AKI Flashcards

1
Q

Define oliguria and anuria

A

Oliguria - little urine <400ml/day

Anuria < 100ml/day

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2
Q

Define AKI. What is it measured in?

A

Acute Kidney Injury is a syndrome of decreased renal function (decline in actual GFR) that occurs over hours/days <2 weeks. Measured in serum creatinine or urine output decline.

Increase in SCr > 26.5umol/L in 48 hrs
Increase in serum creating by 1.5 x baseline within 7 days
Urine volume <0.5ml/kg/hr for 6 hours

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3
Q

What is the first stage of AKI?

A

SCr > 26.5umol/L or 1.5-2 times the baseline

URine output < 0.5ml/kg/hr for 6-12h

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4
Q

What is the 2nd stage of AKI

A

SCr > 2-2.9 x baseline

Urine output <0.5ml/kg/hr for >12h

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5
Q

What is the 3rd stage of AKI

A

SCr >354umol/L or 3 x baseline or initiated on RRT

<0.3ml/kg/hr for > 24h or anuria for 12h

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6
Q

What are the limitations of using serum creatining

A

Increased muscle mass - increased serum creatinine

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7
Q

Risk factors for AKI

A
Pre-existing CKD
Age
Male sex
Comorbidity
CVS disease
Malignancy
Chronic liver disease
Complex surgery
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8
Q

Causal categories of AKI

A

Pre-renal (reduced perfusion to the kidney)
Renal (intrinsic damage to kidneys)
Post-renal (obstruction to the urine)

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9
Q

Describe pre-renal AKI

A

Decreased renal perfusion
If BP falls below a threshold the kidney is able to maintain blood flow and GFR declines.
reversible if recognised quickly

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10
Q

Give causes of pre-renal kidney failure

A

Hyppovolaemia - haemorrhage, diarrhoea and vomitting, burns, pancreatitis
Systemic vasodilation - sepsis, cirrhosis, drugs, anaphylaxis
Reduced CO - LV dysfunction, MI, cariogenic shock, tamponade
Renal preglomerular vasoconstriction - sepsis, hepatorenal syndrome, hypercalcaemia, drugs - NSAIDs
Postglomerular vasodilation - ACE inhibitors, ATII antagonists

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11
Q

What happens if pre-renal AKI is not treated promptly?

A

Kidney cells become hypoxic

Acute tubular necrosis occurs.

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12
Q

What is acute tubular necrosis?

A

Damage to tubular cells so that they cannot reabsorb water and salt efficiently.
It is caused by ischaemia - fall in renal perfusion
Nephroxins - damage toe epithelial cells - cell death and shedding, all drugs are potentially nephrotoxins
sepsis

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13
Q

Give the possible causes of renal AKI

A

Golmerular:
Acute glomerulonephritis - immune disease affecting the glomerulus
Acute tubular necrosis (prolonged pre-renal diseasE)

Acute tubule-interstitial nephritis - inflammation of the interstitial of the kidneys surrounding tubules:
Drug reaction - NSAIDs, antibiotics, PPIs
Infection - acute pyelonephritis

Vessels - vasculitis, DIC

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14
Q

Describe post-renal AKI and give causes.

A

Obstruction to urine flow after it has left the tubules.
This causes a rise in intratubular pressure, dilation of the renal pelvis and reduced renal function.
Obstruction at ureter, bladder, urethra

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15
Q

Where and how can post-renal AKI obstruction occur?

A

Within the lumen:
Renal stones, blood clot, stricture, tumour of renal tract

Within wall: (usually chronic)
Ureteric stricture, congenital

Pressure from external compression:
Pelvic malignancy, prostatic hypertrophy, aortic aneurism, retroperitoneal fibrosis

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16
Q

Give some exogenous and endogenous nephrotoxins

A

exogenous: NASAIDs, ATII antagonists, ACE-i
endogenous: myoglobin bilirubin

17
Q

What is acute glomerulonephritis?

A

Immune disease of the glomerulus
primary - kidneys only
secondary - part of systemic response

18
Q

What is acute tubulointerstital nephritis

A

Inflammation of the kidney interstitial due to infection or toxins

19
Q

what sign indicates post-renal failure?

A
Anuria
History of renal stones/prostatism/pelvic surgery
Palpable bladder
Pelvic masses
Enlarged prostate
20
Q

Describe the presentation in sepsis

A
Pyrexia and rigors (sudden feeling of cold or shivering)
Vasodilation, warm peripheries
Bounding pulse
Rapid capillary erfill
Hypotension
21
Q

Describe the presentation of cardiac failure

A
Gallop rhythm
Raised BP
Raised JVP
Pulmonary oedema (basal crackers and dyspnoea
Peripheral oedema (sacrum ankle)
22
Q

Give investigations to carry out in AKI, what are they to check for?

A

Serum biochemistry U&E - urea and creatinine
ECG - hyperkaleamia
Urine dipstick - protein, blood
Urine microscopy - different casts
Ultrasound Scan - kidney size/asummetry/stones
CXR -pulmonary oedema/ fluid overload/infection
LFT - hepatorenal sundrome
Immunological test for intrinsic renal disease

23
Q

What serum biochemistry is expected and possible in AKI?

A

Raised urea and creatinine in all AKI

Hyperkalaemia, hyponatraemia, hypocalcaemia, hyperphosphataemia possible

24
Q

ECG changes in hyperkalaemia

A
Tall T
Small/absent P
Increased P-R interval
Wide QRS
Asystole
25
Q

What does proteinuria/haematuria suggest?

A

intrinsic renal disease

26
Q

Describe what is seen on microscopy in pre-renal AKI, ATN, glomerulonephritis

A

Pre-renal - hyaline cast (aggregation of protein in concentrated urine (normal))
ATN - muddy brown casts
Glomerulonephritis - RBC casts

27
Q

What immunological tests should be carried out? What do they indicate?

A

Anti-nuclear antibody (ANA) - systemic lupus erythematous (autoimmune disease)
Anti-neutrophil cytoplasmic antibody (ANCA) - systemic vasculitis
Anti-glomerular basement membrane antibodies (AGBM) - goodpasture’s disease (immune attack of lung and kidney BMs leading to lung bleeding and kidney failure

28
Q

What do small kidneys suggest? Asymmetry?

A

Small - CKD

Asymmetry - renal vascular disease