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Renal Pathology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Function of kidneys

A 
Body fluid homeostasis
- urine production 
Regulation of vascular tone
- BP
Excretory function 
- urea
- creatinine
- drugs
Electrolyte homeostasis
- Na, K, Cl, Ca, P
Acid base homeostasis
- H+
- bicarbonate 
Endocrine function 
- Erythropoietin 
- Vit D metabolism 
- Renin
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2
Q

Traditional definition of acute renal failure

A

Rapid loss of glomerular filtration and tubular function over hours to days

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3
Q

What does retention or urea/creatinine show?

A

Failure of homeostasis

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4
Q

What is urea and creatinine excreted by?

A

The kidneys

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5
Q

What can small rises in creatinine cause?

A

Increased odds of death

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6
Q

Definition of acute kidney injury

A

Increase in serum creatinine
- By >26.5 umol/l (0.3mg/dl) within 48 hours OR
- to 1.5x baseline, which is known or presumed to have occurred within the prior 6 days
Urine volume <0.5ml/kg/h for 6 hours

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7
Q

Stages of AKI

A

AKI 1
AKI 2
AKI 3

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8
Q

What is AKI 1?

A 
Serum creatinine
- 1.5-1.9x baseline
OR
- 26.5 umol/l increase
Urine output
- < 0.5ml/kg/h for 6-12 hours
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9
Q

What is AKI 2?

A

Serum creatinine
- 2.0-2.9 x baseline
Urine output
- <0.5 ml/kg/h for >12 hours

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10
Q

What is AKI 3?

A 
Serum creatinine
- 3x baseline OR
- Increase to >354 umol/l (and above) OR
- initiation of RRT
Urine output
- < 0.3ml/kg/h > 24 hours OR
- Anuria for > 12 hours
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11
Q

Stages of AKI

A 
Antecedents
- normal 
- increased risk 
Intermediate stage
- Damage 
AKI
- Decreased GFR
- kidney failure 
Outcomes
- death 
- complications
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12
Q

What are the stages of AKI defined as?

A

Creatinine

Urine output

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13
Q

How many hospital admissions are complicated by AKI?

A

1 in 7

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14
Q

What are the immediately dangerous consequences of AKI?

A 
AEIOU
A - acidosis
E - Electrolyte imbalance
I - Intoxication TOXINS
O - overload
U - uraemic complications
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15
Q

Mortality of dialysis requiring-AKI in hospital

A

45-75%

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16
Q

Mortality of non dialysis AKI stages

A

AKIN 1 - 8%
AKIN 2 - 25%
AKIN 3 - 33%

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17
Q

What is the blood values where you would act on AKI?

A

Rise in serum creatinine >50% baseline
Baseline creatinine of 80umol/L
Rises to 120umol/L (may still be in normal range)
Significant kidney injury

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18
Q

Pathological causes of AKI

A

Pre renal - blood flow to kidney
Renal (intrinsic) - damage to renal parenchyma
Post renal - obstruction to urine exit

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19
Q

Causes of intrinsic AKI

A 
Acute tubular injury 
- prolonged pre renal AKI
- rhabdomyosis
- haemoglobuineria
- nephrotoxins (Iodinated contrast, NSAIDs, gentamicin) snake venom, heavy metals
Mushrooms
Acute tubular necrosis (ATN)
Tubulointestinal injury 
Acute Glomerulonephritis 
Myeloma
Vasculitis
- Lupus
- ANCA associated
Thrombotic microangiopathy
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20
Q

Causes of pre renal AKI

A 
Sepsis
Hypovolaemia
- haemorrhage
- burns
- vomiting/diarrhoea
- diuretics
Hepatorenal syndrome
Cardiac failure
Liver failure
Hypotension - medications
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21
Q

Causes of post renal AKI

A 
Kidney stones
Clot
Sloughed papilla 
Prostatic hypertrophy 
Tumours
Ureteric stricture 
Retroperitoneal / radiation fibrosis
RPF
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22
Q

Commonest cause of AKI

A

Poor perfusion leading to established tubular damage

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23
Q

Pathology of pre renal AKI

A

Failure of the circulation (loss of volume and/or pressure) to provide sufficient plasma flow to maintain blood chemistry and fluid balance

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24
Q

Outcomes of pre renal AKI

A

If promptly treated, can resolve

If sustained, may lead to acute tubular necrosis

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25
Q

Why are the kidneys susceptible to hypoperfusion?

A

Blood supply
Oxygenation
Metabolic demand

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26
Q

Perfusion of kidneys

A

Cortex richly perfused

Medulla receives around 10-15% of renal blood flow

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27
Q

Does the kidney have the potential to regenerate following an acute kidney injury?

A

Yes

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28
Q

Pathology of initiation of AKI

A

Exposure to toxic/ischaemic insult
Renal parenchymal injury evolving
AKI potentially preventable

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29
Q

Pathology of maintenance of AKI

A

Established parenchymal injury
Usually maximally oliguric now
Typical duration 1 - 2 weeks (up to several months)

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30
Q

Pathology of recovery of AKI

A

Gradual increase in urine output
Fall in serum creatinine (may lag behind diuresis)
If GFR recovers quicker than tubule resorptive capacity, excess diuresis may result (e.g. post obstructive natriuresis)

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31
Q

What is radiocontrast nephropathy (RCN)?

A

AKI following administration of iodinated contrast agent

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32
Q

Presentation of RCN

A

Transient renal dysfunction

Resolving after 72 hours

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33
Q

What may RCN lead to?

A

Permanent loss of function

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34
Q

Risk factors for RCN

A 
DM
Renovascular disease
Impaired renal function 
Paraprotein 
High volume of radiocontrast
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35
Q

What is myeloma?

A

A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains

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36
Q

Who is myeloma common in?

A

Elderly

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37
Q

Presentation of myeloma

A 
Anaemia
Back pain 
Weight loss
Fractures
Infections
Cord compression 
Marked elevated ESR
Hypercalcaemia
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38
Q

Investigations of myeloma

A

Bone marrow aspirate > 10% clonal plasma cells
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones Protein (BJP)
Skeletal survery - lytic lesions

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39
Q

Pathology of renal failure in myeloma

A 
Cast nephropathy 'myeloma kidney'
Light chain nephropathy 
Amyloidosis
Hypercalcaemia
Hyperuricaemia
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40
Q

Investigations of AKI

A 
Fluid status
Drugs
Insults
Renal failure
Urine dipstick 
FBC
USS
Blood gas
Renal biopsy 
Renal USS
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41
Q

What is better than treatment for AKI?

A

Prevention

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42
Q

At risk events for AKI occuring

A

Sepsis (e.g. pneumonia, cellulitis, UTI etc)
Toxins (e.g. X ray contrast, NSAIDs, gentamicin, herbal remidies)
Hypotension
Hypovolaemia
Major surgery

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43
Q

Causes of hypovolaemia

A

Haemorrhage
Vomiting
Diarrhoea

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44
Q

Risk factors for AKI

A 
Age > 75
Previous AKI
Heart failure
Liver disease
Chronic kidney disease
DM
Vascular disease
Cognitive impairment
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45
Q

What is done to identify patients at risk of AKI?

A

In the presence of a risk event and one or more risk factors, consider activating the below STOP AKI Prevention care bundle

  • STOP
  • S = sepsis (if suspected screen and treat promptly - SEPSIS 6)
  • T = Toxins - avoid (e.g. gentamicin, NSAIDs, iodinated contrast)
  • O = optimise BP and volume status - avoid/correct hypovolaemia, review BP meds
  • P = prevent harm - daily U and Es, fluid balance and medication review
46
Q

Examples of nephrotoxic drugs

A

Gentamicin
NSAIDs
Iodinated contrast
Aminoglycosides

47
Q

How should you optimise BP and volume status?

A

Consider IV fluids if hypovolaemic;
- resus fluids 250-500mls IV crystalloid ? bolus over 15 mins and review response
Withhold Antihypertensives
Withhold Diuretics

48
Q

How is fluid balance monitored?

A

Input
Output
Daily weights

49
Q

Treatment of AKI

A 
Remove/treat cause if possible
If pre renal 
- Fluid
- BP support
Renal 
- remove participant 
Post renal 
- catheter 
Treat sepsis 
Stop/avoid potential nephrotoxins 
Optimise BP
- fluids
- withhold antihypertensive drugs
Treatment of complications
50
Q

What are the 5Rs from IV prescribing?

A 
Resuscitation 
Routine maintenance
Replacement
Redistribution 
Reassessment
51
Q

When would patients need replacement fluids?

A

If dont need urgent IV resuscitation but do need IV additional to maintenance to correct existing deficit or ongoing abnormal External losses e.g. diarrhoea, fever

52
Q

When would patients need redistribution fluids?

A

When the patients have abnormal internal fluid redistribution or abnormal fluid handling, particularly with sepsis, or major illness, cardiac, liver or renal disease e.g. tissue oedema, GI tract/thoracic/peritoneal collection

53
Q

How many ml from water are usually on the intake in health?

A

2500ml

25-35ml/kg/day

54
Q

How much output of water is normal? How is water excreted from the body?

A 
Urine
Insensible
- skin 
- lungs
- faeces
55
Q

How much Na and K are taken in on average?

A

1mmol/kg/day both

56
Q

What is the only electrolytes dextrose contains?

A

Glucose

variable K

57
Q

What is the only electrolytes NaCl / glucose solution contains?

A

Na
Variable K
Cl
Glucose

58
Q

What electrolytes does Hartmanns contain?

A 
Na
K
Cl 
Ca
Bicarb precursor (lactate)
59
Q

What electrolytes does plasma contain?

A 
Na
K
Cl
Ca
Bicarb
Glucose
60
Q

What electrolytes does plasma lyte contain?

A

Na
K
Cl
Bicarb precursor (acetate and gluconate)

61
Q

ECG changes in hyperkalaemia

A 
Peaked T waves
- tall tented T waves 
P wave widens and flattens
PR segment lengthens
P waves eventually disappear 
Prolonged QRS interval 
High grade AV block with slow junctional and ventricular escape rhythms 
Sinus bradycardia or slow AF
Development of a sine wave appearance (a pre terminal rhythm)
Cardiac arrest
Asystole
VF
62
Q

Treatment of hyperkalaemia

A 
Stabilise myocardium 
- calcium gluconate 
Shift (K+ intracellularly)
- salbutamol 
- insulin-dextrose
Remove
- diuresis
- dialysis
- anion exchange resins
63
Q

Treatment of morphine toxicity

A

Naloxone

64
Q

Treatment of digoxin toxicity

A

Digibind

65
Q

Indication for dialysis in AKI

A 
Acidosis
- Decreased HCO3
- Increased lactate
- increased pCO2
Electrolytes
- Increased K
- Increased or decreased Na
- Increased Ca
- Increased uric acid
- Increased PO4-
- Increased Mg2+
Intoxication 
- aspirin 
- theophylline
- lithium 
- ethylene glycol 
- methanol 
- metformin 
Overload
- nutrition 
- pulmonary oedema
- HTN
Uraemia
- altered mental status
- Pericarditis
- unexplained bleeding
66
Q

Solute removal in haemodialysis vs hemofiltration

A

Haemodialysis
- removal by diffusion
Haemofiltration
- removed by convection

67
Q

What type of therapy is haemodyalsis?

A

Intermittent

Each session lasting 3 - 5 hours

68
Q

What type of therapy is haemofitration?

A

Continous

69
Q

When is haemofiltration used?

A

In an ITU setting usually to treat AKI but can be used in multiple organ dysfunction or sepsis

70
Q

Advantages of haemodialysis

A

Rapid solute removal
Rapid volume removal
Rapid correction of electrolyte disturbances
Efficient treatment for hypercatabolic patient

71
Q

Disadvantages for haemodialysis

A

Haemodynamic instability
Concern if dialysis associated with hypotension, may prolong AKI
Fluid removal only during short treatment time

72
Q

Advantages of continuous therapy

A

Slow volume removal associated with greater haemodynamic stability
Absence of fluctuation in volume and solute control over time
Greater control over volume status

73
Q

Disadvantages of continuous renal replacement therapy

A

Need for continuous anticoagulation
May delay weaning/mobilisation
May not have adequate clearance in hypercatabolic patient

74
Q

What is the staging system for AKI called?

A

AKIN staging system

75
Q

How many stages are there in AKI?

A

3

76
Q

What is the pneumonic to remember immediate problems of AKI?

A

AEIOU

77
Q

What are the long term problems caused by AKI?

A

Secondary problems / infections

  • pneumonia
  • sepsis
  • MI
78
Q

What is the most common type of cause of AKI?

A

Pre renal AKI

79
Q

What kind of obstruction of pre renal AKI is needed to cause an AKI?

A

Bilateral OR

Unilateral with something else e.g. sepsis

80
Q

Why in prevention of AKI are anti-hypertensives withholded?

A

Hypotension can cause an AKI

81
Q

What medicines should be stopped on sick days? Give examples of “sick days”

A

ACEIs, ARBs, NSAIDs, Diuretics, Metformin

Sick days = vomiting, diarhrhoea, vomiting, fever, sweats, shakes

82
Q

What happens in the body when you are unwell?

A

Stimulate RAAS -> conserve salt and water

Stimulate sympathetic system

83
Q

Can metformin cause an AKI?

A

No, but it can cause lactic acidosis if unwell for another reason e.g. sepsis

84
Q

Most patients with AKI will have a degree of what?

A

Hypovolaemia

85
Q

What does ATN stand for?

A

Acute tubular necrosis

86
Q

How can AKI cause ATN?

A

Insult to the kidneys so severe that they develop necrosis of the tubules

87
Q

What is trimethoprim bad to use in?

A

CKD

88
Q

What can trimethoprim cause in CKD?

A

Hyperkalaemia
Increased creatinine
Does not reduce GFR but inhibits the tubular secretion of creatinine and effects the K channels as well

89
Q

Indications for RRT in AKI

A

Refractory AEIOU

90
Q

What are the uraemic complications?

A

Uraemic encephalopathy

Uraemic pericarditis

91
Q

In hyperkalaemia, what can help stabilise the myocardium and how? Then what can be done once the K > 6.5?

A

Calcium gluconate 10mls/10% / calcium chloride
Does not lower the K but stops an MI
Then have to push potassium back into the cells by
- nebulised salbutamol 2.5-5mg
- insulin dextrose IV 6 - 10 units in 50mls/50% dextrose over 30 mins

92
Q

What do nebulised salbutamol and insulin dextrose IV do?

A

Lower K+

93
Q

Why should you not give diuretics in AKI? (unless in fluid overload)

A

Can worsen AKI

94
Q

When having insulin dextrose, what should be done for a few hours after?

A

Monitor blood glucose

95
Q

What group of patients are more likely to be hyperkalaemic and why?

A

DM patients

Not as much insulin

96
Q

What is renal papillary necrosis?

A

Coagulative necrosis of the renal papillae

97
Q

Causes of renal papillary necrosis

A 
Severe acute pyelonephritis
Diabetic nephropathy 
Obstructive nephropathy 
Analgesic nephropathy (NSAIDs)
Sickle cell anaemia
98
Q

Presentation of renal papillary necrosis

A

Visible haematuria
Loin pain
Proteinuria

99
Q

What investigation is required in the investigation of all patients presenting with an AKI of unknown etiology?

A

Renal USS

100
Q

What is a sign of acute interstitial nephritis? What is it often due to?

A

Eosinophilic casts

Often due to a drug reaction

101
Q

Pathology of rhabdomyolysis

A

The toxicity of myoglobin on the tubular cells directly causes damage and necrosis of the cells - so causing tubular cell necrosis

102
Q

What does a raised anion gap suggest?

A

Increased production or reduced excretion of fixed / organic acids

103
Q

Examples of things causing raised anion gap acidosis

A

Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (DKA)
Drugs / Toxins (salicylates, methanol, ethylene glycol)

104
Q

What is a metabolic acidosis with a normal anion gap due to?

A

Loss of bicarbonate or accumulation of H+ ions

105
Q

Causes of metabolic acidosis with normal anion gap

A

Renal tubular acidosis
Diarrhoea
Addisons disease
Pancreatic fistula

106
Q

What would indicate a AKI caused by dehydration?

A

A urea that is proportionally higher than the rise in creatinine

107
Q

What should be considered in a young female patient who develops AKI after initiation of an ACEI?

A

Fibromuscular dysplasia

108
Q

Causes of renal vascular disease

A 
Renal artery stenosis secondary to atherosclerosis (90%)
Fibromuscular dysplasia (10%)
109
Q

What % of patients with fibromuscular dysplasia are female?

A

90%

110
Q

Presentation of fibromuscular dysplasia

A

HTN
CKD or acute renal failure e.g. 2ndry to ACEI initiation
‘Flash’ Pulmonary oedema

Renal Pathology (13 decks)

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