Acute Kidney Injury Flashcards
Definition
An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products AND the dysregulation of extracellular volume and electrolytes.
KDIGO classification
o Increase in serum creatinine > 26 mmol/L within 48 hrs
o Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
o Urine volume < 0.5 ml/kg/hr for 6 hours
Aetiology - Pre-Renal (90%)
Hypovolaemia (eg haemorrhage, severe vomiting)
Heart failure
Cirrhosis
Nephrotic syndrome
Hypotension (eg shock, sepsis, anaphylaxis)
Renal hypoperfusion (eg NSAIDs, ACE inhibitors, ARBs, renal artery stenosis/thrombosis)
Aetiology - Intrinsic Renal
Glomerular (glomerulonephritis, haemolytic uraemic syndrome)
Tubular (acute tubular necrosis)
Interstitial (acute intersitial nephritis (NSAIDs, autoimmune))
Vasculitides (Wegener’s granulomatosis)
Eclampsia
Aetiology - Post-Renal
Due to obstruction (calculi, urethral stricture, prostatic hypertrophy or malignancy, bladder tumour)
Risk Factors
Age (>75) Pre-existing chronic kidney disease Comorbidities (eg heart failure, liver disease) Sepsis Hypovolaemia Hypotension Use of nephrotoxic medications (eg NSAIDs, gentamicin) Emergency surgery Diabetes mellitus
Epidemiology
15% of adults admitted to hospital will develop an AKI
Most common in the elderly
Presenting Symptoms
· Depends on underlying CAUSE · Oliguria/anuria (NOTE: abrupt anuria suggests post-renal obstruction) · Nausea/vomiting · Dehydration · Confusion
Signs on Physical Examination
· Hypertension
· Distended bladder
· Dehydration - postural hypotension
· Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
· Pallor, rash, bruising (vascular disease)
Investigations
Urinalysis: Blood - suggests nephritic cause Leucocyte esterase and nitrites - UTI Glucose Protein Urine osmolality
Bloods:
FBC, Blood film, U&Es, Clotting, CRP
Immunology -
· Serum immunoglobulins and protein electrophoresis - for multiple myeloma
(Also check for Bence-Jones proteins in the urine)
· ANA - associated with SLE
(Also check anti-dsDNA antibodies (high in active lupus)
· Complement levels - low in active lupus
· Anti-GBM antibodies - Goodpasture’s syndrome
· Antistreptolysin-O antibodies - high after Streptococcal infection
Virology - check for hepatitis and HIV
Ultrasound:
Check for post-renal cause (obstruction)
Look for hydronephrosis
Other Imaging:
CXR - pulmonary oedema
AXR - renal stones
ECG - can show hyperkalaemia
Management Plan
Treat the cause 4 MAIN components: 1 - protect patient from hyperkalaemia (calcium gluconate) 2 - optimise fluid balance 3 - stop nephrotoxic drugs 4 - consider for dialysis
Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
Identify and treat infection
Urgent relief of tract obstruction if present
Refer to nephrology if intrinsic renal disease suspected
Renal replacement therapy IF:
Hyperkalaemia refractory to medical management
Pulmonary oedema refractory to medical management
Severe metabolic acidaemia
Uraemic complications
Possible Complications
· Pulmonary oedema · Acidaemia · Uraemia · Hyperkalaemia · Bleeding
Prognosis
Inpatient mortality varies depending on cause and comorbidities
· Indicators of poor prognosis: o Age o Multiple organ failure o Oliguria o Hypotension o CKD
Patients who develop AKI are at increased risk of developing CKD
AKI is potentially reversible whereas CKD is not