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Medicine II > Nephro: Acute Kidney Injury > Flashcards

Nephro: Acute Kidney Injury Flashcards

1
Q

definition of an AKI

A

rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine, leading to failure to maintain fluid, electrolyte and acid-base homeostasis. this can be reversible over days or weeks

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2
Q

criteria for diagnosing AKI

A
  • rise in creatinine >26umol/L in 48hrs
  • rise in creatinine >1.5x
  • urine output <0.5mL/kg/h for >6 consecutive hours
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3
Q

what is the best biomarker to monitor AKIs currently?

A

creatinine

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4
Q

what are life threatening complications of AKI

A
  • hyperkalaemia

- metabolic acidosis

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5
Q

risk factors

A
  • diabetes
  • high BP
  • old age
  • CKD
  • heart failure
  • liver disease
  • PVD
  • nephrotoxic drug
  • sepsis
  • hypovolaemia
  • contrast use
  • obstruction
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6
Q

define oligouria

A
  • urine output which is not enough to eliminate all the end-products
  • <400ml/24hr for 6 consecutive hours
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7
Q

define anuria

A
  • no urine output

- <100ml/24hrs

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8
Q

define polyuria

A
  • when you piss an abnormally high amount of pee

- >3L/24hrs

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9
Q

how do you classify causes of an AKI

A
  • pre-renal
  • renal
  • post-renal
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10
Q

how do you classify AKI?

A

RIFLE classification (risk, injury, failure, loss, ESRF)

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11
Q

what is the AKIN classification?

A
  • classifies renal failure
  • considers a milder version of AKI
  • depends on the creatinine rise
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12
Q

most common causes of an AKI

A
  • ischaemia
  • sepsis
  • nephrotoxins
  • prostatic disease
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13
Q

pre-renal causes of an AKI

A
  • renal hypoperfusion
  • hypotension
  • renal artery stenosis
  • cirrhosis
  • drugs: ACEi, CCF, NSAIDs
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14
Q

renal causes of an AKI

A
  • injury to the glomerulus, tubule or vessels

- classified into tubular, glomerular, interstitial and vascular

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15
Q

tubular causes of AKI

A
  • ATN (result of pre-renal causes like nephrotoxic drugs)
  • crystal damage
  • myeloma
  • hypercalcaemia
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16
Q

glomerular causes of AKI

A
  • autoimmune conditions like SLE, HSP,
  • drugs
  • infections
  • primary GN
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17
Q

interstitial causes of AKI

A
  • drugs

- infiltration from lymphoma, infection, tumour lysis syndrome

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18
Q

vascular causes of AKI

A
  • vasculitis
  • malignant HTN
  • thrombus
  • cholesterol emboli
  • HUS/TTP
  • large vessel occlusion
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19
Q

post-renal causes of AKI

A
  • luminal (stones, clots, sloughed papilae)
  • mural (malignancy, BPH, strictures)
  • external compression (malignancy, retroperitoneal fibrosis)
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20
Q

pathophysiology of pre-renal AKI

A
  • impaired renal perfusion
  • fall in glomerular capillary filtration pressure
  • increased renal absorption of Na and water
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21
Q

what are the sick day rules for AKI

A
  • stop drugs which are contraindicated in renal disease
  • use a few other drugs with caution
  • monitor the use of radiological contrast
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22
Q

which are the drugs that you should stop?

A
  • diuretics
  • ACEi
  • antihypertensives (with B-blockers, consider lowering the dose rather than withholding them)
  • metformin (risk of lactic acidosis)
  • NSAIDs
  • nephrotoxic antibiotics
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23
Q

which drug should you use with caution?

A

opiates

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24
Q

management for contrast

A
  • imp cause for AKI

- keep the patient hydrated both before and after the procedure

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25
Q

aetiology of AKI

A
  • volume depletion
  • hypotension
  • oedematous states
  • selective renal ischaemia
  • nephrotoxic drugs
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26
Q

from where can fluid be lost and cause AKI

A
  • GI tract
  • renal tract
  • skin or respiratory losses
  • third space sequestration
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27
Q

criteria to differentiate between pre-renal and renal causes of uraemia

A
  • urine gravity/osmolality
  • urine sodium
  • fractional excretion of Na
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28
Q

what are the 2 main classifications of post-renal causes?

A
  • intrarenal

- extrarenal (renal pelvis, ureters, bladder, urethra)

29
Q

what is obstructive nephropathy?

A

renal disease caused by impaired flow of urine or tubular fluid

30
Q

how can you check for post-renal causes?

A
  • catheterise

- CTKUB

31
Q

causes of small vessel disease

A
  • small vessel vasculitis
  • thrombotic microangiopathy
  • renal atheroembolism
32
Q

causes of acute glomerulonephritis

A
  • anti-GBM
  • MPGN
  • post-infectious GN
  • IgA nephropathy
  • lupus nephritis
  • cryoglobunaemia
33
Q

causes of acute tubular necrosis

A
  • ischaemia
  • nephrotoxins
  • rhabdomyalsis
  • radiocontrast agents
  • haemorrhage
  • burns
  • diarrhoea and vomiting
  • pancreatitis
34
Q

causes of acute interstitial nephritis

A
  • drugs
  • infections
  • systemic disease
35
Q

which are the drugs associated with renal AKI

A
  • gold
  • aminoglycosides
  • radiocontrast dye
  • penicillins
  • rifampicin
36
Q

which are the drugs associated with postrenal AKI

A
  • indinavir
  • acyclovir
  • sulfonamide
37
Q

pathogenesis of ATN

A
  • intrarenal microvascular vasoconstriction due to reduced sensitivity to vasodilatory substances
  • tubular cell injury (ischaemic injury causing cell death by apoptosis or necrosis)
  • tubular cell recovery (quickly reversible and thus, can recover quickly from ATN)
38
Q

4Ms for prevention of AKI

A
  • monitor patient
  • minimise kidney insults
  • maintain circulation
  • manage acute illnesses
39
Q

presentation of AKI

A
  • can be asymptomatic
  • malaise, confusion, seizures or coma
  • D, N, V
  • anorexia
  • joint pains, rashes
  • oliguria or abnormal urine colour
  • haematuria
  • haemoptysis
40
Q

what should you ask about in the history?

A
  • symptoms of fluid loss
  • symptoms of infections
  • backache
  • drug history
  • past medical history
  • risk factors
41
Q

physical signs to look out for

A
  • vital parameters
  • signs of jaundice
  • rashes
  • fluid status
  • abdominal masses
  • renal punch
  • catheters
42
Q

how can you check for fluid overload?

A

elevated JVP, crackles on auscultation of lungs, lower limb oedema

43
Q

signs of dehydration

A

hypotension, postural BP drop, tachycardia, decreased skin turgor

44
Q

renal signs to look out for in an examination

A
  • palpable bladder
  • palpable kidneys
  • abdominal/pelvic masses
  • renal bruits
  • rashes
45
Q

what should you assess in severe situations?

A
  • ABCDE
  • fluid status
  • urine output
  • hyperkalaemia
  • acidosis (ABG)
46
Q

investigations for AKI

A
  • creatinine
  • urea and electrolytes
  • CBC
  • ESR, CRP
  • glucose
  • ABG
  • urinalysis and microscopy
  • uPCR and/or uACR
  • MSU for C&S
  • US kidneys
  • CXR
  • HepB, HepC, HIV
  • coagulation screen
47
Q

what type of urine output is unusual in AKI?

A

anuria (suggests obstructive cause)

48
Q

distinguish AKI or CKD

A

persistently high creatinine levels in the past (CKD); small kidneys (CKD)

49
Q

causes of red cells or red cell casts

A
  • GN
  • vasculitis
  • malignant HTN
  • thrombotic microangiopathy
50
Q

causes of white cells or white cell casts

A
  • interstitial nephritis
  • GN
  • pyelonephritis
  • allograft rejection
  • malignant infiltration of the kidneys
51
Q

what are RTE cells

A

renal tubular epithelial cells

52
Q

causes of RTE cells or RTE/pigmented cell casts?

A
  • ATN
  • tubulo-interstitial nephritis
  • acute cellular allograft rejection
  • myoglobinuria
  • haemoglobinuria
53
Q

causes of granular casts

A
  • ATN
  • GN
  • vasculitis
  • tubulo-interstitial nephritis
54
Q

causes of eosinophiluria

A
  • allergic interstitial nephritis

- atheroembolic disease

55
Q

causes of crystalluria

A
  • acute uric acid nephropathy
  • calcium oxalate
  • drugs or toxins (antivirals, amoxicillin, sulfadiazine)
56
Q

specific investigations of AKI

A
  • LFT
  • serum protein electrophoresis
  • serum free light chains
  • immunoglobulins
  • creatinine kinase
  • blood film, LDH
  • ANCA, anti-GBM, ANA, ENA, anti-dsDNA, C3, C4, RF
  • ASOT
  • cryoglobulins
  • anti-phospholipid, anti-cardiolipin
  • blood cultures
  • consider renal biopsy if indicated
57
Q

what type of anaesthetic is used for renal biopsies?

A

local anaesthetic

58
Q

3 types of rapidly progressive GN

A
  • immune complex disease
  • pauci-immune disease
  • anti-GBM disease
59
Q

how would RPGN present?

A

AKI and systemic symptoms like fever, myalgia, weight loss, haemoptysis

60
Q

how would you treat RPGN?

A

aggressive immunosuppression with high dose IV steroids and cyclophosphamide +/- plasma exchange

61
Q

histology in AIN

A
  • mononuclear inflammatory infiltrate
  • no glomerular changes
  • tubules are separated by inflammation and oedema
62
Q

management of AKI

A
  • treat the underlying cause
  • assess circulating volume and fluid administration if required
  • prevent and treat hyperkalaemia
  • prevent and treat metabolic acidosis
  • discontinue nephrotoxic drugs
  • adjust dose of drugs, where necessary
63
Q

ECG changes in mild hyperkalaemia

A
  • peaked T waves

- prolonged PR segments

64
Q

ECG changes in moderate hyperkalaemia

A
  • loss of P wave
  • prolonged QRS complex
  • ST segment elevation
  • ectopic beats and escape rhythms
65
Q

ECG changes in severe hyperkalaemia

A
  • progressive widening of QRS complex
  • sine wave
  • ventricular fibrillation
  • asystole
  • axial deviation
  • bundle branch blocks
  • fascicular blocks
66
Q

management of pulmonary oedema

A
  • sit up
  • high flow O2
  • venous vasodilator
  • furosemide 80-250mg IV/IVI
  • if that does not work, urgent haemodialysis or haemofiltration is needed
  • consider CPAP
  • IV nitrates
67
Q

medical treatment of AKI

A
  • overload: loop diuretics
  • hyperkalaemia: calcium gluconate, dextrose, salbutamol, calcium resonium
  • acidosis: sodium bicarbonate
  • RPGN: immunosuppression
68
Q

red flags in AKI

A
  • intractable hyperkalaemia
  • pulmonary oedema and hypoxia
  • severe acidosis
  • uraemic encephalopathy/pericarditis

Medicine II (16 decks)

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