Commonly associated with sepsis, cardiovascular collapse, congestive heart failure, major surgery, nephrotoxins (such as antibiotics, intravenous contrast, or other drugs), or urinary outflow obstruction.
May present with flank pain, haematuria, hypertension or hypotension, oedema, lethargy, uraemia, or decreased urine output; however, often asymptomatic and only diagnosed by laboratory tests.
An acute increase in serum creatinine is essential for diagnosis. Fluid overload, hyperkalaemia, hyperphosphataemia, metabolic acidosis, and elevated urea nitrogen are common.
The mainstay of treatment is supportive care, with management of the underlying illness; correction of acid/base, electrolyte, and volume complications; removal or minimisation of nephrotoxins; and relief of any associated obstruction being key.
Renal replacement therapy with dialysis may be required and is usually well tolerated.
Failure to treat may be associated with clinical deterioration and death. Outcome is dependent upon the severity of the kidney injury and the underlying disease.
Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in renal 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 renal impairment to severe renal failure. A standardised definition is important to facilitate clinical care and research. AKI may be due to various insults such as impaired renal perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic renal 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
- presence of risk factors
- reduced urine production
- paroxysmal nocturnal dyspnoea
- pulmonary oedema
- orthostatic hypotension
- peripheral oedema
- muscle tenderness
- limb ischaemia
- prostatic obstructive symptoms
- altered mental status
- signs of uraemia
- advanced age
- underlying renal disease
- malignant hypertension
- diabetes mellitus
- myeloproliferative disorders, such as multiple myeloma
- connective tissue disease
- sodium-retaining states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome)
- exposure to nephrotoxins (e.g., aminoglycosides, vancomycin + piperacillin-tazobactam, cancer therapies, non-steroidal anti-inflammatory drugs, or ACE inhibitors)
- drug overdose
- cardiac arrest
- recent vascular intervention
- excessive fluid loss
- drug abuse
- alcohol abuse
- excessive exercise
- recent blood transfusion
- genetic susceptibility
- use of renin-angiotensin system inhibitors
- proton pump inhibitors
- herbal therapy
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.
Dr Richard A. Lafayette would like to gratefully acknowledge Dr Sandra Sabatini, Dr Neil Kurtzman, and Dr Corey D. Ball, the previous contributors to this topic. SS, NK, and CDB declare that they have no competing interests.
Professor of Medicine
Section of Nephrology
Department of Medicine
Baylor College of Medicine
GE declares that he has no competing interests.
North Staffs Royal Infirmary
University Hospital of North Staffordshire
DdT declares that he has no competing interests.
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