Commonly associated with sepsis, hypovolaemia, and/or hypotension (pre-kidney AKI and intrinsic AKI); nephrotoxins such as aminoglycoside antibiotics (e.g., gentamicin), intravenous iodinated contrast, ethylene glycol, or rarer forms of AKI such as vasculitis or interstitial nephritis (intrinsic AKI); or urinary outflow obstruction (post-kidney AKI).
Usually occurs in patients with intercurrent illness, without symptoms or signs specific to the kidneys, and is only diagnosed when kidney function tests are performed. Patients may present in many different ways (e.g., with sepsis, hypotension, decreased urine output, lower urinary tract symptoms, or oedema).
Suspect AKI when there is an acute rise in serum creatinine and/or a fall in urine output. More severe AKI can be complicated by hyperkalaemia and acidaemia along with uraemic encephalopathy or pericarditis. Pulmonary oedema can also occur in patients with AKI secondary to obstructive uropathy or renal artery stenosis (flash pulmonary oedema) but is usually iatrogenic due to over-enthusiastic fluid resuscitation.
The mainstay of management is supportive care, with treatment of the underlying cause. Give particular attention to the prompt treatment of sepsis, optimisation of volume status, correction of acidaemia or electrolyte complications, avoidance of nephrotoxins, and relief of any obstruction.
Renal replacement therapy may be needed for severe AKI with complications that do not respond to medical management.
Prompt recognition and treatment is important; AKI occurs in 10% to 20% of emergency admissions and has an inpatient mortality >20% (>35% for stage 3 AKI).
Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output. The change in terminology emphasises that kidney injury presents as a disease spectrum from mild kidney injury to severe kidney failure. A standardised definition is important to facilitate clinical care and research. AKI may be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic kidney disease. The resulting effects include impaired clearance and regulation of metabolic homeostasis, altered acid/base and electrolyte regulation, and impaired volume regulation.
History and exam
Key diagnostic factors
- risk factors
- kidney insults
- reduced urine production
- lower urinary tract symptoms
- symptoms of volume overload/pulmonary oedema
- fever, rash, and/or arthralgia
- haematuria (visible or non-visible)
- palpable bladder and/or enlarged prostate and/or abdominal distension
Other diagnostic factors
- dizziness and orthostatic symptoms
- altered mental status
- pericardial/pleural rub
- muscle tenderness
- abdominal bruit
- advanced age
- underlying kidney disease
- diabetes mellitus
- iodinated contrast
- exposure to nephrotoxins (e.g., aminoglycosides, vancomycin + piperacillin-tazobactam, cancer therapies, non-steroidal anti-inflammatory drugs, or ACE inhibitors)
- excessive fluid loss
- recent vascular intervention
- cardiac arrest
- malignant hypertension
- myeloproliferative disorders, such as multiple myeloma
- connective tissue disease
- sodium-retaining states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome)
- drug overdose
- drug abuse
- alcohol abuse
- excessive exercise
- recent blood transfusion
- genetic susceptibility
- use of renin-angiotensin system inhibitors
- proton pump inhibitors
- herbal therapy
1st investigations to order
- basic metabolic profile (including urea and creatinine and liver function tests)
- serum potassium
- C-reactive protein
- blood culture
- urine culture
- urine output monitoring
- fluid challenge
- venous blood gases
Investigations to consider
- renal tract ultrasound
- abdominal CT or MRI scan
- nuclear renal flow scan
- urine osmolality
- urine sodium concentration
- fractional excretion of sodium/urea
- urinary eosinophil count
- serum creatine kinase
- ANA (anti-nuclear antibodies)
- complement (C3, C4, CH50)
- anti-glomerular basement membrane antibody
- anti-neutrophil cytoplasmic antibodies (ANCA)
- acute hepatitis profile
- HIV serology
- anti-streptolysin-O antibody
- serum/urine electrophoresis
- kidney biopsy
- novel serum and urinary biomarkers
Andrew Lewington, BSc (Hons), MBBS, MEd, MD, FRCP
Consultant Renal Physician
Honorary Associate Professor
Leeds Teaching Hospitals NHS Trust
AL is Associate Clinical Director of NIHR Leeds In-Vitro Diagnostics Co-operative, Co-Chair of UK Kidney Research Consortium Renal Clinical Study Group, Member of Kidney Research UK Research Grant Committee, Committee Member of NICE Kidney Injury Clinical Guideline Update 2018-20, Committee Member of NICE Diagnostic Assessment for Point of Care Creatinine Testing 2018-19. AL attended the Acute Dialysis Quality Initiative Meeting in San Diego 2018 (accommodation expenses); AL was a speaker at the AKI & CRRT Conference in San Diego 2019 (travel and accommodation expenses), the AKI Conference in Coventry 2019 (travel expenses), and the NIHR AKI and Sepsis Meeting in Leeds 2019 (no expenses).
BMJ Best Practice would like to gratefully acknowledge the previous expert contributor, whose work has been retained in parts of the content:
Richard A. Lafayette MD
Professor of Medicine
Stanford University Medical Center
RAL works as a consultant and researcher for Relypsa, Inc. Although unrelated to this topic area, RAL also works as a consultant for Fibrogen, Inc.; Mallinckrodt, Inc.; and Omeros, Inc.; and as a researcher for Genentech, Inc.; Mallinckrodt, Inc.; GlaxoSmithKline, Inc.; Rigel, Inc.; Aurinia, Inc.; and the NIH.
Newcastle upon Tyne Hospitals NHS Trust
Newcastle Hospitals Haemodialysis Service
Honorary Clinical Senior Lecturer
SK was an expert adviser to the National Confidential Enquiry into Patient Outcome and Death (NCEPOD) report into AKI and is lead author of the UK Renal Association clinical practice guideline on AKI.
Section Editor, BMJ Best Practice
Consultant in Paediatric Emergency Medicine
Royal London Hospital
TD declares that she has no competing interests.
Head of Editorial, BMJ Knowledge Centre
JH declares that she has no competing interests.
Comorbidities Editor, BMJ Best Practice
JC declares that she has no competing interests.
Drug Editor, BMJ Best Practice
AM declares that he has no competing interests.
- Chronic kidney disease
- Increased muscle mass
- Drug side effect
- Acute kidney injury (AKI)
- Acute kidney injury: prevention, detection and management
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