Acute Kidney Injury Flashcards
Acute kidney injury (AKI) is generally defined as a sudden decline in renal function over … or …
Acute kidney injury (AKI) is generally defined as a sudden decline in renal function over hours or days.
AKI is a common medical condition affecting up to 15% of emergency hospital admissions and the mortality associated with severe AKI can be up to 30-40%. A decline in renal function can lead to dysregulation of … balance, …-… homeostasis and e….
AKI is a common medical condition affecting up to 15% of emergency hospital admissions and the mortality associated with severe AKI can be up to 30-40%. A decline in renal function can lead to dysregulation of fluid balance, acid-base homeostasis and electrolytes.
AKI may be classified by a number of systems including RIFLE and K….
AKI may be classified by a number of systems including RIFLE and KDIGO.
Based on the KDIGO criteria, an AKI is defined by one of the following parameters:
An increase in serum creatinine by ≥ 26.5 micromol/L within 48 hours
An increase in serum creatinine to ≥ 1.5 times baseline within 7 days
Urine output < 0.5 mL/kg/hr for six hours
The KDIGO criteria divide AKI into … stages.
The aetiology of AKI can be categorised - what are these?
The aetiology of AKI can be categorised into pre-renal, intrinsic renal and post-renal causes.
AKI is most commonly …-renal in nature, typically occuring secondary to renal hypoperfusion.
AKI is most commonly pre-renal in nature, typically occuring secondary to renal hypoperfusion.
AKI is most commonly pre-renal in nature, typically occuring secondary to renal ….
AKI is most commonly pre-renal in nature, typically occuring secondary to renal hypoperfusion.
Decreased renal … can be related to reduced circulating volume (e.g. hypovolaemia), reduced cardiac output (e.g. cardiac failure), systemic vasodilatation (e.g. sepsis) or arteriolar changes (e.g. secondary to ACE-inhibitor or NSAID use).
Decreased renal perfusion can be related to reduced circulating volume (e.g. hypovolaemia), reduced cardiac output (e.g. cardiac failure), systemic vasodilatation (e.g. sepsis) or arteriolar changes (e.g. secondary to ACE-inhibitor or NSAID use).
Renal hypoperfusion causes …. of the renal parenchyma. Prolonged ischaemia can lead to intrinsic damage and the development of acute tubular necrosis (ATN). ATN is the most common cause of intrinsic renal AKI.
Renal hypoperfusion causes ischaemia of the renal parenchyma. Prolonged ischaemia can lead to intrinsic damage and the development of acute tubular necrosis (ATN). ATN is the most common cause of intrinsic renal AKI.
Acute tubular necrosis (ATN) is the most common cause of … renal AKI.
acute tubular necrosis (ATN). ATN is the most common cause of intrinsic renal AKI.
The hallmark of intrinsic renal AKI is structural damage. It may be categorised according to the location of the pathology:
The hallmark of intrinsic renal AKI is structural damage. It may be categorised according to the location of the pathology:
Vasculature
Glomerular
Tubulointerstitial
Intrinsic renal AKI - vascular
Large vessels are typically affected by atherosclerotic disease, thromboembolic disease and dissections (e.g. aortic). Other important causes include renal artery abnormalities such as renal artery stenosis and renal artery thrombosis.
Small vessel disease can occur secondary to vasculitides (these typically lead to the development of glomerular disease), thromboembolic disease, microangiopathic haemolytic anaemias (e.g. disseminated intravascular coagulation) and malignant hypertension.
Intrinsic renal AKI - glomerular
Glomerular pathology can be divided into primary (not associated with systemic disease) and secondary (associated with systemic disease) causes. Glomerular pathology can lead to a number of classical acute presentations (e.g. nephritic/nephrotic syndrome). They are also a major cause of chronic kidney disease (CKD).
Intrinsic renal AKI - tubulointerstitial
Tubulointerstitial pathology causes damage to the renal parenchyma that can lead to scarring and fibrosis in the long-term. The most common tubulointerstitial cause of AKI is ATN, this frequently occurs secondary to prolonged renal hypoperfusion. Other tubulointerstitial causes include acute interstitial nephritis that can occur secondary to medications (e.g. NSAIDs, PPI’s, penicillins) and infections.
Tubulointerstitial pathology causes damage to the renal parenchyma that can lead to scarring and fibrosis in the long-term. The most common tubulointerstitial cause of AKI is …, this frequently occurs secondary to prolonged renal hypoperfusion. Other tubulointerstitial causes include acute interstitial nephritis that can occur secondary to medications (e.g. NSAIDs, PPI’s, penicillins) and infections.
Tubulointerstitial pathology causes damage to the renal parenchyma that can lead to scarring and fibrosis in the long-term. The most common tubulointerstitial cause of AKI is ATN, this frequently occurs secondary to prolonged renal hypoperfusion. Other tubulointerstitial causes include acute interstitial nephritis that can occur secondary to medications (e.g. NSAIDs, PPI’s, penicillins) and infections.
AKI secondary to post-renal causes result from … (often referred to as … …) and accounts for up to 10% of cases.
AKI secondary to post-renal causes result from obstruction (often referred to as obstructive uropathy) and accounts for up to 10% of cases.
Obstruction to urinary flow can occur anywhere along the urinary tract from renal pelvis to urethra. Common causes of obstructive uropathy include … (3)
Obstruction to urinary flow can occur anywhere along the urinary tract from renal pelvis to urethra. Common causes of obstructive uropathy include urinary stones (urolithiasis), malignancy (inc. intraluminal, intramural and extramural tumours), strictures and bladder neck obstruction (e.g. benign prostatic hyperplasia).
There are a number of risk factors that increase the likelihood of developing an AKI during hospital admission. - what are they? (10)
Age (> 65 years old) History of AKI CKD Urological history (e.g. stones) Cardiac failure Diabetes mellitus Sepsis Hypovolaemia Nephrotoxic drug use Contrast agents
These are the main risk factors for developing what?
AKI
ATN can be divided into three stages:
Initiation: acute decrease in renal perfusion causing a reduced GFR
Maintenance: GFR remains low for days or weeks
Recovery: GFR recovers, regeneration of tubulointerstitial cells, polyuric phase may occur
Acute tubular necrosis (ATN) has many causes, most of which can be thought as ‘…’ or ‘….’ in nature. … causes are those of pre-renal AKI described above. … causes include medications (aminoglycosides, chemotherapies), contrast, myoglobin (in rhabdomyolysis) and multiple myeloma.
Acute tubular necrosis (ATN) has many causes, most of which can be thought as ‘ischaemic’ or ‘nephrotoxic’ in nature. Ischaemic causes are those of pre-renal AKI described above. Nephrotoxic causes include medications (aminoglycosides, chemotherapies), contrast, myoglobin (in rhabdomyolysis) and multiple myeloma.
An accurate fluid balance assessment is key in what?
An accurate fluid balance assessment is key. The patient’s fluid balance is suggestive of the underlying aetiology of AKI and may guide subsequent management.
What is this representing?
Fluid balance - dehydration vs overload
Pre-renal - AKI signs and symptoms (7)
Reduced capillary refill time Dry mucous membranes Reduced skin turgor Thirst Dizziness Reduced urine output Orthostatic hypotension
How do we assess for fluid overload? (I.e what do we look for?) - 6
Ankle swelling Orthopnoea Paroxysmal nocturnal dyspnoea Dyspnoea Raised JVP Ascites
Ankle swelling Orthopnoea Paroxysmal nocturnal dyspnoea Dyspnoea Raised JVP Ascites
All signs of what?
Fluid overload
In patients with renal hypoperfusion in the context of hypervolaemia (e.g. cardiac failure), it is important to assess for …. ….
Fluid overload
Those with intrinsic glomerular pathology may present with features of … syndrome (e.g. haematuria, proteinuria, oliguria and hypertension) or … syndrome (e.g. heavy proteinuria, hypoalbuminaemia and oedema).
Those with intrinsic glomerular pathology may present with features of nephritic syndrome (e.g. haematuria, proteinuria, oliguria and hypertension) or nephrotic syndrome (e.g. heavy proteinuria, hypoalbuminaemia and oedema).
Patients with a … disease (e.g. acute interstitial nephritis) may complain of arthralgia, rashes and fever. Eosinophilia is frequently seen.
Patients with a tubulointerstitial disease (e.g. acute interstitial nephritis) may complain of arthralgia, rashes and fever. Eosinophilia is frequently seen.
Patients with urinary … may present with classical loin-to-groin pain, haematuria, nausea and vomiting. Those with … problems may have lower urinary tract symptoms (e.g. dysuria, frequency, terminal dribbling, hesitancy). Obstruction at the … … might be associated with a palpable bladder and a tender suprapubic area.
Patients with urinary stones may present with classical loin-to-groin pain, haematuria, nausea and vomiting. Those with prostatic problems may have lower urinary tract symptoms (e.g. dysuria, frequency, terminal dribbling, hesitancy). Obstruction at the bladder neck might be associated with a palpable bladder and a tender suprapubic area.
Basic assessment - AKI
Assess the current fluid status of the patient, looking for signs of hypo- or hypervolaemia including checking their urine output. Review their medical chart looking for any potential nephrotoxic drugs and their fluid status over the last few days (e.g. have they had a positive or negative fluid balance).
Bedside investigations for AKI:
Urine dipstick
Urine microscopy
Urine osmolality and electrolytes
ECG
Bloods for AKI:
Basic blood tests should include an FBC, U&Es, bone profile and blood gas (venous/arterial). This allows a quick assessment of the extent of renal injury and the development of any potential complications like hyperkalaemia or metabolic acidosis.
Other bloods can be completed depending on the suspected cause of AKI. Many of these look for intrinsic renal causes of AKI.
Creatine kinase Vasculitis screen (e.g. ANCA, ANA) Clotting Blood film Complement Immunoglobulins Serum electrophoresis Virology (hepatitis B/C)
What is the key radiological investigation in the assessment of AKI?
The key radiological investigation in the assessment of AKI is ultrasound, which can look for evidence of obstructive uropathy (e.g. hydronephrosis). If there is a high degree of suspicion of urinary stones, a non-contrast CT may be completed.
Other radiological investigations may include for AKI: (apart from ultrasound)
CXR (eg. looking for signs of overload)
Renal dopplers (renal vascular assessment)
Magnetic resonance angiography (renal vascular assessment)
The management of an AKI should involve regular assessment and monitoring, controlling volume … and correcting … abnormalities and metabolic ….
The management of an AKI should involve regular assessment and monitoring, controlling volume dysregulation and correcting electrolyte abnormalities and metabolic acidosis.
Patients with AKI can be staged according to the KDIGO criteria. It is suggested that patients who have stage … AKI or a suspected diagnosis that may require specialist intervention (e.g. glomerulonephritis, systemic vasculitis), be discussed with a nephrologist within 48 hours of detection. Patients with post-renal AKI may require discussion with a …
Patients can be staged according to the KDIGO criteria. It is suggested that patients who have stage 3 AKI or a suspected diagnosis that may require specialist intervention (e.g. glomerulonephritis, systemic vasculitis), be discussed with a nephrologist within 48 hours of detection. Patients with post-renal AKI may require discussion with a urologist.
In AKI, a regular assessment of the patients’ fluid status should be completed including monitoring their urine output, which may require a … … and daily ….
Regular assessment of the patients’ fluid status should be completed including monitoring their urine output, which may require a urinary catheter and daily weights.
Regular assessment and monitoring of AKI:
A baseline … should be recorded and serial … taken daily, increased to twice daily in more severe cases.
A baseline creatinine should be recorded and serial U&Es taken daily, increased to twice daily in more severe cases.
What drugs should be stopped in an AKI?
Nephrotoxic drugs should be stopped (e.g. ACEi, NSAIDs, spironolactone) and regular prescriptions should be altered to reflect the change in creatinine clearance.
Volume dysregulation in AKI - what do we do in a hypovolaemic patient?
If patients are hypovolaemic then intravenous fluids should be prescribed. The amount and type of fluids will depend on the clinical status of the patient.
Volume dysregulation in AKI - what do we do in hypervolaemic patient?
If the patient is hypervolaemic they may require fluid restriction +/- the use of diuretics. Diuretics (e.g. furosemide) should be used carefully in renal impairment as they can be nephrotoxic.
Severe hyperkalaemia, variably defined as >…. mmol/L, is a medical emergency.
Severe hyperkalaemia, variably defined as >6.5 or 7 mmol/L, is a medical emergency.
The management of hyperkalaemia is critical to avoid potential life-threatening arrhythmias. It involves:
Protection of the myocardium: 10ml of 10% calcium gluconate.
Reduce extracellular potassium: aim is to drive potassium into the intracellular compartment. Insulin (e.g 10 units ACTRAPID in 100ml 20% dextrose) and beta agonists (e.g. 2.5mg nebulised salbutamol) are given.
Additional: stop or adjust potassium-sparing or potassium-containing medications. Resins can reduce potassium absorption but these take hours/days to have effect.
Other electrolyte problems (apart from hyperkalaemia) in AKI include hypo… and hyper…
Other electrolyte problems (apart from hyperkalaemia) in AKI include hypocalcaemia and hyperphosphataemia.
The handling of acid-base is impaired in the setting of AKI due to a … in the GFR. This can results in a metabolic acidosis. Depending on the severity of acidosis and associated clinical state, choices for management involve the use of sodium bicarbonate or dialysis.
The handling of acid-base is impaired in the setting of AKI due to a reduction in the GFR. This can results in a metabolic acidosis. Depending on the severity of acidosis and associated clinical state, choices for management involve the use of sodium bicarbonate or dialysis.
The handling of acid-base is impaired in the setting of AKI due to a reduction in the GFR. This can results in a … …. Depending on the severity of … and associated clinical state, choices for management involve the use of sodium bicarbonate or dialysis.
The handling of acid-base is impaired in the setting of AKI due to a reduction in the GFR. This can results in a metabolic acidosis. Depending on the severity of acidosis and associated clinical state, choices for management involve the use of sodium bicarbonate or dialysis.
What is most common acid-base disturbance associated with acute kidney injury?
Metabolic acidosis is the most common acid-base disturbance associated with acute kidney injury, developing as the result of impaired excretion of the daily load of metabolic fixed acid.
Complications of AKI (4)
The major complications that can occur in association with AKI include hyperkalaemia, fluid overload, metabolic acidosis and uraemia.
The development of uraemic complications in AKI (e.g. encephalopathy, pericarditis), hyperkalaemia, fluid overload or metabolic acidosis that are refractory to medical therapy warrant urgent ….
The development of uraemic complications (e.g. encephalopathy, pericarditis), hyperkalaemia, fluid overload or metabolic acidosis that are refractory to medical therapy warrant urgent dialysis.
RENAL DRS 26 - A useful mnemonic for assessment and management of any patient presenting with an acute kidney injury.
Pre-renal causes of AKI
Reduced circulating volume (e.g. hypovolaemia).
Reduced cardiac output (e.g. cardiac failure).
Systemic vasodilatation (e.g. septic shock).
Drugs altering glomerular haemodynamics (e.g. ACE-i / NSAIDs).
By what mechanism do NSAIDs adversely affect renal function?
Potentiation of anti-diuretic hormone (ADH)
Prevents prostaglandin mediated vasodilation of the afferent arteriole and decreased renal perfusion pressure
Prevents prostaglandin mediated vasodilation of the efferent arteriole and decreased renal perfusion pressure
Increased expression of Na+/K+/2Cl- co-transporter channels in the ascending loop of Henle
Direct glomerular injury
Prevents prostaglandin mediated vasodilation of the afferent arteriole and decreased renal perfusion pressure
NSAIDs result in unopposed constriction of the afferent arteriole and decreased renal perfusion pressure through the inhibition of … synthesis.
NSAIDs result in unopposed constriction of the afferent arteriole and decreased renal perfusion pressure through the inhibition of prostaglandin synthesis.
Non-steroidal anti-inflammatory drugs, NSAIDs (e.g. ibuprofen, naproxen) adversely affect renal blood flow and have direct effects on the renal tubules, promoting natriuresis. NSAIDs impair prostaglandin synthesis by inhibition of …-… and …-…
Non-steroidal anti-inflammatory drugs, NSAIDs (e.g. ibuprofen, naproxen) adversely affect renal blood flow and have direct effects on the renal tubules, promoting natriuresis. NSAIDs impair prostaglandin synthesis by inhibition of COX-1 and COX-2.
Importantly, renal prostaglandins cause … in the kidneys. Under normal conditions, they are not important in the regulation of renal perfusion. However, in renal hypoperfusion, the synthesis of prostaglandins is increased to help prevent ischaemia secondary to ….
Importantly, renal prostaglandins cause vasodilatation in the kidneys. Under normal conditions, they are not important in the regulation of renal perfusion. However, in renal hypoperfusion, the synthesis of prostaglandins is increased to help prevent ischaemia secondary to vasoconstriction.
Prostaglandins help maintain renal blood flow through a variety of mechanisms: (3)
Results in vasodilation of the afferent arteriole and increased renal perfusion pressure.
Decreases expression of Na+/K+/2Cl- co-transporter channels in the ascending loop of Henle, leading to salt and water retention.
Impairs antagonism of anti-diuretic hormone (ADH).
Results in vasodilation of the afferent arteriole and increased renal perfusion pressure.
Decreases expression of Na+/K+/2Cl- co-transporter channels in the ascending loop of Henle, leading to salt and water retention.
Impairs antagonism of anti-diuretic hormone (ADH).
How are these mechanisms maintained?
Prostaglandins help maintain renal blood flow through a variety of mechanisms
Oliguria is defined as which of the following? Urine output < 70 mls / hr Urine output < 35 mls / hr Urine output < 1.0 mls / kg / hr Urine output < 0.5 mls / kg / hr Urine output < 0.1 mls / kg / hr
Oliguria is defined as urine output < 0.5 mls / kg / hr.
In a typical 70 kg patient, this means a urinary output < … mls / hour is considered oliguria. Due to interpatient variability, it is more appropriate to diagnose oliguria based on mls / kg / hr rather than exact amounts.
In a typical 70 kg patient, this means a urinary output < 35 mls / hour is considered oliguria. Due to interpatient variability, it is more appropriate to diagnose oliguria based on mls / kg / hr rather than exact amounts.
Based on the KDIGO classification, if a urinary output < 0.5 mls / kg / hr continues for > … hours, it is consistent with a diagnosis of acute kidney injury.
Based on the KDIGO classification, if a urinary output < 0.5 mls / kg / hr continues for > 6 hours, it is consistent with a diagnosis of acute kidney injury.
Based on the KDIGO classification, if a urinary output < ….mls / kg / hr continues for > 6 hours, it is consistent with a diagnosis of acute kidney injury.
Based on the KDIGO classification, if a urinary output < 0.5 mls / kg / hr continues for > 6 hours, it is consistent with a diagnosis of acute kidney injury.
According to the KDIGO criteria, which of the following does not meet the requirements for an acute kidney injury (AKI)?
An increase in serum creatinine by ≥ 26.5 micromol / L within 48 hours
An increase in serum creatinine by ≥ 1.5 times within 7 days
Urine output < 1.0 ml / kg / hour for 12 hours
Urine output < 0.5 ml / kg / hour for 6 hours
Patient requiring renal replacement therapy (RRT)
Urine output < 1.0 ml / kg / hour for 12 hours (correct answer)
You see an 83-year-old male who is 5 days post-surgery for a traumatic neck of femur fracture. His catheter was removed yesterday as he was mobilising. He has since developed a painfully distended abdomen and the nurse reports that he has not passed urine.
What is the most appropriate next course of action? A Clinical examination B Bladder scan C Abdominal X-ray D Emergency dialysis E Urinary catheter
A - clinical exam
This patient has developed acute urinary retention post a failed ‘trial without catheter’ (TWOC).
A patient complaining of acute abdominal pain requires a clinical assessment with an ABC approach if appropriate followed by a history and clinical examination.
In this scenario, it is likely the patient has developed urinary retention and will need placement of a urinary catheter. A bladder scan (US) is a useful bedside test that allows you to estimate the volume of urine in the bladder.
Approximately, what is the percentage reduction in glomerular filtration rate (GFR) required for creatinine to begin to rise?
50%
A greater than 50% reduction in GFR is needed before creatinine begins to rise.
A greater than …% reduction in GFR is needed before creatinine begins to rise.
A greater than 50% reduction in GFR is needed before creatinine begins to rise.
An 84-year-old woman is being treated for a simple urinary tract infection (UTI). Her latest blood results come back from the lab.
Sodium: 143 (135-145)
Potassium: 6.8 (3.3-5.5)
Creatinine: 210 (< 90)
Urea: 10.6 (2.5-8.0)
You perform an ECG which is shown below.
This patient should be placed on cardiac monitoring and given IV calcium gluconate over a period of 5-10 minutes.
This patient is suffering from hyperkalaemia, most likely secondary to an acute kidney injury from her UTI. Despite there being no changes on her ECG, a K+ > 6.5 warrants urgent attention. Calcium gluconate protects the myocardium from the deleterious effects of hyperkalaemia.
ECG changes, if present, include tall tented T-waves, a wide QRS complex and eventually a sinusoidal pattern and asystole.
A dextrose and insulin infusion +/- nebulised salbutamol constitutes the next stage in management. Refractory hyperkalaemia is an indication for emergency dialysis, but it is not indicated at this point.
A 25-year-old male presents to A&E with general malaise and bilateral thigh pain. This has been ongoing for 5 days after participating in a spinning class for the first time. He has been taking naproxen for the last 3 days without relief. He also complains of passing dark brown urine. Bloods demonstrate a raised creatinine kinase (CK) level of 14,980 U/L (26-192 U/L) with an eGFR of 20.
What is the most likely diagnosis?
A Exercise-induced nephropathy B Renal artery stenosis C Exercise-induced myalgia D Naproxen-induced AKI E Rhabdomyolysis
This patient is likely suffering from an AKI secondary to exercise-induced rhabdomyolysis.
Rhabdomyolysis refers to the breakdown of skeletal muscle. Muscular pain or discomfort is common, alongside dark urine due to myoglobinuria. Diagnosis is confirmed by an elevated serum creatine kinase (CK) level. Fluid hydration is the mainstay of therapy.
Which of the following is not considered an indication for emergency dialysis?
A Refractory pulmonary oedema B Refractory hyperkalaemia C Severe metabolic acidosis D Anuria > 12 hours E Severe uraemia
Anuria is not an indication for emergency dialysis.
The indications for emergency dialysis include:
- Refractory pulmonary oedema
- Refractory hyperkalaemia
- Severe metabolic acidosis
- Severe uraemia +/- complications
The indications for emergency dialysis include:
- Refractory … …
- Refractory ….
- Severe …. ….
- Severe u… +/- complications
The indications for emergency dialysis include:
- Refractory pulmonary oedema
- Refractory hyperkalaemia
- Severe metabolic acidosis
- Severe uraemia +/- complications
You review an 89-year-old female with a urinary tract infection complicated by an acute kidney injury (AKI). She is currently being treated with IV fluids and IV co-amoxiclav on the high-dependency unit (HDU). Her regular medications include paracetamol, sertraline, bisoprolol, cholecalciferol, GTN spray, lisinopril and ibuprofen.
Which combination of medications are particularly deleterious in AKI?
A Bisoprolol and GTN spray B Sertraline and cholecalciferol C Ibuprofen and lisinopril D Ibuprofen and paracetamol E Lisinopril and bisoprolol
ACE-Inhibitors (e.g. lisinopril) and NSAIDs (e.g. ibuprofen) are a particularly nephrotoxic combination in the setting of AKI.
Both agents adversely affect the bodies ability to autoregulate renal blood flow. Other potentially deleterious agents include diuretics and angiotensin-receptor blockers (ARBs). Importantly many medications require adjustment in the advent of impaired renal function and severe illness.
….-Inhibitors (e.g. lisinopril) and … (e.g. ibuprofen) are a particularly nephrotoxic combination in the setting of AKI.
ACE-Inhibitors (e.g. lisinopril) and NSAIDs (e.g. ibuprofen) are a particularly nephrotoxic combination in the setting of AKI.
AKI can occur when there is a sudden … in glomerular filtration rate (GFR).
AKI can occur when there is a sudden decrease in glomerular filtration rate (GFR).
GFR is maintained by sufficient blood flow into the kidneys, functioning nephrons and a clear pathway for outflow of urine from the kidney. If there are alterations to this system, an … can occur.
At the glomerular level, GFR is dependent on a … … between the incoming blood at the afferent capillaries and the pressure in Bowman’s space.
GFR is maintained by sufficient blood flow into the kidneys, functioning nephrons and a clear pathway for outflow of urine from the kidney. If there are alterations to this system, an AKI can occur.
At the glomerular level, GFR is dependent on a pressure gradient between the incoming blood at the afferent capillaries and the pressure in Bowman’s space.
Pre-renal AKI occurs when there is … perfusion to the kidney. This can occur in hypovolaemic, euvolaemic or hypervolaemic states.
Pre-renal AKI occurs when there is reduced perfusion to the kidney. This can occur in hypovolaemic, euvolaemic or hypervolaemic states.
Causes of pre-renal AKI include:
Absolute hypovolaemia: haemorrhage, over-diuresis, vomiting and diarrhoea
Low effective arterial blood volume (EABV): heart failure, cirrhosis, sepsis, third spacing of fluid
Anatomical: renal artery stenosis
Drug-induced: NSAIDs, ACE inhibitors, diuretics
Intra-renal AKI occurs when there is a structural or functional change at the level of the nephron. This can occur independently or as a transformation of a pre-renal AKI.
Causes of intra-renal AKI include:2
occurs due to ischaemic or toxic injury to the cells of the proximal convoluted tubules
Acute interstitial nephritis (AIN): most often eosinophilic nephritis that can be drug-induced (e.g. NSAIDs, penicillin), infection-induced (e.g. tuberculosis, legionella) or immune-mediated (e.g. sarcoidosis, SLE or IgG-related disease (IgG4-RD))
Glomerular disease: includes nephrotic and nephritic syndromes which may be primary renal disease (e.g. anti-glomerular basement membrane (anti-GBM), or part of systemic disease with immune complex deposition (e.g. IgA vasculitis) or without immune complex deposition (e.g. granulomatosis with polyangiitis (GPA))
Intra-tubular obstruction: multiple myeloma with paraprotein, pigment (e.g. rhabdomyolysis)
Other: scleroderma renal crisis, malignant hypertension
Post-renal AKI is associated with an obstructive pathology leading to congestion of the kidneys.
Causes of post-renal AKI can be divided anatomically:
Ureters: nephrolithiasis, retroperitoneal fibrosis
Bladder: bladder cancer
Prostate: benign prostatic hyperplasia (BPH), prostate cancer
Urethra: urethral stricture
External: retroperitoneal mass, ovarian tumours
Unless there is a … kidney, a unilateral obstruction may not cause post-renal AKI as the unaffected kidney may be able to compensate for the reduced function of the affected kidney. This puts patients with a … kidney at increased risk of AKI.3
Unless there is a solitary kidney, a unilateral obstruction may not cause post-renal AKI as the unaffected kidney may be able to compensate for the reduced function of the affected kidney. This puts patients with a solitary kidney at increased risk of AKI.3
Risk factors for acute kidney injury include:
Chronic kidney disease (adults with an eGFR < 60 ml/min/1.73 m2 are at high risk)
Heart failure
Liver disease
Diabetes
History of acute kidney injury
Oliguria (< 0.5 ml/kg/hour)
Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
Hypovolaemia
Use of drugs that can cause or exacerbate kidney injury (Table 1)
Use of iodine-based contrast media within the past week
Symptoms or history of urological obstruction, or conditions that may lead to obstruction
Sepsis
Deteriorating early warning scores
Age 65 years or over
ACE inhibitors
Angiotensin receptor blockers (ARBs)
Cyclosporin
NSAIDs
Tacrolimus
What nephrotoxic effect do these medications have?
GFR alteration
Affect the vascular tone of the afferent and efferent arterioles, altering interglomerular blood flow
Aminoglycosides
Amphotericin B
Cisplatin
What nephrotoxic effect do these medications have?
Tubular cell toxicity
Direct toxicity to the epithelial cells of the proximal convoluted tubules
NSAIDs
Rifampin
What nephrotoxic effects do these medications have?
Interstitial nephritis
Inflammatory reaction within the interstitium of the kidney
Acyclovir
Ampicillin
What nephrotoxic effects do these medications have?
Crystal nephropathy
Can result in precipitates of insoluble crystals
NSAIDs can be implicated in multiple causes of renal impairment so their use should be restricted in patients at risk of AKI:
Pre-renal: NSAIDs block … mediated vasodilation of the afferent arteriole, which limits the kidney’s ability to regulate local blood flow
Intra-renal: NSAIDs can cause … … … (AIN)
Post-renal: long term NSAID use can cause renal papillary … where the medullary papilla sloughs off, causing obstruction to urine flow
Pre-renal: NSAIDs block prostaglandin mediated vasodilation of the afferent arteriole, which limits the kidney’s ability to regulate local blood flow
Intra-renal: NSAIDs can cause acute interstitial nephritis (AIN)
Post-renal: long term NSAID use can cause renal papillary necrosis where the medullary papilla sloughs off, causing obstruction to urine flow
Important areas of the history for suspected AKI to cover include:
Reason for admission to hospital (e.g. sepsis, burns)
Underlying medical conditions (e.g. heart failure, cirrhosis, SLE)
Use of medications known to be nephrotoxic (e.g. NSAIDs, diuretics, penicillin, cisplatin)
Recent imaging investigations using iodinated contrast, particularly if delivered arterially (e.g. CT with contrast, angiogram)
Lower urinary tract symptoms (e.g. frequency, urgency, incomplete emptying)
Known to have a solitary kidney
Typical clinical findings of AKI may include:
Oliguria or anuria
Signs of hypovolaemia: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
Signs of uraemia: ecchymosis due to platelet dysfunction, uraemic encephalopathy (e.g. asterixis, confusion, seizures)
Signs of post-renal obstruction: palpable or tender distended bladder
AKI is detected biochemically by checking …
AKI is detected biochemically by checking urea and electrolytes. Subsequent investigations are guided by history and examination, but an algorithmic approach will yield baseline information that can guide tailored/specialised testing.
Many hospitals are using an ABCDE checklist to prompt AKI management:
A: Address drugs B: Boost blood pressure C: Calculate fluid balance D: Dip urine E: Exclude obstruction
Renal replacement therapy (RRT) is indicated in more severe cases of AKI:8
Metabolic acidosis pH < 7.15 or worsening acidaemia
Refractory electrolyte abnormalities (hyperkalaemia >6.5mmol)
Presence of dialysable toxins (toxic alcohols, aspirin, lithium)
Refractory fluid overload (diuretic resistant fluid overload in setting of AKI)
End-organ uraemic complications (e.g. pericarditis, encephalopathy, uraemic bleeding)
Indications for RRT can be remembered by the mnemonic AEIOU:
Acidosis Electrolyte abnormalities Ingested toxins Fluid Overload Uraemia
Additionally, note that oligo/anuria will often accelerate the need for RRT.
The … criteria are the most commonly used criteria for diagnosing AKI, with an increase in serum creatinine and reduced urine production being the key diagnostic features.
The KDIGO criteria are the most commonly used criteria for diagnosing AKI, with an increase in serum creatinine and reduced urine production being the key diagnostic features.
Recognition and management of AKI are essential to prevent permanent damage or progression to …
Recognition and management of AKI are essential to prevent permanent damage or progression to chronic kidney disease (CKD).
