SAP - Acute Kidney Injury Flashcards

1
Q

What are the functions of the Kidney?

A

Water, inorganic ion and acid-base balance.

Removal of metabolic waste products from the blood

Removal of foreign chemicals from the blood

Production of some Hormones –
Erythropoietin, which controls red cell production
Renin – can influence blood pressure
Involved in Vitamin D processing

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2
Q

How do we measure how well the kidney is working?

A

1) Glomerular Filtration Rate (GFR) = volume of plasma filtered by kidney in unit time.
Units – ml/min – often corrected for body surface.
Normal > 90ml/min/1.73m2
Usually measured indirectly from plasma creatinine

2) Measure levels of nitrogenous waste e.g. urea
3) Measure levels of electrolytes
4) Measure haemoglobin and bone health
5) Test the urine for blood and protein macromolecules - specifically albumin

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3
Q

Relationship between Serum Creatinine and Creatinine Clearance

A

Important: a normal serum creatinine does not mean a normal creatinine clearance

Serum creatinine does not rise above the normal range until there is a reduction of 50-60% in the GFR.

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4
Q

What is an Acute Kidney Injury?

A

Defined as an abrupt loss of renal function resulting in retention of nitrogenous waste and dysregulation of extracellular volume and electrolytes.

Acute Renal Failure has multiple definitions. KDIGO define it as a GFR < 15 mls/min/1.73m2, or requirement for renal replacement therapy (e.g. Dialysis)
Acute Renal Failure is a severe form of Acute Kidney injury that is clinically important.

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5
Q

AKI values

A

GFR <15

urine volume <0.5 mls/kg/hour for 6 hours

increase in serum creatinine by >1.5 times the baseline - >26.5 micromol/l with 2 days

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6
Q

Stages of AKI

A

1, 2, 3

1 = 1.5-1.9 TIMES BASELINE

2= 2.0-2.9 TIMES BASELINE

3= 3 TIMES BASELINE or INCREASE IN SERUM CREATININE TO >353micromole/L

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7
Q

risk factors for AKI

A

CKD (eGFR <60ml/min/1.73m^2)

HF

Liver disease

Oliguria

Diabetes

Nephrotoxics

Recent use of iodinated contrast agents.

Age over 65

Sepsis

Symptoms or history of urological obstruction

Neurological or Cognitive Impairment or Disability

Hypovolemia

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8
Q

3 main causes of AKI

A

Pre renal

intrinsic renal

post renal

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9
Q

Causes of AKI: Pre-Renal

A
  1. Ineffective perfusion of the kidney =
    hypovolaemic states e.g. acute haemorrhage or diarrhoea.
    Heart Failure – impaired cardiac pump efficiency.
    Acute decompensated liver disease with portal hypertension.
  2. Selective renal ischaemia
    Drug reduction of afferent perfusion (NSAIDS).
    Drug reduction of efferent tone (RAAS blockers).
    Renal Artery Stenosis
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10
Q

Renal Cause of AKI: Acute Tubular Necrosis

A

prolonged period of impaired renal perfusion –> renal ischaemia
–> 1) VASOCONSTRICTION (RAAS increase, endothelin increase)

2)Tubule cell injury –> obstruction/tubular back leak/TGF –> RAAS and vasoconstrction.

=====> REDUCED GFR

  • Acute Tubular Necrosis = impaired renal function and morphologic evidence of tubular injury.
  • There are three major causes of ATN: renal ischemia, sepsis, and nephrotoxins.
  • There is effacement and loss of the proximal tubule brush border, patchy loss of tubular cells and focal areas of proximal tubule dilatation.
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11
Q

There are three major causes of ATN:

A

renal ischemia, sepsis, and nephrotoxins.

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12
Q

Post renal causes of AKI

A

any cause of urinary tract obstruction.
eg in lumen:
calculus, blood clot, tumour of renal pelvis
eg in wall:
ureteric stricture, urethral stricture, congenital bladder neck obstruction.
eg in pressure from outside:
pelviureteric compression eg bands, tumours, diverticulitis, aortic aneurysm

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13
Q

overall Causes of AKI

A
ATN – 45% 
Pre renal disease – 21%
Acute on Chronic Renal Failure – 13%
Urinary Tract Obstruction – 10%
Glomerulonephritis or Vasculitis – 4%
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14
Q

Identifying cause of AKI

A

Difficult distinguishing between pre-renal causes and ATN.
Urine helpful
=> Urinary sodium is low if there is avid tubular reabsorption (i.e. low if pre-renal insult).

Clinical assessment is pivotal – a history of fluid loss, or hypotension would suggest a pre-renal cause. Any response to fluid challenge?

Consider Ultrasound Renal Tract to exclude obstruction

NICE CG169 advise performing urine dipstick. Advise to think about acute nephritis if ‘urine dipstick [shows] haematuria and proteinuria.’

NICE advise to offer USS if no cause of the AKI has been identified; or if pyonephrosis is suspected (i.e. infected and obstructed kidney)

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15
Q

Clinical Features of AKI

A

Potentially symptoms of uraemia: anorexia, nausea, vomiting and pruritus.

Potential complications:
Hyperkalaemia is common, especially following trauma to muscle.
Metabolic Acidosis
Hyponatraemia secondary to water overload.
Pulmonary Oedema
Uraemic complications – i.e. Uraemic Pericarditis or Encephalopathy.

Uraemia can proceed to drowsiness, fits, coma and hemorrhagic episodes.
Underlying causes of the AKI may feature as well.

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16
Q

Hyperkalaemia

A

This is a life threatening complication – risk of arrhythmia.
Can lead to muscle weakness, cardiac conduction problems including sinus bradycardia, sinus arrest, VT, VF and asystole.

Shows on the ECG as tall peaked T wave
loss of P wave

widened QRS with tall T wave

17
Q

NICE advise considering renal replacement therapy if any of the following are not responding to medical management:

A
High Potassium
Metabolic Acidosis 
Symptoms or complications of uraemia 
Fluid Overload 
Pulmonary oedema – fluid on the lungs.
18
Q

Hyperkalaemia, Pulmonary Oedema and Oliguria are potential complications of AKI.

A

.

19
Q

AVERAGE GFR

A

180