Acute Kidney Injury Flashcards
Definition
Sudden decline in kidney function following an insult to the kidneys. characterised by:
- increased creatine = > 26 umol/L within 48 hours or 1.5 * baseline in 7 days
- decreased urine output < 0.5 ml/kg/hr for 6 or more hours consecutive
Epidemiology
Males
Elderly >65
Risk Factors
CKD
HF
Diabetes
Liver disease
Nephrotoxic meds =
- NSAIDS
- ACE-I
Iodine-based contrast media
Sepsis
Pre-renal Aetiology
Inadequate blood supply to the kidneys, reducing the filtration of blood (MC)
- Hypovolaemia (e.g. cannot maintain oral intake, haemorrhage, gastrointestinal losses, renal losses, burns)
- Reduced cardiac output (e.g. organ failure (cardiac/liver failure), sepsis, drugs)
- Drugs that reduce blood pressure, circulating volume, or renal blood flow = ACE-I (causes constriction of afferent arteriole = decreased perfusion to glomerulus)
Renal Aetiology
Intrinsic disease in the kidney leading to reduced filtration of blood
- Toxins and drugs (e.g. antibiotics, contrast, chemotherapy)
- Vascular causes (e.g. vasculitis, thromboembolism, microangiopathic haemolytic anaemia)
- Tubular causes (e.g. acute tubular necrosis, rhabdomyolysis, myeloma)
- Glomerulonephritis
- Interstitial causes (e.g. interstitial nephritis, lymphoma infiltration)
Post-renal Aetiology
Obstruction to outflow of urine causing back pressure into the kidneys and reduced kidney function. AKA obstructive uropathy:
- Renal stones
- Blocked urinary catheter
- Enlarged prostate
- Genitourinary tract tumours
- Retroperitoneal fibrosis
- Neurogenic bladder
Pre-renal pathophysiology
Less blood going into kidney = less being filtered = AZOTAEMIA (high blood urea nitrogen + creatinine)
Less blood going into kidney = RAAS activated = Na+ and urea is reabsorbed + water follows = oliguria (less urine output)
Urine more concentrated (>500 mOsm/kg)
Renal pathophysiology
Tubular = acute tubular necrosis due to prolonged ischaemia causes epithelial cells of the tubules to die
Pre-renal causes mean less blood flow into kidneys
Nephrotoxins can kill epithelial cells. When cells die they can block the tubules = higher pressure in tubules
So fluid is trying to go from high pressure glomeruli to high pressure tubule (less filtered -> low eGFR) = azotaemia, hypercalcaemia, metabolic acidosis
Glomerular = glomerular nephritis = antigen-antibody complexes build up in glomeruli = activates compliment system = other immune cells comes = release lysosomal enzymes which damage podocytes = inflammation = large molecules (e.g. proteins) can get from blood into tubules + pass the podocytes
Interstitial = acute interstitial nephritis can be caused by NSAIDs which cause neutrophils + eosinophils to build up in the interstitium (between tubules) -> inflammation
Post-renal Pathophysiology
Intra-abdominal tumours = can press on ureter
Benign prostatic hyperplasia = can press on ureter
Pressure backs up into kidneys = increases tubular pressure = lowers pressure gradient between glomeruli + tubules -> GFR reduces
High pressure in tubules forces reabsorption of Na+, water and urea. Eventually tubular epithelium die due to high pressure so less Na+ + urea reabsorbed
Signs
Signs of hypovolaemia may be present, for example:
- Dry mucous membranes
- Decreased skin turgor
- Reduced blood pressure
Uraemic skin changes: e.g. uraemic frost if severe
Signs of volume overload may be present (e.g. due to obstructive AKI), for example:
- Bibasal crackles
- Raised JVP
- Peripheral oedema
Palpable bladder
Symptoms
Reduced urine output +/- change to urine colour
- MUDDY BROWN CASTS IN URINE
Confusion or drowsiness
Dyspnoea +/- swollen legs
Suprapubic pain: e.g. if caused by urinary retention
Haematuria: e.g. if caused by glomerulonephritis
Post renal specific signs
Palpable prostate
Loin to groin pain with stones
Prostatic issues:
- dysuria
- terminal dribbling
- hesitancy
Symptoms of complications
Hypovolaemia
- arrhythmias, muscle weakness
Uraemia
- fatigue, weakness, anorexia, N+V, confusion, pruritus’, bruising
Volume overload
- oedema, pulmonary oedema
Impaired platelets
- bruising, bleeding
Diagnosis
Establish prerenal, renal, post-renal: Urea :Creatinine ratio:
>100:1 = pre
<40:1 = renal
40-100 = post
Urea and electrolytes: to confirm the diagnosis and check serum potassium (hyperkalaemia)
Full blood count and CRP
Venous blood gas: metabolic acidosis
Chest X-ray: to investigate for pulmonary oedema
Ultrasound urinary tract: to investigate for obstruction or hydronephrosis
Diagnostic criteria
RIFLE criteria:
- A rise in serum creatinine of 26 micromol/L or greater within 48 hours
- A 50% or greater rise in serum creatinine (more than 1.5 times baseline) known or presumed to have occurred within the past 7 days
- A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours (if it is possible to measure this, for example, if the person has a catheter)
Staging
Once an AKI has been detected you can calculate the severity of the AKI with the widely used KDIGO system.
Stage 1:
Rise in creatinine to 1.5-1.9 times baseline, or
Rise in creatinine by ≥26.5 µmol/L, or
Fall in urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage 2:
Rise in creatinine to 2.0 to 2.9 times baseline, or
Fall in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3:
Rise in creatinine to ≥ 3.0 times baseline, or
Rise in creatinine to ≥353.6 µmol/L or
Fall in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, fall in eGFR to <35 mL/min/1.73 m2
Management
First-line:
Treat complications: such as hyperkalaemia
Intravenous fluids
Fluid-balance chart +/- catheter
Treat the underlying cause: start antibiotics (if infection/sepsis suspected), stop offending drug (if applicable), remove the obstruction (if necessary)
Second-line:
Renal-replacement therapy: used when patients do not respond to the medical treatment. It is indicated in the following circumstances:
- Hyperkalaemia refractory to medical management
- Severe metabolic acidosis refractory to medical management
- Volume overload refractory to diuretic agents
- Uraemic manifestations such as encephalopathy or pericarditis
Nephrotoxic medications
NSAIDS
ACE-I
Angiotensin II Inhibitors
Diuretics
May have to be stopped if AKI as increased risk of toxicity but doesn’t usually worsen AKI itself:
- Metformin
- Lithium
- Digoxin
Safe medications
Paracetamol
Warfarin
Statins
Aspirin at 75mg
Clopidogrel
Beta-blockers
Complications
Metabolic: hyperkalaemia, hyperphosphataemia, hyponatremia, hypocalcaemia
Metabolic acidosis
Respiratory: pulmonary oedema (+/- peripheral oedema)
Renal: uraemia, chronic kidney disease, end-stage renal disease
