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NEPHRO > ACUTE KIDNEY INJURY > Flashcards

ACUTE KIDNEY INJURY Flashcards

1
Q

Which medication class is most likely to interfere with renal autoregulation by inhibiting renal prostaglandin production?

A. NSAIDs
B. ACE inhibitors
C. Beta-blockers
D. Calcium channel blockers

A

A. NSAIDs

Rationale: NSAIDs inhibit renal prostaglandin production, reducing afferent arteriolar vasodilation and impairing the kidney’s ability to autoregulate in low perfusion states.

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2
Q

Which compensatory mechanism helps maintain glomerular filtration rate (GFR) in mild hypovolemia?

A. Afferent arteriolar vasoconstriction
B. Efferent arteriolar vasoconstriction mediated by angiotensin II
C. Increased systemic vascular resistance
D. Decreased cardiac output

A

B. Efferent arteriolar vasoconstriction mediated by angiotensin II

Rationale: Angiotensin II–mediated efferent vasoconstriction helps preserve GFR by maintaining glomerular capillary hydrostatic pressure during reduced renal blood flow.

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3
Q

What is a key distinguishing feature of prerenal azotemia compared to intrinsic acute kidney injury (AKI)?

A. Persistent kidney damage despite resolution of the underlying cause
B. Elevated serum creatinine and BUN levels
C. Reversibility upon restoration of renal perfusion
D. Presence of urinary casts

A

C. Reversibility upon restoration of renal perfusion

Rationale: Prerenal azotemia involves no intrinsic kidney damage and is reversible once normal perfusion and hemodynamics are restored.

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4
Q

Which drug combination poses the highest risk for developing prerenal azotemia?

A. NSAIDs and beta-blockers
B. ACE inhibitors and ARBs
C. NSAIDs with ACE inhibitors or ARBs
D. Diuretics and calcium channel blockers

A

C. NSAIDs with ACE inhibitors or ARBs

Rationale: NSAIDs reduce afferent vasodilation, while ACE inhibitors and ARBs impair efferent vasoconstriction, together posing a significant risk of reducing GFR and causing prerenal azotemia.

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5
Q

At what systolic blood pressure does renal autoregulation typically fail, even in healthy adults?

A. 100 mmHg
B. 90 mmHg
C. 80 mmHg
D. 70 mmHg

A

C. 80 mmHg

Rationale: Renal autoregulation fails once systolic blood pressure falls below 80 mmHg, leading to decreased glomerular perfusion and filtration.

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6
Q

What is the likely outcome of prolonged prerenal azotemia if not corrected?

A. Complete recovery without any sequelae
B. Progression to acute tubular necrosis (ATN)
C. Development of nephrolithiasis
D. Formation of renal cysts

A

B. Progression to acute tubular necrosis (ATN)

Rationale: Prolonged prerenal azotemia may cause ischemic injury to tubular cells, leading to ATN, a form of intrinsic AKI.

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7
Q

What mechanism helps maintain GFR in the setting of decreased perfusion pressure?

A. Afferent arteriolar vasoconstriction
B. Increased production of prostaglandins and angiotensin II
C. Decreased sympathetic tone
D. Inhibition of renin-angiotensin-aldosterone system

A

B. Increased production of prostaglandins and angiotensin II

Rationale: In response to decreased perfusion pressure, prostaglandins mediate afferent arteriolar vasodilation, and angiotensin II causes efferent arteriolar vasoconstriction to maintain glomerular capillary pressure and GFR.

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8
Q

What effect do NSAIDs have on renal perfusion and GFR during decreased perfusion pressure?

A. NSAIDs increase vasodilatory prostaglandins, preserving GFR
B. NSAIDs decrease vasodilatory prostaglandins, leading to reduced GFR
C. NSAIDs inhibit angiotensin II, leading to increased GFR
D. NSAIDs have no significant effect on GFR during reduced perfusion

A

B. NSAIDs decrease vasodilatory prostaglandins, leading to reduced GFR

Rationale: NSAIDs inhibit cyclooxygenase enzymes, reducing prostaglandin synthesis. This diminishes afferent arteriolar vasodilation, causing reduced renal perfusion and a decline in GFR.

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9
Q

How do ACE inhibitors or ARBs affect GFR during decreased perfusion pressure (Panel D)?

A. They increase prostaglandin production to preserve GFR
B. They inhibit efferent arteriolar vasoconstriction, reducing GFR
C. They promote afferent arteriolar constriction, increasing GFR
D. They decrease renin secretion, leading to increased GFR

A

B. They inhibit efferent arteriolar vasoconstriction, reducing GFR

Rationale: ACE inhibitors and ARBs block the action of angiotensin II, which reduces efferent arteriolar vasoconstriction. This leads to a drop in glomerular capillary pressure and subsequently lowers GFR.

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10
Q

What is the main compensatory mechanism impaired by NSAIDs under low perfusion pressure conditions?

A. Afferent arteriolar dilation
B. Efferent arteriolar dilation
C. Sodium reabsorption in the proximal tubule
D. Tubuloglomerular feedback

A

A. Afferent arteriolar dilation

Rationale: NSAIDs impair the production of vasodilatory prostaglandins, which are critical for maintaining afferent arteriolar dilation under conditions of low perfusion pressure.

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11
Q

Which condition is likely in a patient with anemia, hyperphosphatemia, and monoclonal spike in serum or urine electrophoresis?

A. Tumor lysis syndrome
B. Multiple myeloma
C. Hemolysis
D. Rhabdomyolysis

A

B. Multiple myeloma

Rationale: Multiple myeloma leads to renal impairment due to light chain deposition in the tubules, presenting with hyperphosphatemia, anemia, and monoclonal spikes on serum or urine electrophoresis.

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12
Q

What is a typical feature of nephrotoxin-associated AKI due to aminoglycoside antibiotics?

A. High BUN/creatinine ratio
B. Granular casts in the urine sediment
C. Elevated FeNa >2%
D. Eosinophilia and sterile pyuria

A

B. Granular casts in the urine sediment

Rationale: Aminoglycosides can cause tubular injury, which often results in granular casts and renal epithelial cells in the urine sediment, indicative of intrinsic AKI.

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13
Q

Which condition is characterized by elevated creatine kinase and myoglobin in the serum?

A. Hemolysis
B. Tumor lysis syndrome
C. Rhabdomyolysis
D. Multiple myeloma

A

C. Rhabdomyolysis

Rationale: Rhabdomyolysis is caused by muscle breakdown, leading to the release of myoglobin and creatine kinase into the bloodstream, which can cause nephrotoxic AKI.

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14
Q

Which clinical feature is most commonly associated with ischemia-associated AKI?

A. History of volume depletion or hemorrhage
B. Systemic hypotension, often with underlying CKD
C. Exposure to nephrotoxic antibiotics
D. Presence of eosinophilia and pyuria

A

B. Systemic hypotension, often with underlying CKD

Rationale: Ischemia-associated AKI is commonly caused by systemic hypotension, especially in patients with pre-existing CKD, leading to reduced renal perfusion and tubular injury.

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15
Q

Which laboratory feature is most consistent with prerenal azotemia?

A. Low BUN/creatinine ratio
B. High urinary sodium concentration (>40 mmol/L)
C. BUN/creatinine ratio above 20:1
D. High fractional excretion of sodium (FeNa >2%)

A

C. BUN/creatinine ratio above 20:1

Rationale: Prerenal azotemia is characterized by a BUN/creatinine ratio greater than 20:1 due to increased urea reabsorption secondary to decreased renal perfusion.

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16
Q

Which of the following surgical procedures carries the highest risk of postoperative AKI?

A. Orthopedic surgery
B. Cardiac surgery with cardiopulmonary bypass
C. Thyroidectomy
D. Breast cancer surgery

A

B. Cardiac surgery with cardiopulmonary bypass

Rationale: Cardiac surgery, especially with cardiopulmonary bypass, is associated with a high risk of postoperative AKI due to factors such as ischemia, inflammation, and hemolysis.

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17
Q

Which is NOT a common risk factor for postoperative AKI?

A. Underlying CKD
B. Older age
C. Hyperthyroidism
D. Diabetes mellitus

A

C. Hyperthyroidism

Rationale: Hyperthyroidism is not a recognized risk factor for postoperative AKI. Key risk factors include CKD, older age, diabetes, heart failure, and emergency procedures.

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18
Q

What is the primary mechanism of AKI associated with atheroembolic disease following vascular surgery?

A. Inflammatory cytokine release
B. Cholesterol crystal embolization
C. Direct nephrotoxic injury by vasopressors
D. Hemodynamic instability

A

B. Cholesterol crystal embolization

Rationale: Atheroembolic AKI results from cholesterol crystal embolization, causing partial or total occlusion of small renal arteries and a foreign body reaction, leading to gradual vascular damage.

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19
Q

Which factor related to cardiopulmonary bypass contributes to postoperative AKI?

A. Hypercoagulability
B. Extracorporeal circuit activation of leukocytes and inflammatory processes
C. Reduced systemic vascular resistance
D. Increased renal perfusion

A

B. Extracorporeal circuit activation of leukocytes and inflammatory processes

Rationale: During cardiopulmonary bypass, leukocyte activation, inflammation, and hemolysis contribute to postoperative AKI.

20
Q

What is the most common clinical course of contrast nephropathy?

A. A rapid rise in serum creatinine within 24 hours, peaking in 12 hours
B. A rise in serum creatinine 24–48 hours after contrast exposure, peaking in 3–5 days
C. Immediate renal failure following contrast administration
D. A gradual decline in renal function over several weeks

A

B. A rise in serum creatinine 24–48 hours after contrast exposure, peaking in 3–5 days

Rationale: Contrast nephropathy typically presents with a rise in serum creatinine 24–48 hours following exposure, peaking in 3–5 days, and resolves within 1 week.

21
Q

Which patient population is most at risk for developing contrast nephropathy?

A. Healthy adults with normal renal function
B. Patients with diabetes and normal renal function
C. Patients with preexisting chronic kidney disease, particularly diabetic nephropathy
D. Children under 10 years of age

A

C. Patients with preexisting chronic kidney disease, particularly diabetic nephropathy

Rationale: Patients with preexisting chronic kidney disease, particularly those with diabetic nephropathy, are at higher risk for contrast-induced nephropathy.

22
Q

Which of the following is NOT a proposed mechanism of contrast nephropathy?

A. Hypoxia in the renal outer medulla due to microcirculatory perturbations
B. Direct cytotoxic damage to renal tubules
C. Increased blood flow to the renal tubules
D. Transient tubule obstruction due to contrast material precipitation

A

C. Increased blood flow to the renal tubules

Rationale: Contrast nephropathy is thought to occur due to hypoxia in the renal outer medulla, cytotoxic damage, and transient obstruction by contrast material. Increased blood flow to the renal tubules is not a contributing factor.

23
Q

What is the primary risk associated with gadolinium-based contrast agents in patients with advanced kidney disease?

A. Acute renal failure
B. Nephrogenic systemic fibrosis (NSF)
C. Chronic interstitial nephritis
D. Hyperkalemia

A

Nephrogenic systemic fibrosis (NSF)

Rationale: Gadolinium-based contrast agents, particularly group I agents, have been associated with nephrogenic systemic fibrosis (NSF) in patients with advanced kidney disease. This risk is very low with group II gadolinium-based contrast agents.

24
Q

Which of the following antimicrobial agents is most likely to cause nonoliguric AKI?

A. Aminoglycosides
B. Amphotericin B
C. Acyclovir
D. Foscarnet

A

A. Aminoglycosides

Rationale: Aminoglycosides are associated with nonoliguric AKI, characterized by a urine volume >400 mL/day, in 10–30% of cases. This type of AKI typically occurs after 5–7 days of therapy.

25
Q

What is a common electrolyte abnormality associated with amphotericin B nephrotoxicity?

A. Hyperkalemia
B. Hypomagnesemia
C. Hypercalcemia
D. Hyponatremia

A

B. Hypomagnesemia

Rationale: Amphotericin B nephrotoxicity frequently results in hypomagnesemia, hypocalcemia, and nongap metabolic acidosis due to its direct tubular toxicity and effects on electrolyte handling.

26
Q

What is the typical clinical presentation of AKI caused by aminoglycosides?

A. Rapid onset of oliguria within 24 hours of therapy
B. Gradual onset of AKI after 5–7 days of therapy, even post-discontinuation
C. Acute glomerulonephritis with hematuria and proteinuria
D. Persistent anuria with hyperkalemia

A

B. Gradual onset of AKI after 5–7 days of therapy, even post-discontinuation

Rationale: Aminoglycosides accumulate in the renal cortex, causing gradual tubular necrosis that manifests as AKI after 5–7 days of therapy or even after the drug has been stopped.

27
Q

Which antimicrobial agent is most likely to cause AKI via tubular obstruction due to precipitation in the tubules?

A. Amphotericin B
B. Acyclovir
C. Rifampin
D. Tenofovir

A

B. Acyclovir

Rationale: Acyclovir can precipitate in the renal tubules, especially when given at high doses or under hypovolemic conditions, leading to intratubular obstruction and AKI.

28
Q

Which of the following antimicrobial agents is most commonly associated with acute interstitial nephritis?

A. Vancomycin
B. Penicillins
C. Tenofovir
D. Amphotericin B

A

B. Penicillins

Rationale: Acute interstitial nephritis is commonly associated with antibiotics like penicillins, cephalosporins, quinolones, sulfonamides, and rifampin.

29
Q

What is a common feature of nephrotoxicity caused by amphotericin B?

A. Rapid development of tubular obstruction
B. Renal vasoconstriction and direct tubular toxicity via reactive oxygen species
C. Formation of immune complexes in the glomeruli
D. Decreased filtration due to intratubular cholesterol crystal embolism

A

B. Renal vasoconstriction and direct tubular toxicity via reactive oxygen species

Rationale: Amphotericin B causes renal vasoconstriction and direct tubular damage mediated by reactive oxygen species, leading to polyuria and electrolyte disturbances.

30
Q

What is the primary renal toxicity mechanism associated with cisplatin?

A. Glomerular sclerosis
B. Proximal tubular necrosis and apoptosis
C. Immune-mediated glomerulonephritis
D. Cholesterol crystal embolization

A

B. Proximal tubular necrosis and apoptosis

Rationale: Cisplatin and carboplatin are accumulated by proximal tubular cells, where they cause necrosis and apoptosis. Hydration regimens help mitigate this toxicity.

31
Q

What renal complication is commonly associated with ifosfamide?

A. Acute interstitial nephritis
B. Type II renal tubular acidosis (Fanconi syndrome)
C. Nephrotic syndrome with proteinuria
D. Renal artery thrombosis

A

B. Type II renal tubular acidosis (Fanconi syndrome)

Rationale: Ifosfamide may cause tubular toxicity, leading to Fanconi syndrome, characterized by polyuria, hypokalemia, and a modest decline in GFR.

32
Q

Which antineoplastic agent is most likely to cause thrombotic microangiopathy with resultant AKI?

A. Bevacizumab
B. Mitomycin C
C. Cisplatin
D. Ifosfamide

A

B. Mitomycin C

Rationale: Mitomycin C and gemcitabine are known to cause thrombotic microangiopathy, leading to AKI due to glomerular and microvascular injury.

33
Q

Which renal adverse effect is associated with antiangiogenesis agents like bevacizumab?

A. Acute interstitial nephritis
B. Proteinuria and hypertension
C. Renal tubular acidosis
D. Acute tubular necrosis

A

B. Proteinuria and hypertension

Rationale: Bevacizumab and other antiangiogenesis agents can cause proteinuria and hypertension due to injury to the glomerular microvasculature, sometimes resulting in thrombotic microangiopathy.

34
Q

Which of the following is a preventative strategy to reduce cisplatin nephrotoxicity?

A. Administration of corticosteroids
B. Use of ACE inhibitors
C. Intensive hydration regimens
D. Concomitant use of aminoglycosides

A

C. Intensive hydration regimens

Rationale: Intensive hydration regimens are used to reduce cisplatin nephrotoxicity by diluting the concentration of cisplatin in the renal tubules and increasing urinary flow.

35
Q

What is the key diagnostic test for differentiating TTP from HUS?

A. Serum creatinine levels
B. ADAMTS13 activity levels
C. Complement C3 levels
D. Platelet count

A

B. ADAMTS13 activity levels

Rationale: ADAMTS13 is a von Willebrand factor cleaving protease, and its deficiency is a hallmark of TTP. Testing for Shiga toxin is also crucial for identifying HUS caused by Shiga toxin–producing E. coli.

36
Q

What is the primary genetic abnormality in most cases of atypical HUS?

A. Mutations in the von Willebrand factor gene
B. Mutations in genes regulating the alternative complement pathway
C. Deficiency of ADAMTS13
D. Overproduction of Shiga toxin

A

B. Mutations in genes regulating the alternative complement pathway

Rationale: Atypical HUS is commonly associated with mutations in genes that encode proteins regulating the alternative complement pathway, leading to uncontrolled complement activation.

37
Q

Which of the following is most commonly associated with atypical HUS in adults?

A. Infection with Shiga toxin–producing Escherichia coli
B. Genetic mutations in complement pathway proteins
C. Vitamin B12 deficiency
D. High-dose corticosteroid therapy

A

B. Genetic mutations in complement pathway proteins

Rationale: In adults, atypical HUS is primarily due to mutations in complement regulatory proteins, whereas typical HUS is associated with Shiga toxin.

38
Q

Which laboratory finding is most specific for the diagnosis of Goodpasture syndrome?

A. Depressed complement levels
B. High titers of antinuclear antibodies (ANAs)
C. Positive anti-glomerular basement membrane (anti-GBM) antibodies
D. Presence of cryoglobulins

A

C. Positive anti-glomerular basement membrane (anti-GBM) antibodies

Rationale: Anti-GBM antibodies are highly specific for Goodpasture syndrome, which is characterized by rapidly progressive glomerulonephritis and pulmonary hemorrhage.

39
Q

Which of the following tests is most helpful in diagnosing membranous nephropathy?

A. Antiphospholipase A2 receptor antibodies
B. Antineutrophil cytoplasmic antibodies (ANCAs)
C. Cryoglobulins
D. Anti-glomerular basement membrane (anti-GBM) antibodies

A

A. Antiphospholipase A2 receptor antibodies

Rationale: The presence of antiphospholipase A2 receptor antibodies is highly indicative of primary membranous nephropathy, aiding in its differentiation from secondary causes.

40
Q

What is the most likely finding in laboratory blood tests of a patient with systemic lupus erythematosus (SLE)-associated glomerulonephritis?

A. Elevated C3 and C4 complement levels
B. Depressed complement levels and high titers of antinuclear antibodies (ANAs)
C. Positive anti-glomerular basement membrane (anti-GBM) antibodies
D. Positive antiphospholipase A2 receptor antibodies

A

B. Depressed complement levels and high titers of antinuclear antibodies (ANAs)

Rationale: SLE-associated glomerulonephritis typically shows low complement levels (C3 and C4) due to immune complex deposition and high ANA titers, which are characteristic of SLE.

41
Q

Which antibody is most commonly associated with granulomatosis with polyangiitis (Wegener’s)?

A. Anti-glomerular basement membrane (anti-GBM) antibodies
B. Cryoglobulins
C. c-ANCA (anti-proteinase 3 antibodies)
D. p-ANCA (anti-myeloperoxidase antibodies)

A

C. c-ANCA (anti-proteinase 3 antibodies)

Rationale: c-ANCA, directed against proteinase 3, is strongly associated with granulomatosis with polyangiitis (Wegener’s), while p-ANCA is more commonly associated with microscopic polyangiitis.

42
Q

In chronic kidney disease (CKD), kidneys are typically smaller than normal. Which of the following is an exception where kidneys may remain normal-sized or enlarged?

A. Hypertensive nephrosclerosis
B. Diabetic nephropathy
C. Polycystic kidney disease
D. Membranous nephropathy

A

B. Diabetic nephropathy

Rationale: In CKD, kidneys are typically small due to fibrosis and loss of functional tissue. However, exceptions include diabetic nephropathy, HIV-associated nephropathy, and infiltrative diseases, where kidneys can remain normal-sized or enlarged.

43
Q

What urine output over 2 hours following a bolus of intravenous furosemide (1.0–1.5 mg/kg) indicates a higher risk of severe AKI progression?

A. >500 mL
B. >200 mL but <500 mL
C. <200 mL
D. No response

A

C. <200 mL

Rationale: A urine output of <200 mL within 2 hours of furosemide administration is associated with a poor prognosis and an increased likelihood of requiring renal replacement therapy.

44
Q

What is the recommended total energy intake for patients with AKI according to KDIGO guidelines?

A. 15–20 kcal/kg per day
B. 20–30 kcal/kg per day
C. 30–40 kcal/kg per day
D. 40–50 kcal/kg per day

A

B. 20–30 kcal/kg per day

Rationale: KDIGO guidelines recommend a total energy intake of 20–30 kcal/kg per day for patients with AKI to balance nutritional needs without overloading the system.

45
Q

What is the suggested protein intake for a patient with noncatabolic AKI who does not require dialysis?

A. 0.6–0.8 g/kg per day
B. 0.8–1.0 g/kg per day
C. 1.0–1.5 g/kg per day
D. 1.5–2.0 g/kg per day

A

B. 0.8–1.0 g/kg per day

Rationale: Protein intake for noncatabolic AKI patients not on dialysis is set at 0.8–1.0 g/kg per day to meet metabolic demands without exacerbating azotemia.

46
Q

At what threshold is metabolic acidosis typically treated in AKI patients?

A. pH <7.35 and serum bicarbonate <20 mmol/L
B. pH <7.30 and serum bicarbonate <18 mmol/L
C. pH <7.25 and serum bicarbonate <16 mmol/L
D. pH <7.20 and serum bicarbonate <15 mmol/L

A

D. pH <7.20 and serum bicarbonate <15 mmol/L

Rationale: Metabolic acidosis in AKI is generally treated only when it becomes severe, as defined by a pH <7.20 and serum bicarbonate <15 mmol/L, to avoid overtreatment and maintain a careful balance in metabolic homeostasis.

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