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Nephrology > 304 AKI > Flashcards

304 AKI Flashcards

1
Q

Common causes of community acquired AKI

A 
Volume depletion
Heart failure
Adverse effect of medications
Obstruction of urinary tract
Malignancy

MOA VH

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2
Q

Common causes of hospital acquired AKI

A

Sepsis
Major surgery
Critical illness involving heart and liver
Nephrotoxic medication

SM CN
SM City

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3
Q

Common conditions associated with pre renal azotemia

A

Hypovolemia
Decreased cardiac output
NSAIDs
Inhibitors of angiotensin II

HINDe

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4
Q

When does renal auto regulation occur

A

SBP falls below 80 mmHg

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5
Q

Effect of NSAIDs on kidney

A

Renal afferent vasodilation

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6
Q

Effect of ACE-I and ARBs to kidney

A

Rena efferent vasoconstriction

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7
Q

Most common causes of intrinsic AKI

A

Sepsis
Ischemia
Nephrotoxin

SIN

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8
Q

Type 1 hepatorenal syndrome

A

SCr increase 2x or more than 2.5 mg/dl within 2 weeks despite volume administration and withholding diuretics

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9
Q

Very metabolically active part of nephron and most hypoxic region

A

S3 segment of proximal tubule

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10
Q

Most common cause of post renal AKI

A

Bladder neck obstruction

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11
Q

Laboratory feature of prerenal azotemia

A 
BUN crea ratio more than 20
FeNa less than 1
Urine osomolality more than 500 mOsm/kg
Hyaline cast
Urine sp gravity more than 1. 018
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12
Q

Contrast nephropathy. Rise in SCr? Peaks and recovers?

A

Increase in SCr within 1-2 days
Peaks on 3-5 days
Resolves within 7 days

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13
Q

Laboratory findings show hypocomplementemia and eosinophiluria. Other causes of eosinophiluria

A 
Atheroembolic disease (with hypocomplementemia) 
Allergic interstitial nephritis
Pyelonephritis
Cystitis
Glomerulonephritis
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14
Q

Causes. Urinary sediments. Granular casts

A

ATN
GN
Vasculitis
Tubulointerstitial nephritis

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15
Q

Urinary sediments in acute cellular allograft rejection

A

Renal tubular epithelial (RTE) cells
RTE cast
Pigmented cast

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16
Q

Novel biomaker associated with ischemia. Type 1 transmembrane protein expressed in proximal tubule

A

Kidney injury molecule 1 (KIM-1)

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17
Q

Novel biomaker detected in plasma and urine 2 hrs of CABG

A

Neutrophils gelatinase associated lipocalin (NGAL)

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18
Q

Novel biomaker for risk of AKI among critically ill patients

A

Insulin growth factor binding protein 7 (IGFBP7)

Tissue inhibitor of metalloproteinase 2 (TMP-2)

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19
Q

Hallmark of AKI

A

BUN more than 100 mg/dl

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20
Q

Electrolyte abnormalities in AKI

A 
Hyponatremia
Hypocalcemia
Hyperkalemia
Hyperphosphatemia
Hyperuricemia 
Hypermagnesemia
Metabolic acidosis
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21
Q

Total energy intake in AKI

A

20-30 kcal/kg per day

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22
Q

Protein intake in AKI. Not on dialysis. On dialysis

A

Not on dialysis: 0.8-1.0 g/kg

On dialysis: 1.0-1.5 g/kg

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23
Q

Most common form of renal replacement therapy for AKI

A

Hemodialysis

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24
Q

When does AKI in burn patients occur

A

10% BSA

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25
Q

Antibiotics commonly associated with AKI

A

Aminoglycosides

Amphotericin B

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26
Q

Electrolyte imbalance in AKI

A

Hyperkalemia
Hyperphosphatemia
Hypocalcemia

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27
Q

Procedures commonly associated with AKI

A

Cardiac surgery with cardiopulmonary bypass
Vascular procedure with aortic cross clamping
Intraoperitoneal procedurez

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28
Q

Common risk factors for postoperative AKI

A 
CKD
Older age
Diabetes Mellitus
CHF
Emergency procedures
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29
Q

True or false. Longer duration of cardiopulmonary bypass is risk factor for AKI

A

True.

30
Q

How can individuals undergoing massive fluid resuscitation lead to AKi

A

Increased fluid can lead to abdominal compartment syndrome and a pressure of more than 20 mmHg leads to renal vein compression and reduced GFR

31
Q

Microvascular causes of AKI

A

Thrombotic micrioangiopathies: cocaine, chemotherapeutic drugs, APAS, radiation nephritis, malignant hypertensive nephroscleorsis, TTP-HUS
Scleroderma
Atheroembolic disease

32
Q

Large vessel disease associated with AKI

A

Renal artery dissection
Thromboembolism
Renal vein compression or thrombosis

33
Q

How does Hypoalbuminemia contribute to AKI

A

Increased free circulating drug concentration

34
Q

How does contrast induce AKI

A
  1. Hypoxia
  2. Cytotoxic damage
  3. Transient tubular obstruction
35
Q

Cause of Chinese herb nephropathy

A

Aristolochic acid

36
Q

How does acyclovir lead to AKI

A

Precipitates in tubulss and cause tubular obstruction

37
Q

Commonly used drugs that have been associated with acute Tubulointerstitial nephritis

A

PPI and NSAIDs

38
Q

Kind of AKI that accompanies aminoglycosides

A

Non oliguric AKI

39
Q

Character of the AKI caused by aminoglycosides

A

Accumulates in the renal cortex
AKI manifest after 5-7 days of therapy
Hypomagnesemia is a common finding

40
Q

How does amphotericin B cause AKI

A

Renal vasoconstriction from increase in tubuloglomerukar feedback as well as tubular toxicity mediated reactive oxygen species

41
Q

When does acyclovir precipitate in tubules and case AKI?

A

Doses higher than 500 mg/m2 OR

Setting of hypovolemia

42
Q

How does cisplatin and carboplatin cause AKI?

A

Accumulate in Proximal tubular cells and cause necrosis and apoptosis

43
Q

How does ifosphamide cause AKI?

A

Cause hemorrhagic cystitis and tubular toxicity manifested as type renal tubular acidosis (Fanconi syndrome) polyuria, hypokalemia

44
Q

How does ethylene glycol cause AKI

A

It’s metabolites cause direct tubular injury and tubular obstruction

45
Q

Metabolite responsible for tubular injury in diethylene glycol

A

2 hydroxyethoxyacetic acid (HEAA)

46
Q

Most common protein in urine produced in the thick ascending limb of the loop of Henle

A

Uromodulin

47
Q

Serum Uric acid levels that leads to precipitation of Uric acid in the renal tubules and cause AKI

A

Serum Uric acid more than 15 mg/dL

48
Q

Can Glomerulonephritis lead to AKI?

A

Yes in 5% of cases

49
Q

How does obstruction lead to AKI

A

Post renal AKI involved hemodynamic alterations triggered by an abrupt increase in intra tubular pressures

50
Q

How is AKI defined

A

Rise of 0.3 mg/dl from baseline within 48 hours
50% higher than baseline within 1 week
Reduction in urine output less than 0.5 ml/kg per hour for 6 hours

51
Q

How can you differentiate AKI from CKD?

A

Small/shrunken kidneys
Cortical thinning on renal ultrasound
Evidence of renal osteodystrophy
Normocytic anemia

52
Q

How to differentiate pre renal azotemia and ischemia associated AKI

A

Pre renal azotemia: FeNa less than 1%

Ischemia associated AKI: FeNa more than 1%

53
Q

Diseases associated with granular casts

A

ATN
GN
Vasculitis
Tubulointerstitial nephritis

54
Q

Diseases associated with WBC, WBC casts

A 
Interstitial nephritis
GN
Pyelonephritis
Allograft rejection
Malignant infiltration of the kidney
55
Q

Diseases with RBC casts

A

GN
Vasculitis
Malignant hypertension
Thrombotic micrioangiopathies

56
Q

Diseases with Eosinophiluria

A 
Allergic interstitial nephritis
Atheroembolic disease
Pyelonephritis
Cystitis
GN
57
Q

Diseases with pigmented cast, renal tubular epithelial cells

A 
ATN
Tubulointerstitial nephritis
Acute cellular Allograft rejection
Myoglobinuria
Hemoglobinuria
58
Q

How is furosemide challenge done to confirm severe AKI

A

Bolus intravenous furosemide 1-1.5 mg/kg
Urine output of less than 200 ml over 2 hours
Means patient is at high risk of progression to more severe AKI and need renal replacement therapy

59
Q

Important electrolyte complication in AKI

A

Hyperkalemia

60
Q

How is rhabdomyolysis managed? Target fluid per day?

A

Target fluid per day: 10L/ day

75 mmol to 0.45% NaCl

61
Q

Calorie intake of patient with AKI

A

20-30 kcal/day

62
Q

True or false. Hyperuricemia treatment is usually not required except in the setting of tumor lysis syndrome

A

True.

63
Q

How is Hyponatremia managed in AKI

A

Fluid restrictions
Avoid hypotonic solutions
Hypertonic saline rarely needed

64
Q

When is hemodialysis initiated in patient with AKI

A

BUN more than 100 mg/dl

65
Q

True or false. If loop diuretics reaches ceiling, add diuretics acting on DCT, CCD, PCT. Such as thiazide then complete blockade with acetazolamide.

A

True.

66
Q

Caution to using thiazide diuretics

A

Hyponatremia

67
Q

Goal urine output in rhabdomyolysis and urine pH

A

PH 7.0
Urine output 200-300 ml/hr
Goal is to flush myoglobin

68
Q

When to cut dose metformin dose

A

EGFR 30-45 ml/min: half dose

EGFR less than 30: hold

69
Q

When to stop/continue ACEI/ARB in CKD

A

Stop: operation, contrast based imaging
Others: continue

70
Q

What fluids to use in AKI

A

LR as more like plasma

Nephrology (6 decks)

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