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MD2 Renal > AKI > Flashcards

AKI Flashcards

1
Q

What are the diagnostic criteria for AKI stage I?

A

Creatinine increase ≥ 25 umol/L or 1.5-2x

UO 6 hrs less than 0.5 mL/kg/hr

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2
Q

Why is creatinine used as a surrogate measure of GFR?

A

Predominantly excreted by glomerular filtration (only very small amount secreted)

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3
Q

What is the gold standard substance for assessing renal clearance?

A

Inulin (only used in research setting)

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4
Q

What are the diagnostic criteria for AKI stage II?

A

Creatinine increase ≥200-300%

UO 12 hrs less than 0.5 mL/kg/hr

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5
Q

What are the diagnostic criteria for AKI stage III?

A

Creatinine increase ≥300% or creatinine ≥350umol/L after a rise of at least 50 umol/L or RRT
UO 24 hrs less than 0.3 mL/kg/hr, or anuria for 12 hrs

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6
Q

What is the main cause of community-acquired AKI?

A

Hypoperfusion

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7
Q

List 4 broad causes of intrinsic AKI. Which of these are common? Which are uncommon?

A 
Tubular injury (common)
Interstitial nephritis (common)
Glomerular disease (uncommon)
Vascular disease (uncommon)
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8
Q

What processes occur on a cellular level with ATN?

A

Ischaemic depletion of ATP, release of ROS and apoptosis

Cell desquamation, obstructive cast, and back-leak of tubular fluid (pathological absorption of metabolic wastes)

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9
Q

What is the main risk factor for AKI?

A

Background of CKD

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10
Q

List 7 risk factors for AKI

A 
Elderly
CKD
HF
Liver disease
DM
Vascular disease
Nephrotoxic medications
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11
Q

Give 4 examples of acute insults which may tip a person with risk factors into AKI

A 
STOP:
Sepsis and hypoperfusion
Toxicity
Obstruction
Parenchymal disease (e.g. acute GN, myeloma)
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12
Q

What are the 4 main physiological roles of the normal kidney?

A

Fluid balance
Acid-base balance
Excretion of wastes and solutes
Endocrine function

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13
Q

What hormones are produced by the kidneys?

A

Activation of 25-OH vitamin D to 1,25-OH (active) vitamin D

EPO

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14
Q

What disturbances to normal function occur with kidney disease?

A

Na+/H2O imbalance (failure of conservation or excretion)
Accumulation of acids
Accumulation of solutes and waste products
Abnormalities of endocrine function

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15
Q

What specific abnormalities of endocrine function may be expected in kidney disease?

A

Anaemia

Disordered bone metabolism

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16
Q

Of the 4 main disturbances resulting from acute kidney disease, which are the most easily measured and recognisable indicators of loss of function? Which of these may be immediately abnormal and which are time-dependent?

A

Na+/H2O imbalance (immediately abnormal)
Accumulation of acids (time-dependent)
Accumulation of solutes and waste products (time-dependent)

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17
Q

RRT

A

Renal replacement therapy (e.g. haemodialysis)

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18
Q

How is AKI defined in the research setting?

A

Acute elevation in serum creatinine

Oliguria

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19
Q

How is AKI defined pathophysiologically?

A 
Any or all of:
Decreased GFR
Oliguria or polyuria
Acidosis
Hyperkalaemia
Abnormal urinary contents (electrolyte abnormalities, glycuria)
Inflammation leading to malnutrition or systemic injury
Anaemia
Disordered bone metabolism
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20
Q

What phenomena commonly cause a delay in AKI diagnosis?

A

Injury evolution time (delay between injury and drop in GFR)

Delayed actual rise (between drop in GFR and rise in sCr)

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21
Q

Why is it difficult to recognise an increased sCr?

A

Baseline, true and current sCr may be difficult to assess

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22
Q

Why is it difficult to assess the baseline sCr?

A

Interperson variability relating to the influence of age, sex and race on muscle mass

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23
Q

Why is it difficult to assess the true sCr?

A

Analytical variability (~10 uM)

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24
Q

Why may it be difficult to assess the current sCr?

A

Infrequent sampling

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25
Q

Give 3 examples of AKI biomarkers likely to be incorporated into the diagnostic criteria

A 
RIFLE R (AKIN-1)
RIFLE I (AKIN-2)
RIFLE F (AKIN-3)
(In order of increasing levels of damage)
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26
Q

Is community-acquired AKI usually a result of pre-renal, renal or post-renal causes? What is the 2nd most common cause?

A

Pre-renal in 70% of cases

2nd most common cause is obstruction

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27
Q

What proportion of cases of community-acquired AKI are superimposed on pre-existing CKD?

A

About half

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28
Q

What is the main cause of AKI in hospitalised patients? What is the predicted mortality in these cases?

A

ATN (renal cause) in >75% of cases

Mortality >70% in these cases

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29
Q

What is the adaptive physiological response to low renal perfusion? What is the effect of this response on urinary concentration capacity?

A

BP: maintained by SNS and RAAS
Na+/H2O: retention mediated by ADH and aldosterone
Urinary concentration capacity is intact, corresponds to stage I-II early AKI

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30
Q

What occurs with decompensation following prolonged renal hypoperfusion?

A

Excessive SNS and RAAS results in ischaemic injury

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31
Q

What medications may exacerbate the dysautoregulation that occurs in prolonged renal hypoperfusion?

A

NSAIDs

ACEIs

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32
Q

Give 2 causes of tubular injury in AKI (i.e. ATN)

A

Ischaemia/prolonged hypoperfusion

Toxins

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33
Q

Give 5 examples of toxins which may cause ATN

A 
Hb/myoglobin
Aminoglycosides
Statins
Cisplatin
Ethylene glycol ("anti-freeze")
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34
Q

Give 3 causes of interstitial nephritis

A

Drugs
Infection
Infiltration

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35
Q

Give 2 causes of glomerular damage

A

Inflammation (glomerulonephritis)

Thrombosis

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36
Q

Give 2 types of vascular disease which may cause intrinsic AKI

A

Inflammation (vasculitis)

Occlusion (thrombosis or embolism)

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37
Q

Is ATN reversible or irreversible?

A

Most often reversible

38
Q

What occurs following initial hypoperfusion in ATN to worsen the disease process?

A

Reperfusion injury: restoration of blood flow to the damaged vascular network results in further inflammation

39
Q

What are the 3 phases of ATN and what occurs in each?

A

Initiation: acute decrease in GFR to low or very low levels, increased sCr and urea
Maintenance: sustained reduction in GFR, continued increase in sCr and urea
Recovery: increased UO, gradual decrease in sCr and urea to pre-injury levels

40
Q

How long does the recovery phase of ATN generally take? What is the risk here?

A

Up to 2-6 weeks

Risk of longterm chronic damage

41
Q

What are the 5 main questions to ask when clinically evaluating AKI?

A 
Is the impairment acute or chronic?
Has obstruction been excluded?
What is the pt's volume status?
Is there evidence of other intrinsic renal disease apart from ATN?
Has a major vascular occlusion occurred?
42
Q

What clinical finding supports a diagnosis of AKI?

A

Oliguria

43
Q

What 4 risk factors/clinical findings suggest CKD?

A

Pre-existing illness (e.g. DM, HTN, vascular disease)
Increased age
Previous sCr show gradual increase
Small, echogenic kidneys on US

44
Q

What 3 clinical findings suggest obstruction causing AKI?

A

Complete anuria
Palpable bladder O/E
Bilateral hydronephrosis on renal US

45
Q

What does volume depletion suggest about the cause of the pt’s AKI?

A

Implies a pre-renal cause (i.e. renal hypoperfusion)

46
Q

What clinical measures can be used to assess a pt’s volume status?

A

JVP
Postural BP drop
Urinary concentration indices
Fluid challenge

47
Q

What are 4 clinical features which might suggest a major vascular occlusion has occurred?

A

Hx of vascular disease
Renal asymmetry on US
Loin pain with macro haematuria
Complete anuria

48
Q

Distinguish between pre-renal causes of AKI and ATN in terms of urine osmolarity, urine sodium, fraction excretion of sodium, fraction excretion of urea, urinary specific gravity, urine Cr/sCr ratio and urine sediment

A 
Urine osmolarity: high vs low
Urine sodium: low vs high
Fraction excretion of sodium: low vs high
Fraction excretion of urea: low vs high
Specific gravity: >1020 vs
49
Q

How is FENa+ calculated?

A

FENa+ = (urine Na+/plasma Na+) x (sCr/urine Cr) x 100

50
Q

What are the 3 key area for investigation in the clinical assessment of AKI?

A

Volume status
Urine studies
Renal US

51
Q

What clinical findings might suggest a diagnosis of thrombotic microangiopathy/HUS?

A

Thrombocytopaenia

Anaemia

52
Q

What clinical findings might suggest a diagnosis of myeloma?

A 
CRAB:
hyperCalcaemia
Renal failure
Anaemia
Bone lesions
53
Q

List some clinical signs which may indicate rapidly progressive glomerulonephritis (RPGN)

A 
Proteinuria
Microscopic haematuria
Fever, malaise
Anaemia
Nasopharyngeal disease (in Wegener's granulomatosis)
Lung disease
Arthralgias/arthropathy
Rashes
54
Q

Distinguish between proliferative and non-proliferative glomerular disease

A

Proliferative: haematuria, usually proteinuria (nephritic syndrome)
Non-proliferative: predominantly proteinuria, negligible haematuria (nephrotic syndrome)

55
Q

Give 3 causes of proliferative glomerulonephritis

A

IgA nephropathy
Post-infectious GN
Vasculitides/RPGN

56
Q

Give 3 causes of non-proliferative glomerulonephritis

A

Minimal change disease (MCD)
Focal segmental glomerulosclerosis (FSGS)
Membranous nephropathy

57
Q

Give 6 examples of conditions which cause nephrotic sydrome

A 
MCD
FSGS
Membranous nephropathy
DM
Endotheliosis
Amyloidosis
58
Q

Give 5 examples of conditions which cause nephritic syndrome

A 
IgA nephropathy
Post-infectious GN
Vasculitides/RPGN
Thin basement membrane
Alport's syndrome
59
Q

Give 2 examples of conditons causing endotheliosis

A

Pre-eclampsia

VEGF inhibitors

60
Q

Give 5 examples of causes of vasculitides/RPGN

A

SLE
Anti-neutrophil cytoplasmic Ab (ANCA)-associated
Microscopic polyangitis (MPA)
Granulomatosis with polyangitis (Wegener’s granulomatosis, GPA)
Goodpastures disease (anti-GBM disease)

61
Q

List 5 rarer causes of glomerular disease

A 
Fabry disease
c3 glomerulopathy (dense deposit disease)
Fibrillary and immunotactoids Gns
HIV nephropathies
Warfarin-related nephropathy
62
Q

What techniques are used to diagnose RPGN?

A

Morphology
Special stains (e.g. silver for GBM)
Immunohistochemistry/immunofluorescence
Sometimes requires EM

63
Q

What is the drawback of using EM for diagnosis of RPGN?

A

Time delay

64
Q

What background morbidities increase risk of AKI?

A 
Age
CKD
HF
Liver disease
DM
Vascular disease
Background nephrotoxic medications
65
Q

Give 4 examples of acute insults which may precipitate AKI

A

Sepsis and hypoperfusion
Toxicity
Obstruction
Parenchymal kidney disease

66
Q

What is the most important preventative action against AKI?

A

Optimising ECV to prevent volume depletion

67
Q

What are the 4 key steps for prevention of AKI?

A

Monitoring
Maintaining circulation
Minimising kidney insults (e.g. infection, drugs)
Managing the acute illness (e.g. sepsis, HF, liver failure)

68
Q

What 7 investigations should be ordered where AKI is suspected?

A

Urine dipstick (+ RBC morphology if +ive for blood)
Urine PCR
Renal US
LFTs
CRP
CK
Platelet count (+/- blood film, haptoglobin, etc)

69
Q

Define oliguric RF functionally and in terms of UO

A

UO < than that required to maintain solute balance (can’t excrete all solute taken in)
UO <400 mL/24 hr

70
Q

Define anuric RF in terms of UO

A

<100 mL/24 hr

71
Q

What 3 conditions may cause anuric RF?

A 
Complete obstruction
Major vascular catastrophy
Severe ATN (more commonly)
72
Q

What 2 conditions is oliguria more common with?

A

Obstruction

Pre-renal azotemia

73
Q

What class of conditions typically cause non-oliguric RF? Give 3 examples

A

Intrinsic renal causes (e.g. nephrotoxic ATN, acute GN, AIN)

74
Q

Does oliguric or non-oliguric RF have a higher mortality?

A

Oliguric (80% vs 25%)

75
Q

List 4 important aspects of supportive AKI care

A

Discontinue offending agents and any nephrotoxins (e.g. NSAIDs, antihypertensives if low BP)
Review drug doses and adjust accordingly
Assess volume status to prevent overload
Nephrology input to gauge need for dialysis

76
Q

Are loop diuretics indicated in AKI?

A

Controversial - main indication for use is volume overload

77
Q

What are the 6 acute metabolic complications of AKI?

A 
Volume overload
Hyperkalaemia
Metabolic acidosis
Hypocalcaemia
Infections
Nutrition
78
Q

How is volume overload as a result of AKI treated?

A

Salt and water restriction
Diuretics
Dialysis for refractory cases

79
Q

How is hyperkalaemia as a result of AKI treated?

A 
Restrict K+ intake
IV glucose and insulin
Kayexalate
Calcium gluconate
Acute dialysis
80
Q

How is metabolic acidosis as a result of AKI treated?

A

HCO3- (if <7.2)

Dialysis

81
Q

How is hypocalcaemia as a result of AKI treated?

A

Calcium carbonate

Calcium gluconate

82
Q

What are the principles underlying peritoneal dialysis?

A

Visceral peritoneum acts as semi-permeable membrane
Solutes leave the blood via diffusion
Fluids move from blood to dialysate via osmotic and hydrostatic pressures

83
Q

What is the osmotically active agent in peritoneal dialysis?

A

Glucose

84
Q

How does haemodialysis work?

A

Blood circulates at high volume through dialyser composed of many capillary width tubes of semi-permeable membrane
Solutes move via osmosis
Fluids move via ultrafiltration (pressure gradient)

85
Q

How are solutes moved in haemofiltration?

A

Via convection (swept through membrane by moving stream of ultrafiltrate; “solvent drag”)

86
Q

List 8 causes of hyperkalaemia

A 
Metabolic acidosis
Insulin deficiency (i.e. DKA, HHS)
Release from pathological cells
Non-selective B-blockers
Reduced RAAS release or effect
Reduced renal blood flow
Abnormal tubular function (AKD, CKD)
Increased intake
87
Q

How should mild hyperkalaemia be treated?

A

Identify and correct underlying cause

88
Q

How should moderate hyperkalaemia be treated?

A

As for mild

Also identify ECG changes

89
Q

How should severe hyperkalaemia be treated?

A

Stabilise myocardium
Insulin + dextrose
Correct acidosis if volume deplete

90
Q

Define mild, moderate and severe hyperkalaemia

A

Mild: 5.5-5.9 mM
Moderate: 6.0-6.9 mM
Severe: >7.0 mM, or >6.5 mM and rapidly increasing or evidence of ECG changes

91
Q

List 5 causes of hypokalaemia

A 
Diarrhoea
Diuretics
Polyuria
Hyperaldosteronism
Shift into cells
92
Q

What are 3 conditions which may cause K+ to shift into cells, producing a hypokalaemia?

A

Alkalosis
B-agonists
Insulin

MD2 Renal (6 decks)

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