Acute Kidney Injury AKI Flashcards
Definition
Abrupt (<48 hrs) reduction in kidney function
Can only be applied following adequate fluid resuscitation and exclusion of obstruction
Classification
- absolute increase in serum creatinine by >26.4umol/l OR
- reduction in urine output
Urine output decreases
Creatinine level increases
Who gets it
Common in hospitalised patents
Risk factors
Increases with age Diabetes Heart failure CKD Peripheral vascular disease Previous AKI Recent contrast in imaging
What are the 3 main categories of causes?
Pre-renal
Renal
Post-renal
People who have AKI are at increased risk of developing CKD. True or false?
True
Drugs to avoid in patients with AKI
NSAIDs ACE inhibitor ARB Diuretics Gentamicin K+ sparing diuretics
PRE RENAL AKI - definition
Reduction in circulating volume which disrupts the kidneys
Decreased blood flow to kidneys –> decreased blood filtered –> decrease in GFR
PRE RENAL AKI - causes
Hypovolaemia
- haemorrhage
- volume depletion (D+V, severe burns)
Hypotension
- shock
- sepsis
Renal hypoperfusion
- NSAIDs
ACE inhibitors / ARBs
PRE RENAL AKI - clinical features
Decreased urine output (oliguria)
- less than 0.5ml/kg/hr
PRE RENAL AKI - clinical examinations
Blood pressure Heart rate Urine output Cap refill Oedema
PRE RENAL AKI - management
IV crystlloid (0.9% NaCl)
Give 250ml bolus
Reassess patient
Give up to 1000ml and if there is still no improvement, seek help
What can untreated pre-renal AKI result in?
Acute tubular necrosis
Acute tubular necrosis falls into which AKI category?
Renal AKI
What is the commonest form of AKI in hospital
Acute tubular necrosis
RENAL AKI - definition
Diseases causing inflammation or damage to the renal cells
This means the kidneys can’t filter blood effectively and reabsorption/secretion is limited
RENAL AKI - categories
Blood vessels (vascular)
Glomerular disease
Interstitial injury
Tubular injury
RENAL AKI - glomerular diseases
Goodpastures
Lupus nephritis
Post infectious glomerulonephritis
RENAL AKI - interstitial injury
Drugs - antibiotics, PPI
Infection (TB)
RENAL AKI - tubular injury
Acute tubular necrosis
- ischaemia due to pre-renal AKI where there is hypovelaemia
Contrast
RENAL AKI - blood vessel causes
Vasculitis
RENAL AKI - clinical features
Anorexia Weight loss Fatigue Nausea and vomiting Itch Oedema - fluid overload Pulmonary oedema Uraemia Rash (if vasculitis)
RENAL AKI - investigations
U+Es
- renal function marker
FBC + coagulation screen
- abnormal clotting
Urinalysis
- haematoproteinuria
US
- size of kidneys (should be normal)
Renal biopsy
RENAL AKI - Management
Fluid resuscitation
250ml bolus of 0.9% NaCl
Reassess patient and repeat until 1000ml administered
If still not achieving adequate BP then further management
- inotropes
- vasopressors
Manage underlying cause
RENAL AKI - complications
Hyperkalaemia Fluid overload (pulmonary oedema) Severe acidosis
POST-RENAL AKI - definition
Due to obstruction of urine flow leading to back pressure (hydronephrosis) and thus loss of concentrating ability
- i.e. the back pressure causes an increased pressure in the renal tubule so diffusion from high conc glomerulus -> low conc renal tubule no longer works and as a result, less molecules are filtered. This lowers the GFR
POST-RENAL AKI - causes
Obstruction/compression
- malignancy
- stones
- strictures
- BPH
POST-RENAL AKI - clinical features
Oliguria
Urine is concentrated
POST-RENAL AKI - investigations
US
CT
POST-RENAL AKI - management
Relieve obstruction
- catheter
- nephrostomy
