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Urinary System > Acute Renal Injury > Flashcards

Acute Renal Injury Flashcards

1
Q

What is the traditional definition of acute renal failure?

A

The rapid loss of glomerular filtration and tubular function over hours-days

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2
Q

What are the features of acute renal failure according to the traditional definition?

A

Retention of urea/creatinine due to a failure of homeostasis
Can be oliguric or non-oliguric
Potentially recoverable

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3
Q

What are the problems with the traditional definition of acute renal failure?

A

Lack of standardisation
Absolute creatinine, changes in creatinine, urine output and need for dialysis are not determined
Creatinine is an insensitive and late marker
RRT is a hard end-point but very late marker
There is a wide spectrum of renal injury

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4
Q

What are the features of acute renal failure according to the current definition (KDIGO)?

A

Increase in serum creatinine by ≥ 0.3 mg/dl (25.5mol/l) within 48 hours or
Increase in serum creatinine by ≥ 1.5 times the baseline, which is known or presumed to have occurred within the prior 7 days, or
Urine volume < 0.5 ml/kg/hour for 6 hours

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5
Q

In normal/increased risk stages of acute kidney injury outcome, what measures should be taken?

A

Preventative

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6
Q

Once damage and progression occur to the kidneys, what should the treatment strategy be focussed on?

A

Managing the disease

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7
Q

How many hospital admissions are complicated by acute kidney injury?

A

Between 1/7 and 1/5

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8
Q

What is the mortality in hospital with dialysis-requiring AKI? In what patients is the mortality worse?

A

45-75%

Worse in older patients and in those with multi-organ failure

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9
Q

What is the mortality in hospital of non-dialysis requiring AKI? (AKIN classification)

A

2% of people
8% with AKIN 1
25% with AKIN 2
33% with AKIN 3

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10
Q

What is the incidence of long-term renal replacement therapy (RRT) following AKI?

A

Around 20% at 90 days post-discharge of those who had RRT

5/100 per year with AKI

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11
Q

What is the incidence of long-term chronic kidney disease following AKI?

A

8/100 per year with AKI (both with and without dialysis)

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12
Q

What are pre-renal causes of AKI?

A

Drugs

  • NSAIDs
  • ACEIs/ARBS
  • Beta-blockers
  • Diuretics
  • Immunosuppressants

Problems with the blood flow to the kidney

  • Sepsis
  • Hypovolaemia e.g. haemorrhage, burns
  • Hepatorenal syndrome
  • Congestive cardiac failure
  • Hypotension
  • Renal artery occlusion/vasoconstriction
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13
Q

What are renal causes of AKI?

A

Damage to renal parenchyma

  • Acute tubular injury e.g. haemoglobinuria, rhabdomyolysis
  • Tubulointerstitial injury
  • Glomerulonephritis
  • Myeloma
  • Vasculitis
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14
Q

What are post-renal causes of AKI?

A

Obstruction to urine exit

  • Kidney stones
  • Prostatic hypertrophy
  • Tumours
  • Retroperitoneal fibroids
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15
Q

What can happen in pre-renal AKI?

A

There is reduced effective circulation volume due to volume depletion, hypotension, cardiac failure etc. and arterial occlusion

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16
Q

What can happen in renal AKI?

A

Acute tubular necrosis
Acute interstitial nephritis
Acute glomerulonephritis
Intra-renal vascular obstruction e.g. vasculitis, thrombotic microangiopathy

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17
Q

What can happen in post-renal AKI?

A

Obstruction

  • Intraluminal e.g. calculus, clot
  • Intramural e.g. malignancy, ureteric stricture
  • Extramural e.g. malignancy
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18
Q

What is the most common cause of AKI?

A

Poor perfusion leading to established tubule damage

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19
Q

How does damage occur in pre-renal AKI?

A

There is failure of the circulation to provide sufficient plasma flow to maintain blood chemistry due to volume/pressure loss, and fluid imbalance occurs

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20
Q

What can pre-renal AKI lead to if sustained?

A

Intrinsic renal failure (acute tubular necrosis)

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21
Q

What is intrinsic renal failure exacerbated by?

A

Toxic injury e.g. drugs

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22
Q

What are the stages in the course of acute kidney injury?

A

Initiation
Maintenance
Recovery

23
Q

What happens in initiation of AKI?

A

Exposure to toxic/ischaemic insult
Real parenchymal injury evolves
Potentially preventable

24
Q

What happens in maintenance of AKI?

A

Established parenchymal injury
Usually maximally oliguric at this stage
Typical duration of 1-2 weeks (can be up to several months)

25
Q

What happens in recovery of AKI?

A

Gradual increase in urine output
Fall in serum creatinine
If GFR recovers more quickly that tubular resorptive capacity excessive diuresis may result

26
Q

What are potential sources of harm to the kidneys?

A

Drugs e.g. ACEI, NSAIDs
Toxins e.g. drugs, radiocontrast
Sepsis
Myeloma

27
Q

What is radiocontrast nephropathy?

A

AKI following administration of iodinated contrast agent

28
Q

What happens in radiocontrast nephropathy?

A

Usually transient renal dysfunction, resolving after 72 hours
May lead to permanent loss of function

29
Q

What are small reductions in renal function associated with?

A

Significant increase in mortality

30
Q

What are the risk factors for radiocontrast nephropathy?

A 
Diabetes mellitus 
Renovascular disease 
Impaired renal function 
Paraprotein 
High volume of radiocontrast
31
Q

What is myeloma?

A

Cancer arising from plasma cells - monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
Second most common haematological malignancy

32
Q

What is the median age of diagnosis of myeloma and the median survival?

A

Median age of diagnosis - 68

Median survival - 5 years

33
Q

What are the clinical features of multiple myeloma?

A 
Anaemia 
Back pain 
Weight loss 
Fractures 
Infections 
Cord compression 
Markedly elevated ESR 
Hypercalcaemia
34
Q

How is myeloma diagnosed?

A

Bone marrow aspiration (> 10% clonal plasma cells)
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones protein
Skeletal survey

35
Q

List the causes of AKI

A 
Cardiac failure 
Haemorrhage 
Sepsis 
Vomiting and diarrhoea 
Prostate disease 
Tumours 
Stones 
Glomerulonephritis 
Vasculitis 
Radiocontrast 
Myeloma 
Rhabdomyolysis 
Drugs
36
Q

What investigations are done for AKI?

A 
U&amp;Es
Bicarbonate
LFTs
Bone scan 
FBC 
Clotting screen 
Blood gas 
ANCA 
Urine dipstick 
Urine PCR/ACR if indicated
Renal biopsy 
Ultrasound 
X-ray
37
Q

What are important features of the history when suspecting AKI?

A 
PMH of systemic disease
New rash, nose bleeds, sore eyes, joint pain 
Drug exposure 
Uraemic symptoms 
Timing of symptoms
38
Q

What are some common complications of AKI?

A 
Acidosis 
Electrolyte imbalance 
Intoxication 
Overload 
Uraemia complications
39
Q

What is the management of AKI?

A

Remove or treat cause if possible

Pre-renal - consider fluid replacement, BP support

Renal - remove precipitant if possible

Post-renal - consider catheterisation

Volume resuscitation or fluid restriction (deplete vs overload) 
Treat sepsis 
Vasopressors 
Stop nephrotoxic drugs e.g. NSAIDs, ahminoglycosides 
Dopamine
Furosemide 
Atrial natriuretic peptide
IGF 1
40
Q

What are the “five Rs for IV prescribing” in AKI?

A 
Resuscitation 
Routing maintenance 
Replacement 
Redistribution 
Reassessment
41
Q

What are some of the possible ECG changes in hyperkalaemia?

A 
Peaked T waves 
Tall tented T waves 
Widened and flattened P wave 
Lengthened PR segment 
P waves eventually disappear
Prolonged QRS interval
42
Q

What is the treatment of hyperkalaemia?

A

Stabilise myocardium - calcium gluconate
Shift potassium intracellularly - salbutamol, insulin-dextrose
Remove - diuresis, dialysis, anion exchange resins

43
Q

What indications for dialysis in AKI are particularly important?

A

Decreased HCO3-
Increased K+
Pulmonary oedema
Pericarditis

44
Q

What is haemodialysis?

A

Solute removal by diffusion

Intermittent therapy with sessions lasting 3-5 hours

45
Q

What is haemofiltration?

A

Solute removal by convection
Larger pore size
Continuous therapy

46
Q

What concepts are important in dialysis?

A

Ultrafiltration
Diffusion
Osmosis

47
Q

What is ultrafiltration?

A

Solution moves by pressure gradient, blood enters glomerulus at a high pressure

48
Q

What are the advantages of haemodialysis?

A

Rapid solute removal
Rapid volume removal
Rapid correction of electrolyte disturbances
Efficient treatment of hypercatabolic patients

49
Q

What are the disadvantages of haemodialysis?

A

Haemodynamic instability
Concern if dialysis is associated with hypotension - may prolong AKI
fluid removal only during short treatment time

50
Q

What are the advantages of continuous renal replacement 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

51
Q

What are the disadvantages of continuous renal replacement therapy?

A

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

52
Q

What are the risk events for AKI?

A 
Post-surgery 
Volume depletion 
Hypovolaemia 
Hypotension 
Rhabdomyolysis 
Radiocontrast
Sepsis 
Toxins
53
Q

What are patient-related AKI risk factors?

A 
Age > 75 
Previous AKI 
Heart failure 
Liver disease 
Chronic kidney disease 
Vascular disease 
Cognitive impairment 
Acutely unwell e.g. MI 
Co-morbidities e.g. diabetes mellitus
54
Q

How can you reduce the risk from contrast?

A

Saline hydration
Sodium bicarbonate
N-acetyle cysteine
Osmolarity of radiocontrast

Urinary System (22 decks)

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