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Nephrology > 304: Acute Kidney Injury > Flashcards

304: Acute Kidney Injury Flashcards

1
Q

Common diagnostic features

A

increased sCr often associated with reduction in urine volume

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2
Q

Patients who survive and recover from an episode of severe AKI requiring dialysis are at increased risk for the later development of dialysis-requiring end-stage kidney disease

A

True

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3
Q

Common causes of community acquired AKI

A 
volume depletion
heart failure
adverse effects of medications
UTO
malignancy
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4
Q

Common causes of hospital acquired AKI

A

sepsis
major surgical procedures
critical illness involving heart or liver failure
nephrotoxic medication administration

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5
Q

Most common form of AKI

A

Prerenal

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6
Q

Define Prerenal Azotemia

A

rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration

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7
Q

Causes of prerenal

A

Hypovolemia
Dec CO
Dec ECV (CHF, Liver Failure)
Impaired renal autoreg (NSAIDs, ACE-I, ARBs, Cyclosporine)

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8
Q

Homeostatic responses to decreased ECV or CO

A

Renal vasoconstriction
Salt and water reabsorption
Myogenic reflex
Tubuloglomerular feedback

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9
Q

Mediators of homeostatic responses to maintain BP and increase intravascular volume

A

Ang II
NE
ADH/Vasopressin

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10
Q

Explain the myogenic reflex

A
  • dilation of afferent arteriole in the setting of low perfusion pressure
  • infrarenal biosynthesis of prostaglandins (Prostacyclin, PGE2), NO, kinins
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11
Q

Explain the TG feedback

A

decreased solute delivery to the macula densa (distal tubule) leads to afferent arteriolar dilation

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12
Q

Renal auto regulation fails once SBP falls below?

A

below 80 mmHg

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13
Q

Atherosclerosis, longstanding hypertension, and older age can lead to hyalinosis and myointimal hyperplasia, causing structural narrowing of the intrare- nal arterioles and impaired capacity for renal afferent vasodilation.

A

True

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14
Q

action of NSAIDs and ACEi/ARBs

A

NSAIDS - limits afferent arteriolar vasodilation

ACE-i/ARBS - limit efferent vasoconstriction

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15
Q

How does CLD cause Prerenal azotemia?

A

Mary arterial vasodilation in the Splanchnic circulation leading to activation of vasoconstrictors

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16
Q

Type 1 HRS

A

> 2x increase in SCr to >2.5 mg/dL, within 2 weeks without an alternate cause (e.g., shock and nephrotoxic drugs), persists despite volume administration and withholding of diuretics.

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17
Q

Type 2 HRS

A

steady increase in sCr in refractory ascites

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18
Q

Intrinsic renal failure affecting the Small vessels

A 
Glomerulonephritis
• Vasculitis
• TTP/HUS
• DIC
• Atheroemboli
• Malignant HTN
• Calcineurin inhibitors
• Sepsis
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19
Q

Intrinsic renal failure affecting the tubules

A 
Toxic ATN 
   Endogenous (rhabdo, hemolysis)
   Exogenous (contrast, cisplatin, gentamicin)
Ischemic ATN
Sepsis
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20
Q

Intratubular Intrinsic AKI

A 
Endo
   Myeloma
   Tumor lysis
   Cellular debris
Exogenous
   Acyclovir
   Methotrexate
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21
Q

Interstitium Intrinsic AKI

A

Allergic (PCN, PPIs, NSAIDs, rifampin, etc.)

  • Infection (severe pyelonephritis, Legionella, sepsis)
  • Infiltration (lymphoma. leukemia)
  • Inflammatory (Sjogren’s, tubulointerstitial nephritis uveitis), sepsis
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22
Q

Large vessel intrinsic AKI

A
  • Renal artery embolus, dissection, vasculitis
  • Renal vein thrombosis
  • Abdominal compartment syndrome
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23
Q

Decreases in GFR with sepsis can occur even in the absence of overt hypotension

A

True

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24
Q

Pathophysiology of sepsis associated AKI

A

Tubular injury, inflammation, mitochondrial dysfunction, interstitial edema

Generalized arterial vasodilation

efferent arteriole vasodilation, particularly early in the course of sepsis

renal vasoconstriction from activation of the SNS, RAAS, ADH, and endothelin

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25
Q

one of the most hypoxic regions in the body

A

renal medulla

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26
Q

Ischemia alone in a n mal kidney is usually not sufficient to cause severe AKI.

A

True

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27
Q

AKI more commonly develops when ischemia occurs in the context of limited renal reserve (e.g., CKD or older age) or coexisting insults such as sepsis, vasoactive or nephrotoxic drugs, rhabdomyolysis, or the systemic inflammatory states associated Pathophysiology of Ischemic Acute Renal Failure with burns and pancreatitis

A

True

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28
Q

Which segment of the nephron is damaged in ischemic AKI

A

S3 segment of the PT

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29
Q

Mechanism of postop AKI

A

Ischemia

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30
Q

procedures most commonly associated with AKI

A

cardiac surgery with cardiodiopulmonary bypass (particularly for combined valve and bypass procedures), vascular procedures with aortic cross clamping, and intraperitoneal procedures

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31
Q

Common risk factors for postoperative AKI

A 
CKD
older age
diabetes mellitus
congestive heart failure
emergency procedures
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32
Q

Cardiopulmonary bypass is a unique hemodynamic state characterized by nonpulsatile flow and exposure of the circulation to extracorporeal circuits. Longer duration of cardiopulmonary bypass is a risk factor for AKI.

A

True

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33
Q

AKI from PCI of aorta

A

cholesterol crystal embolization

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34
Q

AKI is an ominous complication of burns, affecting 25% of individuals with how many % total body surface area involvement.

A

> 10%

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35
Q

abdominal compartment syndrome, where markedly elevated intraabdominal pressures, usually at what pressure, lead to renal vein compression and reduced GFR.

A

> 20 mmHg

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36
Q

Causes of TMA

A 
cocaine
certain chemotherapeutic agents
APAS
radiation nephritis
malignant HPNNS
TTP-HUS
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37
Q

risk factors for nephrotoxicity

A

older age
CKD
prerenal azotemia
Hypoalbuminemia

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38
Q

risk of AKI, or “contrast nephropathy,” is negligible in those with normal renal function but increases in the setting of CKD, particularly diabetic nephropathy

A

True

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39
Q

most common clinical course of contrast nephropathy

A

rise in SCr beginning 24–48 h f ing exposure, peaking within 3–5 days, and resolving within 1 week

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40
Q

Contrast nephropathy is thought to occur from a combination of factors (3)

A

(1) hypoxia in ROM
(2) cytotoxic damage to the tubules directly or via the ROS
(3) transient tubule obstruction with precipitated contrast material

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41
Q

When does Vancomycin cause AKI

A

When trough levels are high and when used in combination with other nephrotoxic antibiotics

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42
Q

Characteristics of aminoglycoside induced AKI

A
  • Nonoliguric AKI accompanies 10–30% even when plasma levels are in the therapeutic range
  • accumulate within the renal cortex
  • manifests after 5–7 days of therapy (delayed for 3-5 days to 2 weeks)
  • present even after the drug has been discontinued
  • Hypomagnesemia
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43
Q

Characteristics of amphotericin b induced AKI

A
  • renal vasoconstriction from an increase in TGF
  • direct tubular toxicity by
  • dose and duration dependent
  • binds to tubular membrane cholesterol and introduces pores.
  • features : polyuria, hypomagnesemia, hypocalcemia, and nongap metabolic acidosis.
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44
Q

Characteristics of Acyclovir induced AKI

A

Tubular obstruction from precipitates in tubules when given at high doses (500 mg/m 2) or IV bolus

45
Q

Antibiotics causing allergic interstitial nephritis

A 
penicillins
cephalosporins
quinolones
sulfonamides
rifampin
46
Q

Cisplatin and Carboplatin causes AKI through necrosis and apoptosis of tubular cells in which segment of the nephron

A

Proximal tubule

47
Q

Cyclophosphamide and ifosfamide cause he orrhagic cystitis and tubular toxicity manifested as?

A

Type II RTA (Fanconi’s syndrome)
Polyuria
Hypokale,ia

48
Q

Bevacizumab, mitomycin C, gemcitabine cause AKI through

A

TMA

49
Q

Ethylene glycol present in automobile a freeze, is metabolized to which compounds that may cause AKI through direct tubular injury and tubular obstruction

A

oxalic acid
glycolaldehyde
glyoxylate

50
Q

Metabolite responsible for tubular injury in diethylene glycol poisoning

A

2-hydroxyethoxyacetic acid (HEAA)

51
Q

Mechanism of Melamine induced AKI

A

intratubular obstruction or possibly direct tubular toxicity

52
Q

Cause of Chinese herb n athy” and “Balkan nephropathy”

A

Aristolochic acid

53
Q

Causes of rhabdomyolysis

A
  • traumatic crush injuries
  • muscle ischemia during vascular or orthopedic surgery
  • compression during coma or immobilization
  • prolonged seizure activity
  • excessive exercise
  • heat stroke or malignant hyperthermia
  • infections
  • metabolic disorders (e.g., hypophosphatemia, severe hypothyroidism)
  • myopathies (drug-induced, metabolic, or inflammatory)
54
Q

Pathogenic factors for AKI due to endogenous toxins

A
  • intrarenal vasoconstriction
  • direct proximal tubular toxicity
  • mechanical obstruction of the distal nephron lumen when myoglobin or hemoglobin precipitates with Tamm-Horsfall protein (uromodulin, the most common protein in urine and produced in the thick ascending limb of the loop of Henle), a process favored by acidic urine.
55
Q

Tumor lysis syndrome leads to massive release of uric acid. At which level does it cause precipitation in the renal tubules and AKI

A

15 mg/dl

56
Q

How does hypercalcemia (especially in MM) cause AKI

A

intense renal vasoconstriction and volume depletion

57
Q

Normal urinary flow rate does not rule out the presence of partial obstruction, because the GFR is normally two orders of magnitude higher than the urinary flow rate and hence a preservation of urine output may be misleading in hiding the postrenal partial obstruction.

A

True

58
Q

Instances when obstruction can cause AKI

A 
- affect both kidneys
     Bladder neck obstruction
     Prostatic disease
     Neurogenic bladder
     Anticholinergic drugs
- Unilateral obstruction in the setting of significant underlying CKD
- reflex vasospasm of the contralateral kidney
-
59
Q

Course of post renal AKI

A
  • initial period of hyperemia from afferent arteriolar dilation
  • intrarenal vasoconstriction
60
Q

Definitions of AKI

A
  • rise from baseline of at least 0.3 mg/dL within 48 h
  • at least 50% higher than baseline within 1 week
  • a reduction in urine output to <0.5 mL/kg per h for longer than 6 h
61
Q

Livedo reticularis and AKI

A

Atheroembolic disease

62
Q

What raises the possibility of renal artery disease

A

Asymmetric kidneys

63
Q

absence of systemic features of hypersensitivity, however, does not exclude the diagnosis of interstitial nephritis, and a kidney biopsy should be considered for definitive diagnosis.

A

True

64
Q

AKI, fever, arthralgias, and a pruritic erythematous rash.

A

allergic interstitial nephritis

65
Q

AKI accompanied by palpable purpura, pulmonary hemorrhage, or sinusitis

A

systemic vasculitis with glomerulonephritis

66
Q

Conditions resulting to Complete anuria early in the course of AKI

A

complete UTO
renal artery occlusion
overwhelming septic shock
severe ischemia (often with cortical necrosis)
severe proliferative glomerulonephritis or vasculitis.

67
Q

Define oliguria

A

<400 mL/24 h

68
Q

Preserved urine output can be seen in nephrogenic diabetes insipidus characteristic of which conditions

A
  • long-standing urinary tract obstruction
  • Interstitial disease
  • nephrotoxicity from cisplatin or aminoglycosides
69
Q

When is pigment nephropathy suspected

A

Red or brown urine color persists in the supernatant after centrifugation

70
Q

In the absence of preexisting proteinuria from CKD, AKI from ischemia or nephrotoxins leads to mild proteinuria (<1 g/d)

A

True

71
Q

pigmented “muddy brown” granular casts and tubular epithelial cell casts

A

Intrinsic

72
Q

dysmorphic red blood cells or red blood cell casts

A

Glomerulonephritis

73
Q

white blood cell casts.

A

Interstitial nephritis

74
Q

Urine eoinophils

A 
interstitial nephritis
pyelonephritis
cystitis
atheroembolic disease
glomerulonephritis
75
Q

oxalate crystals in AKI

A

ethylene glycol toxicity

76
Q

epithelial cell toxins such as aminoglycoside antibiotics and cisplatin, the rise in SCr is characteristically delayed for how many days after initial exposure.

A

3–5 days to 2 weeks

77
Q

Findings in TMA

A

thrombocytopenia
schistocytes on PBS
elevated LDH
low haptoglobin

78
Q

Most diagnostic for Prerenal azotemia

A

response to restoration of hemodynamics

79
Q

lab findings in tumor lysis syndrome

A

Hyperphosphatemia, hypocalcemia, hyperuricemia

hyperkalemia

80
Q

Clinical features and Conditions predisposing to TTP/HUS

A

Neurologic abnormalities and/or AKI
Recent diarrheal illness
Use of calcineurin inhibitors
Pregnancy or postpartum; spontaneous

81
Q

laboratory features in atheroembolic disease

A

Hypocomplementemia, eosinophiluria (variable), variable amounts of proteinuria

82
Q

RBC casts

A

GN
Vasculitis
Malignant HPN
TMA

83
Q

co-occurrence of an increased anion gap and an osmolal gap may suggest

A

Ethylene glycol poisoning

84
Q

Causes of disproportionate BN elevation

A 
Prerenal azotemia
UGIB
Hyperalimentation
increased tissue catabolism
glucocorticoid use
85
Q

other causes of FeNa <1%

A

sepsis
rhabdo
contrast nephropathy

86
Q

How is Furosemide test for oliguric AKI done?

A

urinary flow rate in response to bolus intravenous furosemide 1.0–1.5 mg/kg can be used a prognostic test: urine output of less than 200 mL over 2 h after intravenous furosemide may identify patients at higher risk of progression to more severe AKI, and the need for renal replacement therapy

87
Q

type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin

A

Kidney Injury Molecule-1 (KIM-1)

88
Q

highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 h of cardiopulmonary bypass– associated AKI

A

Neutrophil gelatinase associated lipocalin (NGAL, also known as lipocalin-2 or siderocalin

89
Q

cell-cycle arrest biomarkers used as predictive biomarkers for higher risk of AKI development in critically ill patients

A

insulin- like growth factor binding protein 7 (IGFBP7)

tissue inhibitor of metalloproteinase-2 (TIMP-2)

90
Q

Hallmark of AKI

A

buildup of nitrogenous wastes (elevated BUN)

91
Q

BUN levels causing mental status changes and bleeding complications

A

> 100

92
Q

Major cardiac complications of AKI

A

arrhythmia
pericarditis
pericardial effusion

93
Q

in optimizing renal perfusion for prerenal AKI, composition of replacement fluids should be targeted to the type of fluid lost.

A

True

94
Q

Fluid management in Prerenal AKI

A
  • Severe Blood loss: PRBC
  • Less severe blood loss: isotonic crystalloids/ colloids
  • HES: avoided
  • Crystalloids: less expensive and equally efficacious as colloids
  • Crystalloid > albumin in TBI
95
Q

Bridge therapies in HRS

A

Terlipressin
Octreotide + Midodrine
NE + albumin

96
Q

Glucocorticoids have been used, but not tested in randomized trials, in cases where AKI persists or worsens despite discontinuation of the suspected medication.

A

true

97
Q

Treatment given to AKI due to scleroderma renal crisis

A

ACE-i

98
Q

Treatment for TTP-HUS

A

plasma exchange

99
Q

Fluid requirement for rhabdomyolysis

A

10L/day

100
Q

Effect of alkaline fluids (75 meqs bicarb + 0.45% saline) in rhabdomyolysis

A

prevents tubular injury and cast formation

risk of worsening hypocalcemia

101
Q

goal Urinary flow rate in rhabdomyolysis

A

200-300 ml/h

102
Q

There is no evidence that increasing urine output itself improves the natural history of AKI, but diuretics may help to avoid the need for dialysis in some cases.

A

TRUE

103
Q

Metabolic acidosis is generally treated ONLY when? equipped

A

severe (pH <7.20 and serum bicarbonate <15 mmol/L)

104
Q

total caloric intake per day recommended by the KDIGO

A

20-30 kcal/kg/D

105
Q

recommended Protein intake in AKI

A

0.8-1.0 g/kg/D - non catabolic AKI w/o need for HD

1-1.5 g/kg/D - patients on HD

maximum of 1.7 g/kg/D if hyper catabolic and on continuous HD

106
Q

Treatment for uremic bleeding

A

estrogen
desmopressin
HD

107
Q

Dialysis indications

A
  • volume overload
  • hyperkalemia
  • acidosis
  • in some toxic ingestions
  • when there are severe complications of uremia (asterixis, pericardial rub or effusion, encephalopathy, uremic bleeding)
108
Q

Conditions wherein CRRT is preferred when available

A

hemodynamic instability
cerebral edema
significant volume overload

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