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Renal > AKI > Flashcards

AKI Flashcards

1
Q

What are the risk factors for developing an AKI?

A 
Age >75
Chronic kidney disease
Other organ failure/chronic disease 
Drugs 
Use of iodinated contrast agents 
Sepsis
Poor fluid intake/increased losses
History of renal symptoms/past AKIs
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2
Q

What drugs are associated with increased risk of AKI?

A

NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics

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3
Q

What can the causes of AKI be split up into?

A

Pre-renal
Intrinsic/Intrarenal
Post-renal

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4
Q

What are some causes of pre-renal AKI?

A

Absolute loss of fluid – major haemorrhage, vomiting, diarrhoea, severe burns
Relative loss of fluid – distributive shock, congestive heart failure
Renal Artery – stenosis or embolus
ACE inhibitors

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5
Q

What is the underlying mechanism of pre-renal AKI?

A

Decreased blood flow into kidney

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6
Q

What are the consequences of reduced blood flow in pre-renal AKI?

A

↓blood filtered =↓GFR = ↑creatinine and urea in blood and less urine
RAAS system activates reabsorbs sodium
Increased sodium and water retention

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7
Q

What happens to the UOsm in pre-renal AKI?

A

> 500 Osm/kg

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8
Q

What are some causes of Intra-renal AKI?

A

Acute tubular necrosis
Glomerulonephritis
Acute Interstitial Nephritis

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9
Q

how does acute tubular necrosis cause an AKI?

A

 when cells die they build up and pug renal tubules = creates higher pressure in renal tubules = reduces pressure gradient = less urea and creatinine is filtered out of blood = ↑creatinine and urea in blood and less urine produced = azotaemia and oliguria

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10
Q

what are the causes of acute tubular necrosis?

A

ischaemia, pre-renal AKI, nephrotoxins – aminoglycosides, lead, myoglobin, ethylene glycol, radiocontrast dye, uric acid – tumour lysis syndrome

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11
Q

How does glomerulonephritis cause AKI?

A

damaged membrane permeability increases – large molecules are filtered into urine – proteinuria and haematuria
 Fluid leakage reduces pressure difference – lower GFR – oliguria, more circulating fluid – edema and hypertension

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12
Q

what are the biochemical affects of acute interisitial nephritis AKI?

A

BUN:creatinine <15:1

Una > 40, FEna>2%, or water Uosm < 350

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13
Q

what is the pathophysiology of acute interstitial nephritis

A

infiltration of immune cells - Type 1 or 4 hypersensitivity leading to renal papillary necrosis

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14
Q

what is the mechanism of an intrarenal AKI?

A

damage to tubules, glomerulus or interstium

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15
Q

What is the mechanism of post renal AKI?

A

obstruction to outflow

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16
Q

what are the causes of post-renal AKI?

A

Compression – intra-abdominal tumours, Benign prostatic hyperplasia
Blockage – kidney stones

17
Q

What does obstruction of outflow in post-renal AKI cause?

A

increases renal tubule pressure – reduces pressure gradient = ↓GFR = less urea and creatinine is filtered out of blood = ↑creatinine and urea in blood and less urine produced = azotaemia and oliguria

18
Q

what are the biochemical affects of post-renal AKIs?

A

Initially high pressure causes more Na, urea and water to be reabsorbed
BUN: Creatinine >15:1, urine concentrated
Over time epithelial cells damaged - less urea and Na BUN:creatinine <15, Una>40, FEna >1-2%

19
Q

Clinical Features of AKI

A 
Asymptomatic
reduced urine output
Oedema (pulm, peri)
arrhythmias (acid/base balance)
Uraemia - anorexia, lethargy, pericarditis, encephalopathy
20
Q

what is the diagnositic criterai of a AKI?

A

a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

21
Q

What features of examination could exist in AKIs?

A

palpable bladder, palpable kidneys, abdominal/pelvic masses, renal bruits, rashes

22
Q

What aspects of urinalysis should be looked at in AKI?

A

infection, glomerular disease, microscopy, culture, BJ proteins

23
Q

Which routine bloods should be done in AKI?

A

U&Es, FBC, LFT, clotting, CK, ESR, CRP

24
Q

Which additional bloods should be done in AKI?

A

blood film, renal immunology: immunoglobulins, paraprotein electrophoresis, complement, autoantibodies

25
Q

what is the serum creatinine criteria for stage 1 AKI?

A

Increase >26μmol/L in 48hr OR increase > 1.5 x baseline

26
Q

what is the serum creatinine criteria for stage 2 AKI?

A

Increase 2-2.9 x baseline

27
Q

what is the serum creatinine criteria for stage 3 AKI?

A

Increase >3 x baseline OR >354μmol/L OR commenced on RRT irrespective of stage

28
Q

what is the urine output criteria for stage 1 AKI?

A

<0.5mL/kg/h for >6 consecutive hours

29
Q

what is the urine output criteria for stage 2 AKI?

A

<0.5mL/kg/h for >12h

30
Q

what is the urine output criteria for stage 3 AKI?

A

<0.3mL/kg/h for 24h or anuria for 12h

31
Q

What is the urine specific gravity of pre-renal and intrarenal AKI?

A

Pre-renal >1.020

Intrarenal <1.020

32
Q

What is the urine osmolarity of pre-renal and intrarenal AKI?

A

Pre-renal >500

Intrarenal <350

33
Q

What is the urine sodium of pre-renal and intrarenal AKI?

A

Pre-renal <20

Intrarenal >40

34
Q

what are the complications of AKI?

A
  • Hyperkalaemia
  • Pulmonary Oedema
  • Uraemia
  • Acidaemia
35
Q

what is the general management of an AKI?

A

Assess volume states: aim for euvolemia
Stop nephrotoxic drugs
monitor
nutrition

36
Q

what are the features of management in pre-renal AKIs?

A

correct volume depletion

37
Q

what are the features of management in intrarenal AKIs?

A

refer

38
Q

what are the features of management in post-renal AKIs?

A

catheterise and CT of renal tract

consider cystoscopy and stents or nephrostomy

39
Q

What are the indications for renal replacement therapy?

A

fluid overload, hyperkalaemia, hypocalcaemia, metabolic acidosis, pericarditis, uremic symptoms, GFR <15ml/min/1.73 m2, or poisoning.

Renal (7 decks)

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