Acute Kidney Injury Flashcards
Define
Impairment of renal function over days or weeksOften results in ↑plasma urea/creatinine and oliguria (<400mL/day) and is usually reversible
A spectrum of damage form a mild deterioration in function to a severe injury requiring RRT
→ A rapid reduction in kidney function, as measured by serum urea and creatinine, and leading to a failure to maintain fluid, electrolyte and acid–base homeostasis
KDIGO Classification of AKI
- Increase in serum creatinine > 26 mmol/L within 48 hrs
- Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
- Urine volume < 0.5 ml/kg/hr for 6 hours
Causes
PRE-RENAL
- ↓renal perfusion (40-70%)
- Shock (hypovolemic, septic, cardiogenic)→ renal hypoperfusion
- Hepatorenal syndrome (associated with liver failure)
- Renal artery stenosis
INSTRINSIC RENAL
(10-50%)
- TUBULAR: Acute tubular necrosis (ATN) → COMMONEST, due to damage by ischemia, drugs, toxins (paracetamol, aminoglycosides, NSAIDs, ACE-I, lithium, contrast, myoglobinuria in rhabdomyolysis)
- GLOMERULAR
- Acute glomerulonephritis
- Acute interstitial nephritis → NSAIDs, penicillins, sulphonamides, leptospirosis
- INTERSTITIAL: drugs, infiltration with lymphoma, infection
- VASCULAR: Small or large vessel obstruction
- Renal artery/vein thrombosis, cholesterol emboli,vasculitis, haemolytic microangiopathy (e.g. HUS or TTP)
- Others – myeloma, neuropathy, accelerated phase HTN (e.g. pre-eclampsia), pigment (haemolysis, rhabdo), urate (lympho/myloprolifeative disorders post chemo)
POST-RENAL
(10-20%)
- LUMINAL: Stones, clots
- MURAL: malignancy (e.g. uteric, prostate, bladder), BPH, strictures
- EXTRINSIC compression: Retroperitoneal fibrosis ,
Risk factors
Age
Chronic kidney disease
Comorbidities (e.g. heart failure)
Sepsis
Hypovolaemia
Use of nephrotoxic medications
Emergency surgery
Diabetes mellitus
Epidemiology
common, up to 18% of hospital pts
Symptoms
Depends on underlying CAUSE
Oliguria/anuria
NOTE: abrupt anuria suggests post-renal obstruction
Nausea/vomiting
Dehydration
Confusion
Signs
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
- Look for hydronephrosis
Other Imaging
CXR - pulmonary oedema
AXR - renal stones
Management
Treat the cause
FOUR main components to management:
- Protect patient from hyperkalaemia (calcium gluconate)
- Optimise fluid balance
- Stop nephrotoxic drugs
- Consider for dialysis
- Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
- Identify and treat infection
- Urgent relief of urinary tract obstruction
- Refer to nephrology if intrinsic renal disease is suspected
Renal Replacement Therapy (RRT) considered if:
- Hyperkalaemia refractory to medical management
- Pulmonary oedema refractory to medical management
- Severe metabolic acidaemia
- Uraemic complications
Complications
Pulmonary oedema
Acidaemia
Uraemia
Hyperkalaemia
Bleeding
Prognosis
Inpatient mortality varies depending on cause and comorbidities
Indicators of poor prognosis:
- Age
- Multiple organ failure
- Oliguria
- Hypotension
- CKD
Patients who develop AKI are at increased risk of developing CKD
