Acute kidney injury (URO) Flashcards
Define acute kidney injury (AKI).
Acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output (dysregulation of fluid balance and electrolytes, and retention of nitrogenous waste products)
What are some risk factors of AKI? (8)
- age >65
- Hx of:
- CKD
- HF
- liver disease
- diabetes
- multiple myeloma
- contrast administration
- NSAIDs/ACEi’s or ARBs/diuretics
What are the three types of AKI?
- prerenal - any condition that leads to decreased renal perfusion –> low urinary sodium (anything impairing blood supply to kidney)
- intrinsic (intrarenal) - any condition that leads to severe direct kidney damage –> high urinary sodium
- postrenal - any condition that results in bilateral obstruction of urinary flow from renal pelvis to urethra
What is prerenal AKI commonly associated with? (3)
Sepsis, hypovolaemia and/or hypotension
What is intrinsic AKI commonly associated with? (3)
- nephrotoxins like aminoglycoside Abx (e.g. gentamicin) and NSAIDs
- rare causes include vasculitis or interstitial nephritis
What is postrenal AKI commonly associated with?
Urinary outflow obstruction
What are some prerenal causes of AKI? (5)
- hypovolaemia - haemorrhage, diarrhoea, vomiting
- hypotension - shock, sepsis, anaphylaxis
- heart failure
- renal artery stenosis (investigate with magnetic resonance angiography MRA, asymmetrical kidneys, avoid ACEi)
- drugs - e.g. NSAIDs, ACEi
What is the serum urea:creatinine ratio in prerenal AKI?
Increased
What are some causes of intrinsic AKI? (6 + 4)
- acute tubular necrosis (most common)
- acute interstitial nephritis (drug-induced)
- haemolytic uraemic syndrome (vascular)
- thrombolytic thrombocytopenia purpura (vascular)
- glomerulonephritis
- membranous nephropathy (adult nephrotic syndrome - proteinuria, hypoalbuminemia, hyperlipidaemia etc)
- vasculitides, eclampsia, rhabdomyolysis, tumour lysis syndrome
What is the most common cause of intrinsic AKI seen in clinical practice?
Acute tubular necrosis - damage to tubular cells due to ischaemia (shock or sepsis) or nephrotoxins (contrast or aminoglycosides)
Describe ischaemic acute tubular necrosis (intrarenal AKI).
Damage to tubular cells due to prolonged and severe ischaemia:
- shock
- heart failure
- renal artery stenosis
- excessive GI fluid loss
Give examples of endogenous toxins that can cause acute tubular necrosis (intrarenal AKI)? (3)
- myoglobin from rhabdomyolysis (raised CK)
- uric acid from tumour lysis syndrome
- monoclonal light chains from multiple myeloma
Give examples of exogenous toxins that can cause acute tubular necrosis (intrinsic AKI)? (5)
- aminoglycosides e.g. gentamicin
- NSAIDs
- cisplatin
- contrast agents
- anti-freeze
What is seen on microscopy of acute tubular necrosis (intrinsic AKI)?
Muddy brown granular casts in urine
Describe urine sodium and osmolality in acute tubular necrosis (intrinsic AKI)?
High urine sodium
Low urine osmolality
What is the most common drug-induced cause of intrinsic AKI?
Acute interstitial nephritis - caused by penicillin/Abx or NSAIDs
What are some systemic symptoms of acute interstitial nephritis (intrinsic AKI)? (4)
- fever
- arthralgia
- rash
- eosinophilia (allergic-type reaction –> type IV hypersensitivity)
What might you find on urinalysis, urine dip and bloods of acute interstitial nephritis (intrinsic AKI)?
- urinalysis: white cell casts because an immune reaction is occurring
- urine dip: leukocytes +++
- bloods: raised IgE, eosinophilia
List two types of vascular disease causing intrinsic AKI. (2)
- haemolytic uraemic syndrome (HUS)
- thrombotic thrombocytopenia purpura (TTP)
What are the clinical features of haemolytic uraemic syndrome (intrinsic AKI)? (3)
- haemolytic (normocytic) anaemia - jaundice, schistocytes
- thrombocytopenia - petechiae, purpura
- AKI following blood diarrhoeal illness - due to Shiga-toxin producing E.coli O157:H7
What is the management for haemolytic uraemic syndrome (HUS - intrinsic AKI)?
Supportive management
What is thrombotic thrombocytopenia purpura (TTP -intrinsic AKI)?
Abnormally large and sticky multimers of VWF cause platelets to clump within vessels
List clinical features of thrombotic thrombocytopenia purpura (TTP - intrinsic AKI)? (3)
- overlap with HUS (haemolytic anaemia, thrombocytopenia)
- fever
- neurological signs - headache, confusion, seizures
How is thrombotic thrombocytopenia purpura (TTP) measured? (2)
- plasmapheresis
- rituximab
What are the two ways that glomerulonephritis (intrinsic AKI) can present? (2)
- nephrotic syndrome (proteinuria)
- nephritic syndrome (haematuria)
List some causes of postrenal AKI. (4)
- kidney stones
- BPH
- external compression of ureter e.g. due to tumour
- neurogenic bladder due to MS, spinal cord lesions or peripheral neuropathy
What is the criteria used to stage AKI?
KIDIGO criteria
- stage 1:
- creatinine rise of 1.5x baseline OR
- creatinine rise of >=26pmol/L in 48h OR
- urine output <0.5ml/kg/hour for 6 hours
- stage 2:
- creatinine rise of 2x baseline OR
- urine output <0.5ml/kg/hour for 12 hours
- stage 3:
- creatinine rise of 3x baseline OR
- urine output <0.3ml/kg/hour for 24 hours OR
- anuria for 12 hours OR
- serum creatinine >354 pmol/dl
What are the clinical features of AKI? (6)
- decreased urine output –> oliguria (reduced) or anuria (absence)
- signs of volume depletion (prerenal AKI) - hypotension, tachycardia, reduced skin turgor, orthostatic hypertension, thirst
- signs of fluid overload (Na+ and H2O retention) - peripheral/pulmonary oedema, hypertension, HF, SOB
- signs of uraemia (due to failure of kidneys to excrete urea) - anorexia, nausea, encephalopathy, asterixis, pericarditis
- signs of renal obstruction (postrenal AKI) - distended bladder (suprapubic distension), lower urinary tract symptoms due to incomplete voiding, pain over bladder or flanks, haematuria
- arrhythmias due to hyperkalaemia (–> muscle weakness, paraesthesia)
What are the clinical signs of volume depletion in prerenal AKI? (5)
- hypotension
- tachycardia
- reduced skin turgor
- orthostatic hypotension
- thirst
What are the clinical signs of fluid overload in AKI? (4)
- peripheral or pulmonary oedema
- hypertension
- HF
- SOB
What are the clinical signs of uraemia in AKI? (5)
- anorexia
- nausea
- encephalopathy
- asterixis
- pericarditis
What are the clinical signs of renal obstruction in postrenal AKI? (4)
- distended bladder (suprapubic distension)
- incomplete voiding –> overload –> lower urinary tract symptoms
- pain over bladder or flanks
- haematuria
What arrhythmia can occur in AKI and what are some clinical features of this? (1 + 2)
Hyperkalaemia
- muscle weakness
- paraesthesia
In AKI, what can fever, rash and arthralgia be a sign of?
Small-vessel vasculitis or (acute) interstitial nephritis - intrinsic AKI
What are the 1st line investigations for AKI? (8)
- U&Es
- creatinine
- LFTs
- serum potassium
- FBC
- bicarbonate
- urinalysis (dipstick)
- VBG/ABG
What will investigations generally show if AKI? (3)
- increase in serum creatinine
- decrease in urine output
- hyperkalaemia
When is hyperkalaemia considered severe? (2)
- if K+>6.5 OR
- ECG changes:
- tall tented T-waves
- loss of P waves
- broad QRS complexes
What does blood on urinalysis indicate (AKI)?
Nephritic cause
What does leukocyte esterase and nitrites on urinalysis indicate?
UTI
What does glucose on urinalysis indicate?
Osmotic diuresis
What does protein on urine dipstick indicate?
- rules out prerenal and postrenal causes of AKI
- indicates intrinsic cause - glomerular disease
What will acute ischaemic necrosis show on a urine dipstick?
Leukocytes +++
What does glomerulonephritis show on urine dipstick?
Positive blood
What do you see on blood film in haemolytic uraemic syndrome?
Schistocytes
What do you do after initial investigation if no obvious cause of AKI can be found?
Renal ultrasound to look for obstruction in postrenal AKI
What can VBG/ABG show in suspected AKI?
An anion gap metabolic acidosis is seen in AKI due to impaired excretion of non-volatile acids
What can cause false positive creatinine rises? (2)
- use of trimethoprim
- serum creatinine falls during pregnancy so rise after recent delivery may be false +ve
What are some differential diagnoses for AKI?
- CKD (hypocalcaemia, small kidneys US)
- HUS (AKI+haemolytic anaemia+thrombocytopenia)
- rhabdomyolysis (falls, seizures)
- pre-renal uraemia
- acute tubular necrosis
- nephritic syndromes (sudden onset haematuria, oliguria, hypertension, oedema)
- nephrotic syndrome (proteinuria, hypoalbuminemia, oedema, no haematuria)
- increased muscle mass
- drug side effects (cimetidine, trimethoprim)
- orthostatic proteinuria
What is the general 1st line management plan for AKI? (5)
- stop nephrotoxic substances
- manage volume status (hypovolaemia or hypervolaemia)
- treat hyperkalaemia
- patient may require catheterisation if postrenal AKI
- identify and treat underlying cause of AKI
What nephrotoxic substances are stopped in AKI? (4)
DAMN substances:
- diuretics
- ACEi & aminoglycosides (gentamicin)
- metformin if eGFR<45 (does not worsen AKI but can accumulate –> lactic acidosis)
- NSAIDs
What NSAID can be continued in AKI?
Aspirin at cardio-protective doses i.e. 75mg to prevent cardiovascular events
How can we manage hypovolaemic (pre-renal) AKI?
- immediate IV fluid resuscitation with 500mL bolus IV fluid over 15mins
- if hyperkalaemia >5.5 or suspected (e.g. rhabdomyolysis): normal saline at 0.9% NaCl
- if still hypotensive: vasopressors (IV norepinephrine)
How can we manage hypervolaemic AKI?
- loop diuretic e.g. furosemide
- sodium and fluid restriction
- renal replacement therapy (dialysis) if these do not work
How can we manage different stages of hyperkalaemia in AKI?
- mild (5.5-5.9mmol/L): identify and treat underlying cause, CONSIDER cation-exchange resin/polymer
- moderate (6.0-6.4 and normal ECG): PLUS insulin (Actrapid)+dextrose to drive K+ into cells
- severe (>6.5 or ECG changes): PLUS calcium chloride/gluconate (IV gluconate 10% 30mL to stabilise cardiac membrane) PLUS salbutamol
What can remove potassium from the body in hyperkalaemia (AKI)?
Calcium resonium
What do we consider in patients with AKI and metabolic acidosis?
Sodium bicarbonate
How do we manage hypervolaemic AKI with pulmonary oedema? (3)
- upright position
- high-flow oxygen
- glyceryl trinitrate (GTN)
What are the indications for renal replacement therapy (haemodialysis) in AKI? (5)
- refractory metabolic acidosis
- refractory hyperkalaemia
- refractory pulmonary oedema
- refractory hypervolaemia
- uraemia (complications e.g. pericarditis/encephalopathy)
- (NB refractory = non-responsive to treatment)
What is an acronym we can use that indicates whether referral for renal replacement therapy in AKI is needed?
AEIOU BLAST
- Acidosis (pH<7.2 or HCO3<10)
- Electrolyte (persistent hyperkalaemia i.e. >7mmol/L)
- Intoxication (OD of Barbiturates, Lithium, Alcohol, Salicylates, Theophylline)
- Oedema (pulmonary that is refractory)
- Uraemia (urea>40 or complications e.g. encephalitis)
What are some complications of AKI? (5)
- hyperkalaemia
- hyperphosphatemia
- uraemia
- chronic progressive kidney disease
- end-stage kidney disease
What can cause AKI in elderly patients?
A ‘long lie’ following a fall = prolonged immobility –> rapid breakdown of muscles –> myoglobulin products that are toxic to glomerulus –> AKI
Raised CK = rhabdomyolysis
What is an electrolyte difference between AKI and CKD?
Both can have hyperkalaemia (due to impaired K+ excretion) but CKD often has hypocalcaemia too (lack of 1-a-hydroxylase)
