteriole
1. B 2. C 3. A
Obstructive nephropathy can be categorized as crystal nephropathy or nephrolithiasis. 1. Which of the 2 is "precipitation in the distal tubular lumens leading to intratubular obstruction"? 2. Which of the 2 is "precipitation in the collecting system causing kidney stones"?
1. Crystal nephropathy 2. Nephrolithiasis
What are the 6 variants of drug-induced kidney disease?
1. Hemodynamically mediated kidney injury 2. Renal tubular epithelial cell (RTEC) damage 3. Obstructive nephropathy 4. Glomerular disease 5. Tubulointerstitial disease 6. Renal vasculitis, thrombosis and cholesterol emboli
What are some non-specific signs/symptoms of AKI?
1. Malaise 2. Anorexia 3. Vomiting 4. Volume overload 5. Shortness of Breath 6. Edema 7. Hypertension 8. Changes in urine output (volume/color) --> *more specific* 9. Weight gain 10. Flank/abdominal pain
Signs and symptoms of Uremia include:
1. Malnutrition 2. Anorexia 3. Nausea & vomiting 4. Fatigue 5. Sexual dysfunction 6. Platelet dysfunction 7. Pericarditis 8. Neuropathy
The afferent arteriole is associated with _____1______ while the efferent arteriole is associated with____2______. *Word bank: Prostaglandin-mediated Vasodilation OR Angiotensin-II mediated vasoconstriction*
1. Prostaglandin-mediated Vasodilation 2. Angiotensin-II mediated vasoconstriction
*KNOW* A combination of NSAIDs + ACEI/ARBs + diuretics has a _______ increased risk of AKI. A. 30% B. 60%
A
94% of kidney transplant patients are prescribed calcineurin inhibitors but they can lead to AKI. A. True B. False
A
A patient with underlying CKD is considered to have acute on chronic AKI. A. True B. False
A
Changes occur primarily in the interstitium rather than the tubules in tubulointerstitial nephritis. These changes may be acute or chronic. A. True B. False
A
Diabetics receiving contrast dye are thought to be at increased risk for metformin-induced lactic acidosis but are generally only at risk if they have a preexisting renal impairment. A. True B. False
A
Drug-induced kidney disease should be monitored for temporal relation to initiation of new drug therapy. A. True B. False
A
Early detection of AKI BEFORE overt functional changes (i.e, SrCr, UO, etc.) with early treatment/prevention. A. True B. False
A
The characteristics below signify/characterize: - Metabolic acidosis - Bicarbonaturia - Glycosiuria (w/o hyperglycemia) - Low Phos, K, Mag, uric acid (increased urinary losses) A. Proximal tubule damage B. Distal tubule damage
A
The description below characterizes: - Rapid loss of kidney function - Systemic symptoms - Generally reversible A. Acute allergic interstitial nephritis (AIN) B. Chronic Interstitial nephriitis (CIN)
A
The following AKI risk factors can be categorized as: - Chronic diseases - Age >65 yo - Infection/sepsis - Male gender - Dehydration A. Community acquired B. Hospital acquired C. ICU-acquired
A
The kidneys receive 25% of cardiac output. A. True B. False
A
The mechanism for RTEC (Renal Tubular Epithelial Cell) damage is direct cellular toxicity or ischemia most often localized in the proximal & distal tubular epithelia. A. True B. False
A
Which of the following type of RRT (Renal Replacement Therapy) matches the description below: - Most common "dialysis" - Has a higher risk of hypotension due to rapid fluid removal - Generally 3 times/week for a few hours A. Intermittent hemodialysis (IHD) B. Continuous renal replacement therapy (CRRT)
A
Loops should ONLY be used for the management of fluid overload NOT for the purpose of prevention or treatment of AKI. A. True B. False
A *Diuretics should be avoided in prerenal AKI patients since they are already dehydrated*
Analgesic nephropathy is as a result of chronic tubulointestitial nephritis with papillary necrosis. A. True B. False
A *Evolves slowly over years & occurs due to analgesic use: ASA, NSAIDs, Tylenol or products with caffeine* *Affects more women than men*
When treating an AKI patient with isotonic saline, the high chloride content is not a problem if everything is functioning OK but if not, it could lead to hyperchloremic metabolic acidosis. A. True B. False
A *Hypoalbuminemia: may be resistant to crystalloids so consider colloids (albumin)*
Acute tubular necrosis (ATN) caused by Amphotericin B is largely related to cumulative dose given (generally seen after a total of 2-3 g). A. True B. False
A *Risk of ATN decreases with liposomal formulation*
ACEI's/ARB's result in: A. Indirect vasodilation of efferent arteriole B. Indirect vasoconstriction of afferent arteriole C. Dose-related vasoconstriction of afferent arteriole
A *With an ACEI/ARB, we loose the vasoconstriction & perfusion pressure in the kidneys*
Glomerular disease is as a result of direct cellular toxicity and immune mediated toxicity. Which of the following results from *direct cellular toxicity*? *Select all that apply* A. Minimal change glomerular disease B. Focal segmental glomerulosclerosis C. Membranous nephropathy
A & B
*KNOW* Which of the following is TRUE regarding the prevention & treatment of ATN induced by Amphotericin B? A. Set a SCr threshold for when to discontinue or switch to liposomal formulation (i.e: SCr >2 x 2 days) B. Extend infusion time & limit cumulative dose C. Use NS 0.9% 10-15 mL/kg prior to EACH dose of amphotericin B D. Replacement of electrolytes as needed E. Prevention is key & will improve in some patients but MAY be irreversible so consider alternative & d/c therapy
ALL!!!
Prevention is key in AKI but once a patient develops AKI, which of the following options can be used for supportive management? *Select all that apply* A. Hydration, electrolyte, acid/base and waste management B. Hemodynamic support (BP) C. Renal replacement therapies (RRT) D. Nutritional support E. Avoidance of nephrotoxins
ALL!!!
Risk factors for radiographic contrast media-induced nephropathy (CIN) include: *Select all that apply* A. Larger volumes/doses of contrast B. Ratio of volume:CrCl >3.7 C. Preexisting kidney disease (GFR <60) & other diseases reducing blood flow D. High osmolality of contrast agent E. Intra-arterial administration method
ALL!!!
Which of the following agents cause DIRECT crystal nephropathy due to low urine volume or urine pH changes? *Select all that apply* A. Sulfonamides B. Indinavir C. Triamterene D. Acyclovir E. Foscamet F. Methotrexate G. Ciprofloxacin
ALL!!!
Which of the following are considered causes of diuretic resistance? *Select all that apply* A. Acute tubular necrosis (ATN) B. Nephrotic syndrome C. Interstitial edema D. Reduced renal blood flow E. Excess sodium
ALL!!!
Which of the following can be used in early detection of AKI? *Select all that apply* A. NephroCheck Test B. Neutrophil gelatinase-associated lipocalin (NGAL) C. Kidney injury molecule-1 (KIM-1) D. Interleukin-18 (IL-18) E. Liver-type fatty acid binding protein
ALL!!!
Which of the following is TRUE regarding ATN induced by Aminoglycosides (AGs)? *Select all that apply* A. Incidence is usually higher in critically ill patients B. Usually presents within 5-7 days of therapy initiation C. Characterized by gradual but progressive increase in SCr/BUN with maintained urine output & possible microscopic hematuria/proteinuria D. Full recovery achievable if discontinued E. Can be prevented by hydration and appropriate PK monitoring
ALL!!!
Which of the following is TRUE regarding Acute phosphate nephropathy? *Select all that apply* A. Its generally seen with conditions that increase calcium (hyperparathyrodism, malignancy, excessive calcium supplementation) B. Mechanism: Excessive calcium leads to deposition of calcium phosphate crystals resulting in tubular calcification C. Often occurs in patients receiving oral sodium phosphate solution for bowel preparation (OSPS; osmoprep) D. Its more of an increased phosphate intake issue rather than calcium E. It has an increased risk in elderly and preexisting kidney disease
ALL!!!
Which of the following is TRUE regarding diuretics and AKI? *Select all that apply* A. Loop diuretics are used if patient is fluid overloaded B. Loop diuretics increase urine output C. Loop diuretics decrease risk of tubular obstruction D. Loop diuretics enhance renal blood flow E. Loop diuretics do NOT reduce the incidence of AKI nor improve patient outcomes
ALL!!!
Which of the following is TRUE regarding drug dosing in AKI? *Select all that apply* A. Choose agents primarily metabolized by the liver not kidney B. eGFR and CrCl are NOT good estimates of renal function in the setting of AKI C. For patients on RRT, use specific dialysis dosing guidelines D. Always adjust doses when AKI resolves E. Patients with edema may need loading doses if rapid onset is needed due to increased volume of distribution
ALL!!!
Drugs causing acute allergic interstitial nephritis (AIN) include: *Select all that apply* A. Antimicrobials B. Diuretics C. Neuropsychiatric/seizure drugs D. NSAIDs E. PP1s/H2 blockers
ALL!!! *And many more*
Laboratory abnormalities associated with AKI include: *Select all that apply* A. Increased SCr B. Increased BUN C. Decreased GFR D. Metabolic acidosis E. Electrolyte abnormalities (↑K and Phos)
ALL!!! *Fluid/volume status changes (dehydration, fluid overload)* *Hemodynamic status changes (hypotension)*
Which of the following should be monitored in the treatment of AKI with hydration? *Select all that apply* A. Weight B. Fluid intake and urine output C. Pulmonary and peripheral edema D. Blood pressure E. Electrolytes
ALL!!! *Target urine output is >0.5 mL/kg/hr*
*Class Q* Which of the following is TRUE regarding NSAID-induced AIN? A. Patient are typically younger than 50 yo B. A patient may present with proteinuria of >3.5 g/day C. Onset is usually within 2 weeks after therapy initiation D. Patients typically present with fever, rash, and eosinophilia
B
*KNOW* A combination of NSAIDs + ACEI/ARBs + diuretics + age>75 or preexisting kidney disease has a _______ increased risk of AKI. A. 30% B. 60%
B
Metolazone, a diuretic commonly used in overcoming diuretic resistance is still effective at CrCl? A. <30 mL/min B. <20 mL/min C. >50 mL/min
B
The characteristics below signify/characterize: - Metabolic acidosis - Hyperkalemia - Polyuria (failure to maximally concentrate urine) A. Proximal tubule damage B. Distal tubule damage
B
The description below characterizes: - Interstitial fibrosis - Irreversible - No or minimal systemic symptoms A. Acute allergic interstitial nephritis (AIN) B. Chronic Interstitial nephriitis (CIN)
B
The following AKI risk factors can be categorized as: - Volume depletion - Hypotension - Sepsis - Low CO - Radiocontrast dyes A. Community acquired B. Hospital acquired C. ICU-acquired
B
Which of the following types of injuries is most common for *hospital/ICU acquired*? A. Prerenal AKI B. Intrinsic AKI C. Postrenal AKI
B
Which of the following etiologies of AKI match the description below: - Vascular damage - Glomerular damage - Acute tubular necrosis (ATN) - Acute interstitial nephritis (AIN) A. Prerenal AKI B. Intrinsic AKI C. Postrenal AKI
B *Damage = Intrinsic AKI*
Which of the following type of RRT (Renal Replacement Therapy) matches the description below: - Used for hemodynamically unstable patients - Has a higher risk of thrombosis/thromboformation - Generally several hours everyday A. Intermittent hemodialysis (IHD) B. Continuous renal replacement therapy (CRRT)
B *We generally do CRRT to avoid the hypotension associated with IHD*
*CASE #2* Based on the following labs, what type of AKI would you suspect? No urinary sediment Urine Na 16 mEq/L FENa 0.7% BUN 46 mg/dL SrCr 1.3 mg/dL
BUN/SCr = 46/1.3 = 35 *BUN/SCr is above >20 = Prerenal* *Urine is still concentrated (low urine Na (<20), low FENa (<1%))*
Amphotericin B causes ATN by direct tubular epithelial cell toxicity & afferent arteriolar vasoconstriction resulting in: A. Necrosis of proximal tubular cells B. Ischemic tubular injury C. Both A & B
C
Contrast media administration results in: A. An increased AKI risk B. Increased metformin-induced lactic acidosis risk C. Both A & B
C
Glomerular disease is as a result of direct cellular toxicity and immune mediated toxicity. Which of the following results from *immune mediated toxicity*? A. Minimal change glomerular disease B. Focal segmental glomerulosclerosis C. Membranous nephropathy
C
Radiographic contrast media-induced nephropathy (CIN) can lead to renal ischemia and oxidative stress. This occurs through: A. *Acute renal vasoconstriction* from contrast with/without hypotension *resulting in reduced renal blood flow* up to 25% for several hours post contrast administration B. Direct cellular toxicity from contrast C. Both A & B
C
The following AKI risk factors can be categorized as: - Sepsis/septic shock - Major surgery - Multiorgan failure - Hypotension - Low CO A. Community acquired B. Hospital acquired C. ICU-acquired
C
What is the most common type of RTEC (Renal Tubular Epithelial Cell)? A. Proximal tubule damage (PTD) B. Distal tubule damage (DTD) C. Acute tubular necrosis (ATN) D. Osmotic nephrosis
C
*KNOW* Which of the following does the KDIGO guidelines recommend as nutritional support to AKI patients? A. 20-30 kcal/kg/day B. Higher protein requirements in patients receiving dialysis & CRRT C. Both A & B
C *AKI patients are found to be malnourished & have derangements in glucose, lipid & protein metabolism*
*KNOW* Acute allergic interstitial nephritis (AIN) can be managed with: A. Discontinuing offending therapy B. Corticosteroid therapy; Prednisone 1 mg/kg/day for 4-6 weeks then taper over 4 more weeks C. A or B
C *Discontinue steroid therapy if no improvement in kidney function after 3-4 weeks (i.e: SCr, BUN)*
Which of the following etiologies of AKI match the description below: - Bladder outlet obstruction - Ureteral obstruction - Renal pelvis/tubular obstruction A. Prerenal AKI B. Intrinsic AKI C. Postrenal AKI
C *Obstructions = Post-renal AKI*
Calcineurin inhibitors result in: A. Indirect vasodilation of efferent arteriole B. Indirect vasoconstriction of afferent arteriole C. Dose-related vasoconstriction of afferent arteriole
C *Results in increased renal vascular resistance* *They have a similar action as NSAID's except that this is related to dose NOT prostaglandin (NSAID's)*
*Class Q* Which of the following statements is true regarding contrast-media induced nephrotoxicity (CIN)? A. Metformin causes CIN directly B. Metformin should be held for 72 hours after contrast dye administration to prevent CIN C. Per guidelines, metformin should be held in all patients undergoing contrast administration D. None of the above are true
D
*KNOW* 1 mg of Bumetanide is equivalent to: A. 40 mg of Furosemide B. 20 mg of Torsemide C. 50 mg of Ethacrynic acid D. All the above
D
*KNOW* Metformin itself does NOT cause CIN (radiographic contrast media-induced nephropathy) but the American College of Radiology recommends: A. Holding metformin at the time of or prior to contrast administration B. Holding metformin for 48 hrs after contrast dye administration if eGFR < 30 mL/min OR currently in AKI C. Does not recommend holding metformin after contrast dye in patients with eGFR >30 mL/min & have no evidence of AKI D. All the above
D
*KNOW* Which of the following KDIGO classifications below establishes if a patient has AKI? A. Increase in SCr of >0.3 mg/dL within 48 hours B. Increase in SCr to >1.5x baseline within prior 7 days C. Urine volume <0.5 mL/kg/hr lasting for at least 6 hours D. All the above
D
AKI can be classified 3 ways with separate criteria for serum creatinine (SCr) and Urine output (UO). These classifications include: A. RIFLE (Risk, Injury, Failure, Loss of kidney function & End stage renal disease) B. AKIN (Acute Kidney Injury Network) C. KDIGO (Kidney Disease: Improving Global Outcomes) D. All the above
D
Changes in intraglomerular hemodynamics (i.e: afferent/efferent arteriole vasodilation/vasoconstriction) can be caused by: A. NSAID's B. ACEI's/ARBs C. Calcineurin inhibitors D. All the above
D
Extracellular volume depletion (reduced blood flow to the kidneys) can be caused by: A. Loop diuretics B. Negative ionotropes C. Vasodilators D. All the above
D
Triamterene, antibacterials and antiretrovirals cause nephrolithiasis. These agents do not present with typical GFR changes but present with symptoms such as: A. Pain B. Hematuria C. Infection D. All the above
D
Which of the following agents cause INDIRECT crystal nephropathy? A. Chemo agents B. Warfarin C. Statins D. All the above
D
Which of the following are goals in the treatment/management of AKI? A. Minimize damage to the kidneys B. Reduce extrarenal complications C. Facilitate renal recovery to pre-AKI baseline D. All the above
D
Which of the following are risk factors for calcineurin-induced AKI? A. Age >65 yo B. Higher doses C. Older kidney allograft age D. All the above
D
Which of the following is TRUE regarding the prevention and treatment of analgesic nephropathy? A. Hydrate B. Avoid combination analgesics C. Treatment is discontinuation of analgesics D. All the above
D
The most common clinical manifestations of AIN (Acute allergic interstitial nephritis) presenting 14 days after therapy initiation include: A. Fever B. Maculopapular rash C. Arthralgia D. All the above
D *Known as the classic triad* *Others include: eosinophillia, oliguria, pyuria, hematuria, proteinuria*
Chronic interstitial nephritis (CIN) is progressive and irreversible. It is caused by: A. Lithium B. Analgesics C. Calcineurin inhibitors D. All the above
D *Limited set of drugs compared to acute interstitial (AIN)*
Lack of functioning kidneys leads to: A. Accumulation of waste products B. Metabolic disturbances C. Water retention D. All the above
D *There is no good treatment to directly reverse injury thus need to recognize early and prevent*
Which of the following are ways we could prevent AKI? A. Avoid/remove nephrotoxic agents (to the extent possible) B. Hydrate (2L/day) C. Vasopressors if needed for hemodynamic support D. All the above
D *Vasopressors can be used in combination with fluids in shock* *Hydrate with crystalloids (i.e: isotonic saline) > colloids (i.e: albumin)*
*KNOW* Prevention of radiographic contrast media-induced nephropathy (CIN) is through: A. Hydration before, during and after administration with either isotonic saline or sodium bicarbonate plus N-acetylcysteine B. Isotonic saline at 1-1.5 mL/kg/hr starting 3-12 hrs before and for 6-24 hrs after (goal urine flow: 150 mL/hr) C. Sodium bicarbonate at 3 mL/kg/hr 1 hr before then 1 mL/kg/hr during & 6 hrs after (goal: 150 mEq/L) D. N-acetylcysteine at 600-1200 mg PO Q12 hrs for 2-3 days (with 1-2 doses prior to exposure) E. All the above
E
*KNOW* Which of the following is TRUE regarding NSAID-induced AIN? A. Patients are typically above 50 years old B. Delayed onset; normally 6 months after start of treatment C. Typically has NO fever, rash, eosinophillia D. Patients may present with proteinuria of >3.5 g/day E. All the above
E
*KNOW* Which of the following is TRUE regarding radiographic contrast media-induced nephropathy (CIN)? A. Its the most common cause of ATN B. It presents as a nonoliguric increase in SCr starting at 24-48 hrs post exposure/procedure C. SCr peaks 3-4 days post-exposure & recovery is usually within 7-10 days D. Has a high mortality rate E. All the above
E
ACEI/ARBs are often used to prevent progression of CKD but can cause AKI. Which of the following are risk factors for ACEI/ARB-induced AKI? A. Congestive heart failure (CHF) B. CKD C. Renal artery stenosis D. Volume depletion E. All the above
E
Acute Kidney Injury (AKI) is a clinical syndrome generally defined by an ABRUPT reduction in kidney function as evidenced by changes in: A. Laboratory values B. Serum creatinine (SCr) C. Blood urea nitrogen (BUN) D. Urine output E. All the above
E
The primary prevention method of drug-induced AKI is to avoid nephrotoxic agents but if that's not possible, which of the following are ways we could prevent drug-induced AKI? A. Appropriately dose medications for renal function B. Appropriate hydration (2L/day) C. Monitor D. Limit multiple nephrotoxic agents at once E. All the above
E
Which of the following are risk factors for NSAID-induced AKI? A. CHF B. CKD & advanced age (>60 yo) C. Lupus D. Hepatic disease E. All the above
E
Which of the following is TRUE regarding Calcineurin inhibitors & AKI? A. AKI caused by calciuneurin inhibitors usually occurs within days of therapy B. A biopsy is sometimes needed to differentiate kidney rejections from drug induced AKI C. AKI caused by calcineurin inhibitors can be treated by reducing dose or discontinuing agent D. AKI can be prevented by therapeutic drug monitoring, avoiding other nephrotoxins & use of CCB's to antagonize vasoconstriction effects E. All the above
E
Which of the following is TRUE regarding NSAIDs & AKI? A. AKI caused by NSAIDs usually occurs within 2-7 days of initiating therapy B. AKI caused by NSAIDs usually results in reduced urine output, weight gain and edema C. AKI caused by NSAIDs is reversible if discontinued within a few days (rarely severe) D. Prevention is key but also hydrate, avoid concurrent hypotensive medications or diuretics if possible, use low doses & for the shortest duration possible E. All the above
E
Which of the following is TRUE regarding lithium-induced chronic interstitial nephritis? A. Its observed after 5+ years of therapy B. May lead to ESRD after 10-20 years of treatment C. Often asymptomatic, progressive & slowed increase in SCr/BUN D. Often associated with nephrogenic diabetes insipidus (no hyperglycemia) E. All the above
E
Which of the following is TRUE regarding osmotic nephrosis? A. Caused by drugs such as mannitol, dextran, IV immunoglobulin (sucrose, maltose) & radiographic contrast media B. Often undetected but may lead to ATN C. Usually reversible D. Causes damage by creating an oncotic gradient due to hyperosmolar substances resulting in cellular swelling E. All the above
E
Which of the following is TRUE regarding treatment of AKI with hydration? A. Maintains/restores intravascular volume & adequate perfusion to the kidneys B. Use crystalloids over colloids (i.e: isotonic saline) C. Avoid overhydrating (can make it worse) D. Consider vasopressors in critically ill patients/shock (i.e: NE, vasopressin, dopamine) E. All the above
E
*KNOW* Which of the following are ways we could prevent and treat lithium induced CIN? A. Monitor lithium concentrations (toxic >1.5 mEq/L) B. Avoid dehydration C. Monitor SCr/BUN D. Amiloride 5-10 mg PO daily E. All the above
E *Amiloride should be titrated to 20 mg PO if polyuria is NOT resolved within 7-10 days of treatment*
Which of the following diagnostic tools do we use to determine if a patient has AKI? A. Urinalysis B. Imaging (CT, KUB, ultrasonography) C. Lab tests D. Biopsy E. All the above
E *Biopsy is used as a last resort*
Which of the following are ways to overcome diuretic resistance? A. Use loop diuretics as IV infusion instead of intermittent boluses B. Use higher doses C. Switch to a different diuretic (ex: one with better bioavailability; torsemide or bumetanide) D. Combine loop with a different class of diuretic (Ex: Metolazone) E. All the above
E *If you try all this and it doesn't help produce urine; STOP IT!* *When switching diuretics, remember to increase dose while switching; don't assume they work the same way*
Which of the following drugs cause Acute tubular necrosis (ATN)? A. Aminoglycosides B. Amphotericin B C. Radiographic contrast media D. Calceinurin inhibitors E. All the above *Which of the above is the most common cause of ATN?*
E *Radiographic contrast media*
Which of the following is TRUE regarding ACEI/ARBs & AKI? A. Avoid concurrent hypotensive agents/diuretics with ACEI/ARB's B. Monitor SCr and potassium (start low & go slow) C. Expect a 30% increase in SCr (3-5 days) from baseline; stabilizes within 1-2 weeks D. If SCr is >30% over 1-2 weeks; discontinue agent E. All the above
E *Reversible if discontinued* *Not a concern clinically if SCr increase is limited to 30%*
Which of the following is TRUE regarding cholesterol emboli? A. Its caused by warfarin & thrombolytics B. Its irreversible C. It presents as purple discoloration of toes and mottled skin over the legs D. Results in necrosis of vessels within weeks/months of therapy initiation E. All the above
E *Treatment with supportive care*
Hemodynamically mediated kidney injury; similar to "pre-renal" AKI can be caused by: A. Loop diuretics B. Negative ionotropes C. Vasodilators D. NSAID's E. ACEI/ARB's F. Calcineurin inhibitors G. All the above
G
What is the problem with using SCr to detect AKI?
With SCr, there is a delay; we don't immediately see the increase in SCr (you see it in 1-2 days).
What is the problem with using UO (urine output) to detect AKI?
With UO, if you have a decreased urine output; you most likely have AKI but if you have AKI, it doesn't necessarily mean you have a decreased UO.
