Acute kidney injury
Overview
Definition Clinically acute kidney injury (AKI) is characterised by a rapid reduction in
kidney function over hours or days, resulting in a failure to maintain
fluid, electrolyte and acid–base homeostasis. Untreated this can lead to
pulmonary oedema, hyperkalaemia and metabolic acidosis.
AKI is defined when one of the following criteria is met.
● Increase in serum creatinine of ≥26 micromol/L within 48 hours
● Increase in serum creatinine of ≥50% from baseline (the lowest serum creatinine value recorded within 3 months of the event), which is known or presumed to have occurred within the past 7 days
● Fall in urine output to <0 .5="" for="" hour="" kg="" ml="">6 consecutive hours in adults and >8 hours in children Causes Prerenal AKI ( ≈80% of cases) Blood flow to the kidney is reduced which, if left untreated, can lead to ischaemic injury to the kidney (known as acute tubular necrosis or ATN). Common causes of prerenal AKI include:
● hypotension
● dehydration
● sepsis
● significant blood loss, e.g. gastrointestinal bleeding
● cardiac or liver failure
● severe burns Some medications may cause prerenal AKI, such as NSAIDs, ACE inhibitors, ARBs and diuretics (see ‘Further reading’ for more detailed information). Postrenal AKI ( ≈10% of cases) Obstruction to urine outflow from the kidneys occurs. Common causes of postrenal AKI include: ● benign prostatic hypertrophy
● bladder or prostate cancer
● abdominal tumours compressing the urinary tract
● renal stones Some medications may cause postrenal AKI, either through deposition of crystals (e.g. aciclovir or cytotoxic agents) or through blood clots after bleeding (e.g. antiplatelet or anticoagulant therapy) CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
Acute kidney injury
Intrinsic AKI ( ≈10% of cases) A Damage occurs to the kidney itself, often immunological in origin. Common causes of intrinsic AKI include:
● acute interstitial nephritis (AIN) – a hypersensitivity reaction that may often be drug-related, e.g. proton pump inhibitors (PPIs) and pencillins
● myeloma – through deposition of light chains in the kidney
● autoimmune renal disease, including lupus and vasculitis
● rhabdomyolysis – due to the renal toxicity of myoglobin from muscle breakdown Risk factors
● Age >75 years
● Chronic kidney disease
● Cardiac failure
● Peripheral vascular disease
● Liver disease
● Diabetes mellitus
● Nephrotoxic medications, including iodinated radiological contrast media
● Hypovolaemia
● Sepsis
● Surgical procedures Diagnostic tests
● Drug history
● Vital signs (temperature, heart rate, blood pressure)
● Biochemistry (urea and electrolytes)
● Full blood count
Urine dipstick ± microscopy
● Microbiology:
● Urine culture
● Blood culture
● Urine output
● Hydration status, including jugular venous pressure More specific renal investigations are dependent upon the clinical presentation and may include:
● renal immunology
● urinary biochemistry (electrolytes, osmolality)
● renal tract ultrasound within 24 hours (if renal tract obstruction is suspected)
● kidney biopsy Staging The severity of AKI can be classified into three stages. 2 Stage 1: serum creatinine increase of ≥26 micromol/L within 48 hours or increase to ≥1.5–1.9 times baseline; urine output <0 .5="" for="" hour="" kg="" ml="">6 consecutive hours Stage 2: serum creatinine increased to ≥2–2.9 times baseline; urine output <0 .5="" for="" hour="" kg="" ml="">12 hours Stage 3: serum creatinine increased to ≥3 times baseline or increased to ≥354 micromol/L or commenced on renal replacement therapy, irrespective of stage; urine output <0 .3="" for="" hour="" kg="" ml="">24 hours or anuria for 12 hours CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
Acute kidney injury A Treatment goals AKI has a poor prognosis, with the mortality ranging from 10% to 80%. depending upon the patient population studied. Even small increases in serum creatinine are associated with worse patient outcomes, including prolonged hospital stay and increased morbidity and mortality. 3 The goals of AKI treatment are:
● Prevention
● Early identification and assessment
● Appropriate hydration
● Avoid hypotension (systolic blood pressure
<110 mmhg="" nbsp="" p="">● Prompt treatment of infection and other medical conditions
● Stop nephrotoxic drugs
● Adjust doses of renally excreted drugs Treatment options
● Identify and treat potential causes, e.g. underlying sepsis
● Assess volume status and give appropriate intravenous fluid therapy
● Use potassium-containing solutions (e.g. Hartmann’s) cautiously due to the risk of exacerbating hyperkalaemia
● Daily observations, fluid balance, body weight and urine output should be monitored to ensure appropriate fluid therapy and avoid overload
● Medication review:
● Discontinue/avoid all nephrotoxic medications
● Discontinue antihypertensive medications if patient is hypotensive
● Adjust medication doses as necessary
● Administer vasopressors and/or inotropes to increase blood pressure where appropriate
● Manage biochemical complications, e.g. treatment of hyperkalaemia and/or metabolic acidosis
● Give renal replacement therapy Pharmaceutical care and counselling Assess
● Ensure a detailed drug history is taken, including OTC, herbal and recently stopped medications
● Fluid status
● Medication review Essential intervention Many drugs can precipitate AKI and all nephrotoxic medications or medications that may affect renal haemodynamics should be stopped or avoided, e.g. NSAIDs, ACE inhibitors and diuretics. Advise on suitable alternatives where appropriate Essential intervention Review the side-effect profile of all medicines to identify potential causes of ATN or interstitial nephritis, e.g. amphotericin, PPIs Essential intervention Discontinue non-essential medications where appropriate until AKI has resolved, e.g. statins Essential intervention Advise on appropriate drug dosing in AKI. Many pharmacokinetic parameters, including volume of distribution, clearance and protein binding, are altered in AKI. Drug doses need to be adjusted appropriately with the correct assessment of kidney function to reduce toxicity. Examples include dose reduction of renally excreted drugs such as digoxin or gabapentin, or use of alternative agents that are less renally excreted, e.g. switching from morphine to fentanyl CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
Secondary
A intervention Advise on the appropriate use of intravenous fluids (see Fluid balance entry). Provide recommendations around fluid restriction and minimum infusion volumes for drugs used in fluid-overloaded patients Continued monitoring Daily assessment of renal function and review of medication doses as renal function improves. Consider reintroduction of non-causative medications once AKI has resolved Counselling Counsel a patient regarding any medication changes prior to discharge, in particular any causative agents that have now been stopped. Advise patients about any medications to be avoided in future (e.g. OTC NSAIDs). Advise patients receiving medications that put them at risk of AKI to seek medical advice if they become acutely unwell or think they might be dehydrated. Provide accurate discharge information to general practitioners, including changes to medication, medicines to be restarted after discharge (and when this should occur) and any counselling provided/
● Increase in serum creatinine of ≥26 micromol/L within 48 hours
● Increase in serum creatinine of ≥50% from baseline (the lowest serum creatinine value recorded within 3 months of the event), which is known or presumed to have occurred within the past 7 days
● Fall in urine output to <0 .5="" for="" hour="" kg="" ml="">6 consecutive hours in adults and >8 hours in children Causes Prerenal AKI ( ≈80% of cases) Blood flow to the kidney is reduced which, if left untreated, can lead to ischaemic injury to the kidney (known as acute tubular necrosis or ATN). Common causes of prerenal AKI include:
● hypotension
● dehydration
● sepsis
● significant blood loss, e.g. gastrointestinal bleeding
● cardiac or liver failure
● severe burns Some medications may cause prerenal AKI, such as NSAIDs, ACE inhibitors, ARBs and diuretics (see ‘Further reading’ for more detailed information). Postrenal AKI ( ≈10% of cases) Obstruction to urine outflow from the kidneys occurs. Common causes of postrenal AKI include: ● benign prostatic hypertrophy
● bladder or prostate cancer
● abdominal tumours compressing the urinary tract
● renal stones Some medications may cause postrenal AKI, either through deposition of crystals (e.g. aciclovir or cytotoxic agents) or through blood clots after bleeding (e.g. antiplatelet or anticoagulant therapy) CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
Acute kidney injury
Intrinsic AKI ( ≈10% of cases) A Damage occurs to the kidney itself, often immunological in origin. Common causes of intrinsic AKI include:
● acute interstitial nephritis (AIN) – a hypersensitivity reaction that may often be drug-related, e.g. proton pump inhibitors (PPIs) and pencillins
● myeloma – through deposition of light chains in the kidney
● autoimmune renal disease, including lupus and vasculitis
● rhabdomyolysis – due to the renal toxicity of myoglobin from muscle breakdown Risk factors
● Age >75 years
● Chronic kidney disease
● Cardiac failure
● Peripheral vascular disease
● Liver disease
● Diabetes mellitus
● Nephrotoxic medications, including iodinated radiological contrast media
● Hypovolaemia
● Sepsis
● Surgical procedures Diagnostic tests
● Drug history
● Vital signs (temperature, heart rate, blood pressure)
● Biochemistry (urea and electrolytes)
● Full blood count
Urine dipstick ± microscopy
● Microbiology:
● Urine culture
● Blood culture
● Urine output
● Hydration status, including jugular venous pressure More specific renal investigations are dependent upon the clinical presentation and may include:
● renal immunology
● urinary biochemistry (electrolytes, osmolality)
● renal tract ultrasound within 24 hours (if renal tract obstruction is suspected)
● kidney biopsy Staging The severity of AKI can be classified into three stages. 2 Stage 1: serum creatinine increase of ≥26 micromol/L within 48 hours or increase to ≥1.5–1.9 times baseline; urine output <0 .5="" for="" hour="" kg="" ml="">6 consecutive hours Stage 2: serum creatinine increased to ≥2–2.9 times baseline; urine output <0 .5="" for="" hour="" kg="" ml="">12 hours Stage 3: serum creatinine increased to ≥3 times baseline or increased to ≥354 micromol/L or commenced on renal replacement therapy, irrespective of stage; urine output <0 .3="" for="" hour="" kg="" ml="">24 hours or anuria for 12 hours CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
Acute kidney injury A Treatment goals AKI has a poor prognosis, with the mortality ranging from 10% to 80%. depending upon the patient population studied. Even small increases in serum creatinine are associated with worse patient outcomes, including prolonged hospital stay and increased morbidity and mortality. 3 The goals of AKI treatment are:
● Prevention
● Early identification and assessment
● Appropriate hydration
● Avoid hypotension (systolic blood pressure
<110 mmhg="" nbsp="" p="">● Prompt treatment of infection and other medical conditions
● Stop nephrotoxic drugs
● Adjust doses of renally excreted drugs Treatment options
● Identify and treat potential causes, e.g. underlying sepsis
● Assess volume status and give appropriate intravenous fluid therapy
● Use potassium-containing solutions (e.g. Hartmann’s) cautiously due to the risk of exacerbating hyperkalaemia
● Daily observations, fluid balance, body weight and urine output should be monitored to ensure appropriate fluid therapy and avoid overload
● Medication review:
● Discontinue/avoid all nephrotoxic medications
● Discontinue antihypertensive medications if patient is hypotensive
● Adjust medication doses as necessary
● Administer vasopressors and/or inotropes to increase blood pressure where appropriate
● Manage biochemical complications, e.g. treatment of hyperkalaemia and/or metabolic acidosis
● Give renal replacement therapy Pharmaceutical care and counselling Assess
● Ensure a detailed drug history is taken, including OTC, herbal and recently stopped medications
● Fluid status
● Medication review Essential intervention Many drugs can precipitate AKI and all nephrotoxic medications or medications that may affect renal haemodynamics should be stopped or avoided, e.g. NSAIDs, ACE inhibitors and diuretics. Advise on suitable alternatives where appropriate Essential intervention Review the side-effect profile of all medicines to identify potential causes of ATN or interstitial nephritis, e.g. amphotericin, PPIs Essential intervention Discontinue non-essential medications where appropriate until AKI has resolved, e.g. statins Essential intervention Advise on appropriate drug dosing in AKI. Many pharmacokinetic parameters, including volume of distribution, clearance and protein binding, are altered in AKI. Drug doses need to be adjusted appropriately with the correct assessment of kidney function to reduce toxicity. Examples include dose reduction of renally excreted drugs such as digoxin or gabapentin, or use of alternative agents that are less renally excreted, e.g. switching from morphine to fentanyl CPPC c01.tex V2 - 11/18/2015 1:44 P.M.
Secondary
A intervention Advise on the appropriate use of intravenous fluids (see Fluid balance entry). Provide recommendations around fluid restriction and minimum infusion volumes for drugs used in fluid-overloaded patients Continued monitoring Daily assessment of renal function and review of medication doses as renal function improves. Consider reintroduction of non-causative medications once AKI has resolved Counselling Counsel a patient regarding any medication changes prior to discharge, in particular any causative agents that have now been stopped. Advise patients about any medications to be avoided in future (e.g. OTC NSAIDs). Advise patients receiving medications that put them at risk of AKI to seek medical advice if they become acutely unwell or think they might be dehydrated. Provide accurate discharge information to general practitioners, including changes to medication, medicines to be restarted after discharge (and when this should occur) and any counselling provided/
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