AKI Flashcards
What is AKI?
Acute kidney injury (AKI) is a syndrome of decreased renal function, measured by serum creatinine or urine output, occurring over hours–days. It includes different aetiologies and may be multifactorial.
How is AKI stage?
3 stages based on urine output or creatinine
What are the different stages?
Stage 1 - Serum Cr 1.5-1.9 x baseline or >26.5umol/L; Urine output <0.5ml/kg/h for 6-12 hours
Stage 2 - Serum Cr 2.0–2.9 x baseline; Urine output <0.5ml/kg/h for >12 hours
Stage 3 - Serum Cr >353.6μmol/L (4.0mg/dL) or >3.0 x baseline or
renal replacement therapy; UO <0.3mL/kg/h for >24h or anuria for >12h
What is the framework to manage AKI?
SALFORD
Sepsis and other causes - treat
ACEI/ARB and NSAIDs - suspend/review
Labs and leaflets
Fluid assessment and response
Obstruction - USS within 24 hours in non-resolving AKI 3 of unknown cause
Renal/critical care referral - non-resolving AKI 3, anuric, CKD 4-5, severe complication
Dip urine and document it
What is the commonest causes of AKI?
Pre-renal disease or ATN
What is the aetiology of AKI?
Pre-renal - decreased perfusion to the kidney
Renal - intrinsic renal disease
Post-renal - obstruction to urine
What are pre-renal causes of AKI?
Dehydration, sepsis, hypotension, shock, hepatorenal syndrome, HF
What are the renal causes of AKI?
Glomerulonephritis, ATN, vasculitis, contrast, NSAIDs, ACEI, ARBs, gentamicin, interstitial disease
What are the post-renal causes of AKI?
prostatic hypertrophy, renal stones, pelvic cancer
What should be done on admission to A&E in terms of kidneys?
1) Renal function, blood pressure, temperature and pulse checked
2) risk assessment for the likelihood of developing AKI
3) high serum creatinine, it is important to establish whether this is an acute or acute-on-chronic phenomenon
What are life-threatening complications of AKI? (3)
1) Scoring on NEWS - consider critical care referral
2) Pulmonary oedema
3) Hyperkalaemia
What do you look for O/E in suspected AKI patients?
HR, BP, JVP, Cap refill, palpate for bladder
How do you treat hypovolaemia?
Bolus fluid 250–500mL of crystalloid over less than 15 mins, until volume replete. If 2L given without response, seek expert help.
What monitoring do you carry out? (5)
1) Fluid balance - urinary catheter and hourly urine output
2) K+
3) Observations - every 4 hr
4) lactate - if signs of sepsis
5) daily creatinine
What investigations do you carry out? (5)
1) Urine dip - haematuria/proteinuria may suggest intrinsic renal disease
2) USS within 24 hours. small kidneys –> CKD.
3) check liver function (hepatorenal)
4) check platelets
5) investigate for intrinsic renal disease: Igs, auto-antibodies
How is AKI managed?
Pre-renal: correct volume depletion and/or increase renal perfusion via circulatory/cardiac
support, treat any underlying sepsis.
Renal: refer for likely biopsy and specialist treatment of intrinsic renal disease.
Post-renal: catheter, nephrostomy, or urological intervention
Common to all - manage fluid balance (match to UO + 500mL), acidosis, hyperkalaemia, correct hypovolaemia, stop nephrotoxic drugs, nutritional support, H2-receptor antagonist to stop upper GI bleed, body weight
What are the clinical features of pre-renal AKI? (5)
Tachycardia, postural hypotension, poor peripheral pefusion, metabolic acidosis, hyperkalaemia
What are the clinical features of GN and acute interstitial nephritis? (2)
Patients with glomerulonephritis usually demonstrate significant haematuria and proteinuria
Acute interstitial nephritis - suspected in a previously well patient if there is an acute deterioration of renal function coinciding with the introduction of a new drug treatment
What are the clinical features of post-renal AKI?
bladder enlargement, USS for obstruction, hydronephrosis
What is hydronephrosis
Refers to distension and dilation of the renal pelvis and calyces, usually caused by urinary retention due to obstruction of the free flow of urine from the kidney. Untreated, it leads to progressive atrophy of the kidney.
What is Acute tubular necrosis?
Kidney damage due to hypoperfusion. Usually the result of a combination of factors which have caused renal ischaemia and toxicity, e.g. hypotension and dehydration or sepsis with associated nephrotoxic drugs.
What are the 3 stages of Acute Tubular Necrosis?
Oliguric, maintenance, polyuric
A 72-year-old woman who has been on the ward for the past five days is noted by the nurses not to be passing much urine. She was admitted originally with pneumonia but has since developed diarrhoea. Blood tests show her creatinine has increased from 98 to 172 µmol/l. Which tests is most useful when determining whether there is prerenal uraemia or acute tubular necrosis?
Urinary Sodium
What are the commonest causes of pre-renal AKI?
true volume depletion due to gastrointestinal (diarrhoea, vomiting), renal (diuretics), or third space fluid and electrolyte losses and haemorrhage.
What are risk factors for AKI?
Age, NSAID use, previous AKI, diabetes, HTN
Which 3 groups of drugs have NICE said that if started in the last week is recognised as a risk factor for AKI?
ACE-I, ARB and NSAIDs
Which patients require discussion with the renal team? (4)
- All patients with a renal transplant
- All patients with an AKI 3
- All AKI (stage 1, 2, or 3) patients with blood & protein on urine dipstick
- All patients who have no known cause of their AKI and have deteriorating renal function.
Which complications of AKI require renal replacement therapy? (4)
- uraemic encephalopathy/coma
- Metabolic acidosis that doesn’t respond to medical management
- refractory hyperkalaemia that doesn’t respond to medical management
- severe pulmonary oedema that doesn’t respond to medical management
What electrolyte imbalance does omeprazole cause?
Hyponatriemia
What would urine osmolality and sodium in pre-renal AKI show?
urine osmolality high, urine sodium low
What would urine osmolality and sodium in renal AKI/ATN show?
urine osmolality low, urine sodium high
