Acute kidney injury (AKI) Flashcards
What are the functions of the kidneys?
Define acute kidney injury.
Acute decline in renal function, leading to a rise in serum creatinine and a decrease in urine output.
- The kidneys therefore cannot carry out their functions of:
- Water homeostasis
- Electrolyte balance
- Acid-base homeostasis
- Endocrine function: RAS, EPO, Vit D
- Clearance of waste products
What is the most common form of AKI? What are the top 5 causes of in-patient AKI?
Acute tubular necrosis (ATN) accounts for 45% of cases of AKI. ATN is caused by sepsis in 19% of ICU patients
Top 5 causes of in-hospital AKI:
- Decreased renal perfusion
- Medications
- Radiographic contrast media
- Postoperative
- Sepsis
Source: In-hospital AKI. Nash 2002
What is the aetiology of pre-renal AKI?
Pre-renal causes:
- Reduced renal perfusion e.g. hypovolaemia, haemorrhage, sepsis, renal artery stenosis
- Exogenous toxins e.g. immunoglobins, myoglobin
- Endogenous toxins e.g. ACEi. NSAIDs
What is the aetiology of post-renal AKI?
- Renal obstruction
- Ureteric obstruction
- Urethral obstruction
- Catheter obstruction
What is the aetiology of intrinsic renal AKI?
- Vascular Disease e.g. vasculitis
- Glomerular Disease e.g. glomerulonephritis
- Tubular Disease e.g. ATN
- Interstitial Disease e.g. analgesic nephropathy
What is the pathophysiology of renal AKI?
Most commonly ATN (acute tubular necrosis) due to…
- impaired renal perfusion –> tissue hypoxaemia –> severe ischaemia –> increased ROS and reduced adenosine triphosphate* –> cellular dysfunction/death –> microvascular endothelial injury (most severe in early proximal tubule and outer medullary segments)
What is oliguria?
A urine output of less than 400-500mL per 24 hours in adults
(Normal urine output for an adult is 0.5ml/kg/hr and for children 1ml/kg/hr on average)
What are the risk factors for AKI?
Risk factors for AKI include:
- CKD
- chronic disease e.g. heart failure, liver disease, DM
- history of AKI
- nephrotoxic medications (e.g. NSAIDs, aminoglycosides, ACEi, ARBs and diuretics) within the past week
- use of iodinated contrast agents within the past week
- age 65 years or over
What are the KDIGO criteria for diagnosing AKI?
- Increase in serum creatinine by ≥26.5 micromol/L (≥0.3 mg/dL) within 48 hours; or
- Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
- Urine volume <0.5 mL/kg/hour for 6 hours.
Is there genetic predisposition to AKI?
There is preliminary evidence that a genetic predisposition for AKI may exist, especially with apolipoprotein E (APO-E) genes.
Summarise RAS response to reduced circulating volume.
- Central baroreceptors are activated
- RAS activation
- Vasopressin release
- Sympathetic system activation
- Vasoconstriction, renal sodium retention, increase in CO
*Angiotensin II stimulates aldosterone release promoting water and sodium reabsorption at collecting duct
*Low BP also promotes ADH release and increased tubular water re-absorption concentrating the urine
What two main ix are used to define severity of AKI?
Serum creatinine
Urine output (or eGFR)
What is the pathophysiology of post-renal AKI?
Obstruction –> increased intratubular pressure –> ischaemia and atrophy of renal tubules
Probably due to influx of monocytes and macrophages releasing cytokines, free radicals, proteases and TNF-beta which cause irreverisble injury and fibrosis.
Recognise the presenting symptoms of acute kidney injury (AKI).
Often asymptomatic and diagnosed by laboratory tests.
General symptoms:
- N&V
- Uraemia
- Altered mental status
Recognise the signs of acute kidney injury (AKI) on physical examination
Hypotension, hypertension, pulmonary oedema, peripheral oedema. Asterixis. Altered mental status
Patients with…
- fluid loss, sepsis, or pancreatitis may have hypotension along with other signs of circulatory collapse.
- glomerular disease typically present with hypertension and oedema, proteinuria, and microscopic haematuria (nephritic syndrome).
- rash, petechiae, or ecchymoses may suggest an underlying systemic condition such as vasculitis, thrombotic microangiopathy, or glomerulonephritis.
- after haemorrhage, sepsis, drug overdose, surgery, cardiac arrest, or other conditions associated with hypotension and prolonged renal ischaemia –> ATN
- renovascular disease may have an underlying abdominal bruit
- prostatic obstruction may present with abdominal distension from a full bladder.
Identify appropriate investigations for acute kidney injury (AKI)
Diagnosed based on reduced UO and rising sCr.
Bloods: U&E, VBG, FBC, urinalysis and culture, urinalysis, serological (if AI suspected then ESR, anti-streptolysin O, anti-nuclear antibodies, anti-DNA, complement, anti-glomerular BM antibodies, hepatitis profile, HIV test ect)
Scans: renal USS. CXR, ECG. Later CT, MRI
Invasive: cystoscopy*,
What acronym is used for management of AKI?
STOP AKI
Sepsis - urgent septic screen within 1hr
Toxins - identify and stop e.g. NSAIDs, aminoglycoside abx, contrast
Optimise volume and BP - fluids, vasopressors in ICU
Prevent harm - check reversible causes e.g. U&Es, obstruction, meds
What is the management of pre-renal, renal and post-renal acute kidney injury (AKI)?
Pre renal -
- volume expansion/red blood cell transfuision - crystalloids (Ringer’s lactate/saline)/colloids (only for severe hypoalbuminaeamia). HES not reccommended.
- vasopressor -adrenaline(1microg/min IV), dopamine(1microg/kg/min), to keep MAP >60mmHg.
- diuretic - e.g. furosemide (40-80mg IV)
- RRT - for 4-6hrs
Intrinsic -
- treat underlying condition
- diuretic - furosemide (40-80mg) for volume control
- volume expansion - as above
- RRT
Obstructive -
- bladder catheterisation
- relief of obstruction above bladder neck (e.f. ureteral stenting, lithotripsy, exploratory laparotomy, percutaneous nephrostomy)
- diuretic
- RRT
Identify the possible complications of acute kidney injury (AKI) and its management
hyperphosphataemia - give phosphate binders like calcium acetate/carbonate.
uraemia –> lethargy, confusion, obtundation
volume overload (pulmonary and peripheral oedema)
hyperkalaemia - from impaired excretion of potassium, cell lysis or tissue breakdown
metabolic acidosis - may be managed by oral bicarbonate solutions
Which class of drugs may predispose patients to developing pre-renal AKI? Explain each.
- A.NSAIDs
- B.Calcineurin inhibitors
- C.ACEi or ARBs
- D.Diuretics
- E.All of the above
All of the above:
- NSAIDs - decrease afferent flow
- Calcineurin inhibitors - decrease afferent flow
- ACEi or ARBs - increase efferent flow so decrease filtration
- Diuretics – affect tubular function, decrease preload
When do you refer for emergency RRT?
- Refractory HYPERKAL (potassium >6.5 mmol/L)
- Refractory metabolic ACIDOSIS (pH <7.15)
- Refractory volume OVERLOAD with or without pulmonary oedema
- End-organ complications of URAEMIA (e.g., pericarditis, encephalopathy, uraemic bleeding) or other end-organ involvement (e.g., neuropathy, myopathy)
- Severe AKI and POISONING/drug overdose (e.g., ethylene glyc
What are the KIDGO stages of AKI?
AKI Stage 1:
- sCr : x1.5- 1.9 the reference OR rise of ≥26 µmol/L
- UO: <0.5ml/kg/hr for 6-12 hrs
AKI Stage 2:
- sCr : x2.0-2.9 the reference
- UO: <0.5ml/kg/hr for _>_12hrs
AKI Stage 3:
- sCr : x≥3 the reference OR or rise of ≥354 µmol/L
- UO: <0.3ml/kg/hr for _>_24hrs OR anuria for _>_12 hours
What is the RIFLE criteria for AKI?
RIFLE (Risk, Injury, Failure, Loss of kidney function, and Endstage kidney disease):
Severity groups:
1.Indicates risk:
- Serum creatinine increased 1.5 times; or
- Urine production of <0.5 mL/kg body weight for 6 hours
2. Indicates injury:
- Creatinine increased 2.0 times; or
- Urine production of <0.5 mL/kg for 12 hours.
3.Indicates failure:
- Creatinine increased 3.0 times; or
- Urine output <0.3 mL/kg for 24 hours or anuria for 12 hours.
4.Indicates loss:
- Persistent AKI for more than 4 weeks; complete loss of kidney function.
5.Indicates ESRD:
- ESRD (loss >3 months).
