Acute Kidney Injury Flashcards
How is AKI defined?
Acute kidney injury has variably been defined as an abrupt deterioration in parenchymal renal function, which is usually, but not invariably, reversible over a period of days or weeks
What percentage of people admitted to hospital and ICU develop AKI, respectively?
AKI is seen in 10-15% of people admitted to the hospital and in more than 50% of people admitted to the intensive care unit (ICU)
How can causes of AKI be categorised?
Pre-renal, intrinsic/renal, post-renal
What are common pre-renal causes of AKI?
- Hypovolaemia (GI losses, burns, haemorrhage)
- Reduced CO (Cardiac failure, liver failure, sepsis)
- Drugs that reduce blood pressure, circulating volume or renal blood flow (ACE-I, ARBs, NSAIDs, loop diuretics)
How would you define pre-renal causes of AKI?
Pre-renal causes of AKI are most common and are due to reduced perfusion of the kidneys and leading to a decreased glomerular filtration rate (GFR)
How would you define renal causes of AKI?
Consequences of structural damage to the kidney, for example, tubules, glomeruli, interstitium, and intrarenal blood vessels.
What are common renal causes of AKI?
- Toxins and drugs
- Antibiotics
- Glomerular causes
- Tubular causes
- Interstitial causes
What are glomerular causes of intrinsic AKI?
Glomerulonephritis
What are tubular causes of intrinsic AKI?
Acute tubular necrosis, rhabdomyolysis, myeloma
What are the interstitial causes of intrinsic AKI?
Interstitial nephritis, lymphoma infiltration
What are the vascular causes of intrinsic AKI?
Vasculitis, thrombosis, thromboembolism, dissection
What is acute tubular necrosis?
Acute tubular necrosis (ATN) is common, particularly in hospital practice.
It results most often from renal ischaemia but can also be caused by direct renal toxins including drugs such as the aminoglycosides, lithium and platinum derivatives
How would you define post-renal causes of AKI?
Post-renal causes are least common, accounting for around 10% of acute kidney injury. Due to acute obstruction of the flow of urine resulting in increased intratubular pressure and decreased GFR
What are common post-renal causes of AKI?
Obstruction –> renal stones, blocked catheter, enlarged prostate, genitourinary tract tumours/masses, neurogenic bladder
What are the symptoms and signs of AKI?
Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms:
- Fatigue
- Loss of appetite
- Headache
- Nausea
- Vomiting
- Potassium level disturbances can lead to arrhythmias
- Fluid balance is affected, leading to hyper, hypo or normotension
- Pain in the flanks may be encountered in some conditions (such as clotting of the kidneys’ blood vessels or inflammation of the kidney)
What is the clinical presentation of AKI determined by?
The clinical presentation is often dominated by the underlying cause. The various symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease.
Which groups are specifically at risk of AKI?
- People > 65 age
- History of AKI
- CKD with estimated glomerular filtration rate [eGFR] less than 60mL/min/1.73m2
- Symptoms or history of urological obstruction or conditions which may lead to obstruction
- Chronic conditions such as heart failure, liver disease, and diabetes mellitus.
How is AKI diagnosed?
AKI can be diagnosed if any one of the following is present:
1. Increase in Serum Creatinine by ≥0.3mg/dl (≥26 μmol/l) within 48 hours; or
- Increase in Serum Creatinine to ≥1.5 times baseline, which has occurred within the prior 7 days; or
- Urine volume < 0.5 ml/kg/h for 6 hours
When should you think AKI?
- Nausea and vomiting, or diarrhoea,evidence of dehydration.
- Reduced urine output or changes to urine colour.
- Confusion, fatigue,and drowsiness.
Especially in combination with any of the risk factors
What are the three stages of AKI?
- Stage 1 - risk
- Stage 2 - injury
- Stage 3 - failure
What is the first stage in AKI?
STAGE 1 - risk
1. Creatinine rise of 26 micromol or more within 48 hours OR 2. Creatinine rise of 50–99% from baseline within 7 days (1.50–1.99 x baseline) OR 3. Urine output < 0.5 mL/kg/h for more than 6 hours
What is the second stage in AKI?
STAGE 2 - injury
1. 100–199% creatinine rise from baseline within 7 days (2.00–2.99 x baseline) OR 2. Urine output < 0.5 mL/kg/hour for more than 12 hours
What is the third stage in AKI?
STAGE 3 - failure
1. 200% or more creatinine rise from baseline within 7 days (3.00 or more x baseline) OR 2. Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days OR 3. Urine output < 0.3 mL/kg/hour for 24 hours or anuria for 12 hours
What are the complications linked to AKI?
Complications from acute kidney injury (AKI) arise as a result of impairment of the kidney’s excretory, endocrine, and metabolic actions. The risk of complications is related to the stage of AKI
Complications include:
- Hyperkalaemia
- Electrolyte imbalance
- Metabolic acidosis
- Volume overload
- Uraemia
- CKD and end-stage renal disease
What are the predictors of developing CKD after AKI?
Predictors for CKD after AKI include older age, lower baseline eGFR, higher baseline albuminuria, and higher stages of AKI
How would you treat AKI?
Immediate admission or referral to hospital is not needed for all people with acute kidney injury (AKI).
Assess volume status, renal function, serum potassium
Treat the underlying cause!
Who needs urgent admission following AKI?
- Stage 3 kidney injury
- No identifiable AKI cause
- An underlying cause that requires urgent secondary care
- Risk of urinary tract obstruction
- Sepsis
- Evidence of hypovolaemia and a need for intravenous fluid replacement and monitoring.
- A deterioration in clinical condition or a need for observation
- A complication of acute kidney injury requiring urgent secondary care management such as pulmonary oedema, uraemic encephalopathyor pericarditis, or severe hyperkalaemia.
What is the prognosis for AKI?
The prognosis of AKI varies depending on clinical setting, the underlying cause, and any comorbidities
- There is also evidence that mortality increases with increasing stages of AKI - AKI acquired in the community has a lower mortality rate than hospital acquired AKI - People with chronic kidney disease preceding the episode of AKI there was a four- to five-fold increase in renal outcomes and mortality outcomes were doubled compared with people with AKI alone
What are causes of acute deterioration in chronic kidney disease?
Systemic infection (urinary tract infection (UTI), chest infection, central line)
Drugs (diuretics, angiotensin-converting enzyme (ACE) inhibitors, aminoglycosides.)
Dehydration
Urinary tract obstruction or urinary retention (due to spinal cord compression or neurogenic bladder, or renal vein thrombosis)
