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MD2 Renal > AKI > Flashcards

AKI Flashcards

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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
Give 3 examples of AKI biomarkers likely to be incorporated into the diagnostic criteria
``` RIFLE R (AKIN-1) RIFLE I (AKIN-2) RIFLE F (AKIN-3) (In order of increasing levels of damage) ```
26
Is community-acquired AKI usually a result of pre-renal, renal or post-renal causes? What is the 2nd most common cause?
Pre-renal in 70% of cases | 2nd most common cause is obstruction
27
What proportion of cases of community-acquired AKI are superimposed on pre-existing CKD?
About half
28
What is the main cause of AKI in hospitalised patients? What is the predicted mortality in these cases?
ATN (renal cause) in >75% of cases | Mortality >70% in these cases
29
What is the adaptive physiological response to low renal perfusion? What is the effect of this response on urinary concentration capacity?
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
30
What occurs with decompensation following prolonged renal hypoperfusion?
Excessive SNS and RAAS results in ischaemic injury
31
What medications may exacerbate the dysautoregulation that occurs in prolonged renal hypoperfusion?
NSAIDs | ACEIs
32
Give 2 causes of tubular injury in AKI (i.e. ATN)
Ischaemia/prolonged hypoperfusion | Toxins
33
Give 5 examples of toxins which may cause ATN
``` Hb/myoglobin Aminoglycosides Statins Cisplatin Ethylene glycol ("anti-freeze") ```
34
Give 3 causes of interstitial nephritis
Drugs Infection Infiltration
35
Give 2 causes of glomerular damage
Inflammation (glomerulonephritis) | Thrombosis
36
Give 2 types of vascular disease which may cause intrinsic AKI
Inflammation (vasculitis) | Occlusion (thrombosis or embolism)
37
Is ATN reversible or irreversible?
Most often reversible
38
What occurs following initial hypoperfusion in ATN to worsen the disease process?
Reperfusion injury: restoration of blood flow to the damaged vascular network results in further inflammation
39
What are the 3 phases of ATN and what occurs in each?
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
How long does the recovery phase of ATN generally take? What is the risk here?
Up to 2-6 weeks | Risk of longterm chronic damage
41
What are the 5 main questions to ask when clinically evaluating AKI?
``` 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
What clinical finding supports a diagnosis of AKI?
Oliguria
43
What 4 risk factors/clinical findings suggest CKD?
Pre-existing illness (e.g. DM, HTN, vascular disease) Increased age Previous sCr show gradual increase Small, echogenic kidneys on US
44
What 3 clinical findings suggest obstruction causing AKI?
Complete anuria Palpable bladder O/E Bilateral hydronephrosis on renal US
45
What does volume depletion suggest about the cause of the pt's AKI?
Implies a pre-renal cause (i.e. renal hypoperfusion)
46
What clinical measures can be used to assess a pt's volume status?
JVP Postural BP drop Urinary concentration indices Fluid challenge
47
What are 4 clinical features which might suggest a major vascular occlusion has occurred?
Hx of vascular disease Renal asymmetry on US Loin pain with macro haematuria Complete anuria
48
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
``` 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
How is FENa+ calculated?
FENa+ = (urine Na+/plasma Na+) x (sCr/urine Cr) x 100
50
What are the 3 key area for investigation in the clinical assessment of AKI?
Volume status Urine studies Renal US
51
What clinical findings might suggest a diagnosis of thrombotic microangiopathy/HUS?
Thrombocytopaenia | Anaemia
52
What clinical findings might suggest a diagnosis of myeloma?
``` CRAB: hyperCalcaemia Renal failure Anaemia Bone lesions ```
53
List some clinical signs which may indicate rapidly progressive glomerulonephritis (RPGN)
``` Proteinuria Microscopic haematuria Fever, malaise Anaemia Nasopharyngeal disease (in Wegener's granulomatosis) Lung disease Arthralgias/arthropathy Rashes ```
54
Distinguish between proliferative and non-proliferative glomerular disease
Proliferative: haematuria, usually proteinuria (nephritic syndrome) Non-proliferative: predominantly proteinuria, negligible haematuria (nephrotic syndrome)
55
Give 3 causes of proliferative glomerulonephritis
IgA nephropathy Post-infectious GN Vasculitides/RPGN
56
Give 3 causes of non-proliferative glomerulonephritis
Minimal change disease (MCD) Focal segmental glomerulosclerosis (FSGS) Membranous nephropathy
57
Give 6 examples of conditions which cause nephrotic sydrome
``` MCD FSGS Membranous nephropathy DM Endotheliosis Amyloidosis ```
58
Give 5 examples of conditions which cause nephritic syndrome
``` IgA nephropathy Post-infectious GN Vasculitides/RPGN Thin basement membrane Alport's syndrome ```
59
Give 2 examples of conditons causing endotheliosis
Pre-eclampsia | VEGF inhibitors
60
Give 5 examples of causes of vasculitides/RPGN
SLE Anti-neutrophil cytoplasmic Ab (ANCA)-associated Microscopic polyangitis (MPA) Granulomatosis with polyangitis (Wegener's granulomatosis, GPA) Goodpastures disease (anti-GBM disease)
61
List 5 rarer causes of glomerular disease
``` Fabry disease c3 glomerulopathy (dense deposit disease) Fibrillary and immunotactoids Gns HIV nephropathies Warfarin-related nephropathy ```
62
What techniques are used to diagnose RPGN?
Morphology Special stains (e.g. silver for GBM) Immunohistochemistry/immunofluorescence Sometimes requires EM
63
What is the drawback of using EM for diagnosis of RPGN?
Time delay
64
What background morbidities increase risk of AKI?
``` Age CKD HF Liver disease DM Vascular disease Background nephrotoxic medications ```
65
Give 4 examples of acute insults which may precipitate AKI
Sepsis and hypoperfusion Toxicity Obstruction Parenchymal kidney disease
66
What is the most important preventative action against AKI?
Optimising ECV to prevent volume depletion
67
What are the 4 key steps for prevention of AKI?
Monitoring Maintaining circulation Minimising kidney insults (e.g. infection, drugs) Managing the acute illness (e.g. sepsis, HF, liver failure)
68
What 7 investigations should be ordered where AKI is suspected?
Urine dipstick (+ RBC morphology if +ive for blood) Urine PCR Renal US LFTs CRP CK Platelet count (+/- blood film, haptoglobin, etc)
69
Define oliguric RF functionally and in terms of UO
UO < than that required to maintain solute balance (can't excrete all solute taken in) UO <400 mL/24 hr
70
Define anuric RF in terms of UO
<100 mL/24 hr
71
What 3 conditions may cause anuric RF?
``` Complete obstruction Major vascular catastrophy Severe ATN (more commonly) ```
72
What 2 conditions is oliguria more common with?
Obstruction | Pre-renal azotemia
73
What class of conditions typically cause non-oliguric RF? Give 3 examples
Intrinsic renal causes (e.g. nephrotoxic ATN, acute GN, AIN)
74
Does oliguric or non-oliguric RF have a higher mortality?
Oliguric (80% vs 25%)
75
List 4 important aspects of supportive AKI care
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
Are loop diuretics indicated in AKI?
Controversial - main indication for use is volume overload
77
What are the 6 acute metabolic complications of AKI?
``` Volume overload Hyperkalaemia Metabolic acidosis Hypocalcaemia Infections Nutrition ```
78
How is volume overload as a result of AKI treated?
Salt and water restriction Diuretics Dialysis for refractory cases
79
How is hyperkalaemia as a result of AKI treated?
``` Restrict K+ intake IV glucose and insulin Kayexalate Calcium gluconate Acute dialysis ```
80
How is metabolic acidosis as a result of AKI treated?
HCO3- (if <7.2) | Dialysis
81
How is hypocalcaemia as a result of AKI treated?
Calcium carbonate | Calcium gluconate
82
What are the principles underlying peritoneal dialysis?
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
What is the osmotically active agent in peritoneal dialysis?
Glucose
84
How does haemodialysis work?
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
How are solutes moved in haemofiltration?
Via convection (swept through membrane by moving stream of ultrafiltrate; "solvent drag")
86
List 8 causes of hyperkalaemia
``` 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
How should mild hyperkalaemia be treated?
Identify and correct underlying cause
88
How should moderate hyperkalaemia be treated?
As for mild | Also identify ECG changes
89
How should severe hyperkalaemia be treated?
Stabilise myocardium Insulin + dextrose Correct acidosis if volume deplete
90
Define mild, moderate and severe hyperkalaemia
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
List 5 causes of hypokalaemia
``` Diarrhoea Diuretics Polyuria Hyperaldosteronism Shift into cells ```
92
What are 3 conditions which may cause K+ to shift into cells, producing a hypokalaemia?
Alkalosis B-agonists Insulin

MD2 Renal (6 decks)

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