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*Medicine: Renal & Urology > AKI > Flashcards

AKI Flashcards

1
Q

What is acute kidney injury?

A
  • an acute decline in renal function
  • leading to a rise in serum creatinine and/or fall in urine output
  • previously known as acute renal failure
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2
Q

What is involved in the KDIGO classification of acute kidney injury?

A

Severity is staged according to highest creatinine rise or longest period/severity of oliguria

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3
Q

AKI is commonly asymptomatic so is easily missed. Whenever a patient presents with an acute illness, ensure your history covers characteristics that increase the risk of AKI.

What are risk factors for AKI?

A
  • Advancing age (>65)
  • History of acute kidney injury
  • Chronic kidney disease
  • Comorbidities - heart failure, liver disease, diabetes, dementia, pancreatitis
    • any sodium-retaining states
    • any impairment resulting in reduced oral fluids
  • Radiocontrast
  • Nephrotoxic drugs
  • Myeloproliferative disorder eg. multiple myeolma
  • Trauma, surgery, sepsis
  • Excessive fluid loss
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4
Q

What are examples of nephrotoxic drugs to look out for?

A
  • NSAIDs
  • Aminoglycoside antibiotics (eg. gentamicin)
  • ACE inhibitors / ARBs
  • Diuretics
  • Any hypertensives (eg. beta blockers)
  • Aciclovir, methotrexate, triamterene, indinavir or sulfonamides
  • Recreation drugs
  • OTCs and herbal remedies
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5
Q

How common is AKI and what is the mortality?

A
  • 15% of in-patients develop AKI
  • 25-30% mortality
  • Acute tubular necrosis (ATN) accounts for 45% of cases of AKI (due to sepsis)
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6
Q

What are the four most common causes of AKI?

A
  • Sepsis (41%)
  • Volume depletion (37%)
  • Nephrotoxic drugs (11%)
  • Obstruction (8%)
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7
Q

What is the aetiology of acute kidney injury?

A
  • Pre-renal (40-70%)
    • reduced vascular volume
    • reduced cardiac output
    • systemic vasodilatation
    • renal vasoconstriction
  • Renal (10-50%)
    • glomerular, intersititial or vessel damage
  • Post-renal (10%)
    • within renal tract
    • can be extrinsic compression
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8
Q

What are pre-renal causes of AKI?

A
  • Low volume → haemorrhage, D+V, burns, pancreatitis, DKA
  • Low C/O → cardiogenic shock, MI, PE
  • Systemic vasodil. → sepsis, drugs
  • Renal vasoconstriction → NSAIDs, ACE-I, ARB, hepatorenal syndrome
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9
Q

What are renal/intrinsic causes of AKI?

A
  • Glomerular → glomerulonephritis, ATN, rhabdo
  • Interstitial → drug rxn, infection, infiltration
  • Vessels → vasculitis, DIC, TTP, HUS
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10
Q

What are post-renal causes of AKI?

A
  • Within renal tract → stone, malignancy, stricture, clot, hydronephrosis
  • Extrinsic compression → pelvic malignancy, BPH
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11
Q

What are the features and treatment of rhabdomyolysis?

A
  • Causes → seizure, collapse, ecstasy, crush injury, McArdle syndrome, statins
  • Signs → AKI, raised creatinine/CK/phosphate/K, hypocalcaemia, myoglobinuria, metabolic acidosis
  • Mx → IV fluids + urine alkalinisation
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12
Q

What causes acute interstitial nephritis?

A
  • 25% of drug-induced AKI = acute interstitial nephritis
  • Causes → penicillin, rifampicin, NSAIDs, allopurinol, furosemide, systemic dx (SLE/sarcoidosis/Sjorgen’s), infection
  • Sx → fever, rash, arthralgia, eosinophilia, renal impairment, HTN
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13
Q

What is flash pulmonary oedema a sign of?

A
  • Renal vascular disease, eg:
    • renal artery stenosis
    • fibromuscular dysplasia

Presents as HTN, CKD/AKI and flash pulm oedema

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14
Q

What is the pathophysiology of pre-renal AKI?

A
  • results from impaired renal perfusion and the changes seen are appropriate physiological responses
  • low perfusion pressure causes the kidneys to enhance sodium and water re-absorption
  • baroreceptors in carotid and aortic arch respond to lower BP w/ sympathetic stimulation
  • this, along w/ vasoconstriction of glomerular efferent arteriole and dilation of the afferent arteriole, is intended to maintain glomerular filtration within a relatively narrow range
  • decreasing perfusion promotes activation of RAAS → Ang II (potent vasoconstrictor) → stimulates aldosterone → promotes soidum and water reabsorption at collecting duct
  • low blood volume is also a stimulus to hypothalamus promoting ADH release → increased tubular water reabsorption, concentrating the urine
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15
Q

What is the pathophysiology of renal/intrinsic AKI?

A
  • acute tubular necrosis (ATN) occurs due to prolonged/severe ischaemia
  • it’s preceded by impaird renal perfusion + tissue hypoxaemia
  • this yields direct microvacular endothelial injury + tubular ischaemia typically most severe in early proximal tubule and outer medullary segments
  • hypoxaemia → inc reactive oxygen species → reduction in available adenosine triphosphate → cellular dysfunction + death
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16
Q

What is the pathophysiology of postrenal AKI?

A
  • renal injury associated w/ obstruction results from increased intratubular pressure
  • yields tubular ischaemia and atrophy
  • evidence also suggests injury results from influx of monocytes and macrophages
17
Q

What are the clinical features of AKI?

A

Many pts are initially asymptomatic and diagnosed with lab tests, but the following may be seen:

  • Signs → oliguria/anuria, pulm or peripheral oedema, arrhythmias, hypotension/hypertension
  • Symptoms → N+V, dizziness, orthopnoea
  • Uraemia symptoms are seen in CKD or urea >40hr:
    • pruritus, N+V, encephalopathy, pericarditis, weight loss, muscle cramps
18
Q

What investigations can be carried out for AKI?

A
  • Bedside → vitals, urine output (!), urine dip, ABG (lactate), ECG
    • haematuria / proteinuria may suggest intrinsic renal dx
  • Bloods →
    • FBC for thrombocytopaenia (HUS), anaemia (CKD), leucocytosis
    • LFTs for hepatorenal syndrome
    • U+Es for high creatinine / K / urea (?pre-renal failure)
    • for any intrinsic renal dx, look for IGs, paraprotein, complement, Abs (ANA, ANCA, anti GBM)
  • Imaging →
    • Renal USS (!!): small kidneys ?CKD, asymmetry ?vascular, post-obstructive causes
    • CXR for any pulmonary oedema and/or assoc. HF
19
Q

What are the differences between acute tubular necrosis and prerenal uraemia?

A
20
Q

When would you refer to a nephrologist, for AKI, according to NICE?

A
  1. Renal transplant
  2. ITU patient with unknown cause of AKI
  3. Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
  4. AKI with no known cause
  5. Inadequate response to treatment
  6. Complications of AKI
  7. Stage 3 AKI (see guideline for details)
  8. CKD stage 4 or 5
  9. Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
21
Q

The management of AKI is largely supportive. What are the supportive measures?

A
  • Treat sepsis
  • STOP nephrotoxic meds (refer to image)
  • stop drugs that increase complications → diuretics (esp K-sparing), metformin, antihypertensives
  • check all drug dosages are appropriate for renal impairment
  • consider gastroprotection (eg. PPI) and nutritional support
  • avoid radiological contrast
22
Q

What involves general management of AKI for the underlying aetiology?

A
  • Pre-renal → correct vol depletion and/or inc renal perfusion via circulatory support, treat any underlying sepsis <do><br></br> </do>
  • Renal → refer to likely biopsy and specialist treatment of intrinsic renal disease
  • Post-renal → catheter, nephrostomy or urological intervention

Common to all aetiologies of AKI is the need to manage fluid balance, acidosis, hyperkalaemia and the timely recognition of those who may require renal replacement therapy

23
Q

How do you manage the fluid balance for a patient in AKI?

A

Must assess voume status first, either a) hypovolaemia or b) overload

  • Hypovolaemia → reduced BP and urine output, non-visible JVP, poor tissue turgor, inc HR, daily weight loss
    • examine before + after all fluid given to ensure adequate response and to reduce the risk of fluid overload
    • give 500mL crystalloid over 15min (eg. 0.9% saline), further 250-500mL boluses with clinical review after each one - stop when euvolemic or seek exp help when 2L given
  • Fluid overload → inc BP and JVP, lung creps, peripheral oedema, gallop rhythm
    • oxygen if required
    • fluid restriction, consider oral and IV fluids
    • diuretics, only if symptomatic fluid overload
    • renal replacement therapy: AKI w/ fluid overload and oligo/anuria needs urgent referral to renal/critical care
24
Q

How do you manage acidosis in AKI?

A
  • Treatment of underlying disorder will stop acid production
  • Where the effect of treatment may be delayed, acidosis will persist and RRT may be indicated
  • Sodium bicarbonate treatment is controversial
25
Q

How do you manage hyperkalaemia in AKI?

A

Treat K>6.5 mmol/L or with any ECG changes:

  • 10mL of 10% calcium gluconate → slowly IV (max rate of 2mL/min), repeat dose if necessary until ECG normalises up to a max dose of 40mL
  • dextrose/insulin infusion → 50mL of 50% dextrose w/ 10 units of soluble human insulin, over 15mins - monitor hourly for hypoglycaemia, which may be delayed in renal impairment
  • nebulised salbutamol → 10-20mg can be considered in adjunct to above, 40% of pts do not respond and caution is required in pts w/ tachycardia or IHD
  • cation-exchange resin (calcium polystyrene sulfonate) → to remove potassium from body

RRT for severe refractory hyperkalaemia

26
Q

Renal replacement therapy (e.g. haemodialysis) is used for which life-threatening complicating indications?

A
  • refractory hyperkalaemia - potassium >6.5
  • refractory metabolic acidosis - pH <7.15
  • refractory vol overload +/- pulm oedema
  • end-organ complications of uraemia
  • severe AKI and poisoning/drug overdose

*Medicine: Renal & Urology (23 decks)

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