Acute kidney injury (AKI), previously called acute renal failure, is a sudden decrease in kidney function that develops within seven days, as shown by an increase in serum creatinine or a decrease in urine output, or both.
Causes of AKI are classified as either prerenal (due to decreased blood flow to the kidney), intrinsic renal (due to damage to the kidney itself), or postrenal (due to blockage of urine flow). Prerenal causes of AKI include sepsis, dehydration, excessive blood loss, cardiogenic shock, heart failure, cirrhosis, and certain medications such as ACE inhibitors or NSAIDs. Intrinsic renal causes of AKI include glomerulonephritis, lupus nephritis, acute tubular necrosis, certain antibiotics, and chemotherapeutic agents. Postrenal causes of AKI include kidney stones, bladder cancer, neurogenic bladder, enlargement of the prostate, narrowing of the urethra, and certain medications such as anticholinergics.
The diagnosis of AKI is made based on a person's signs and symptoms, along with laboratory tests measuring serum creatinine and urine output. Other tests include urine microscopy and urine electrolytes. Renal ultrasound can be obtained when a postrenal cause is suspected. A kidney biopsy may be obtained when intrinsic renal AKI is suspected, and the cause is unclear.
AKI is seen in 10–15% of people admitted to the hospital and in more than 50% of people admitted to the intensive care unit. AKI may lead to several complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, effects on other organ systems, and death. People who have experienced AKI are at increased risk of developing chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.
Signs and symptoms The underlying cause often dominates the clinical presentation. The symptoms of acute kidney injury result from various disturbances in kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea, and vomiting. Marked increases in the potassium level can lead to abnormal heart rhythms, which can be severe and life-threatening. Fluid balance is frequently affected, though blood pressure can be high, low, or normal.
Pain in the flanks may be encountered in some conditions (such as clotting of the kidneys' blood vessels or inflammation of the kidney). This is the result of stretching of the fibrous tissue capsule surrounding the kidney. If the kidney injury is the result of dehydration, thirst or evidence of fluid depletion may be seen on physical examination. Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a rash in interstitial nephritis (or vasculitis) and a palpable bladder in obstructive nephropathy.
Causes Prerenal Prerenal causes of AKI ("prerenal azotemia") are those that decrease effective blood flow to the kidney and cause a decrease in the glomerular filtration rate (GFR). Both kidneys need to be affected, as one kidney is still more than adequate for normal kidney function. Notable causes of prerenal AKI include low blood volume (e.g., dehydration), low blood pressure, heart failure (leading to cardiorenal syndrome), hepatorenal syndrome in the context of liver cirrhosis, and local changes to the blood vessels supplying the kidney (e.g. NSAID-induced vasoconstriction of afferent arteriole). The latter includes renal artery stenosis, or the narrowing of the renal artery which supplies the kidney with blood, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.
Intrinsic or intrarenal Intrinsic AKI refers to disease processes that directly damage the kidney itself. It can be due to one or more of the kidney's structures, including the glomeruli, kidney tubules, or the interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis, and acute interstitial nephritis, respectively. Other causes of intrinsic AKI are rhabdomyolysis and tumor lysis syndrome. Certain medication classes such as antibiotics (e.g. amoxicillin/clavulanic acid) and calcineurin inhibitors (e.g., tacrolimus) can also directly damage the tubular cells of the kidney and result in a form of intrinsic AKI.
Postrenal Postrenal AKI refers to acute kidney injury caused by disease states downstream of the kidney and most often occurs as a consequence of urinary tract obstruction. This may be related to:
Benign prostatic hyperplasia Kidney stones Obstructed urinary catheter Bladder stones Cancer of the bladder, ureters, or prostate Damage to the nerves controlling urine flow and bladder function
Diagnosis Definition Introduced by the KDIGO in 2012, specific criteria exist for the diagnosis of AKI.
AKI can be diagnosed if any one of the following is present: Increase in SCr by ≥0.3 mg/dl (≥26.5 μmol/L) within 48 hours Increase in SCr to ≥1.5 times baseline, which has occurred within the prior 7 days Urine volume < 0.5 mL/kg/h for 6 hours
Staging The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative group, aid in assessing the severity of a person's acute kidney injury. The acronym RIFLE is used to define the spectrum of progressive kidney injury seen in AKI:
Risk: A 1.5-fold increase in serum creatinine, or a glomerular filtration rate (GFR) decrease by 25%, or urine output <0.5 mL/kg per hour for six hours. Injury: Two-fold increase in the serum creatinine, or GFR decrease by 50%, or urine output <0.5 mL/kg per hour for 12 hours Failure: Three-fold increase in the serum creatinine, or GFR decrease by 75%, or urine output of <0.3 mL/kg per hour for 24 hours, or no urine output (anuria) for 12 hours Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than 4 weeks End-stage kidney disease: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than 3 months
Evaluation A measurable decrease in urine output may signal deterioration of kidney function. Often, it is diagnosed based on blood tests for substances normally eliminated by the kidneys - urea and creatinine. Additionally, the ratio of BUN to creatinine is used to evaluate kidney injury. Both tests have their disadvantages. For instance, about 24 hours are needed for the creatinine level to rise, even if both kidneys have ceased to function. Several alternative markers have been proposed (such as NGAL, HAVCR1, IL18, and cystatin C), but none is sufficiently established as of 2018 to replace creatinine as a marker of kidney function.
These may include urine sediment analysis, kidney ultrasound, and/or kidney biopsy. Indications for kidney biopsy in the setting of AKI include the following: Unexplained AKI in a patient with two nonobstructed, normally sized kidneys AKI in the presence of the nephritic syndrome Systemic disease associated with AKI Kidney transplant dysfunction
In medical imaging, acute changes in the kidney are often examined with renal ultrasonography (US) as the first-line modality, where CT scan and magnetic resonance imaging (MRI) are used for follow-up examinations and when US fails to demonstrate abnormalities. In the evaluation of the acute changes in the kidney, the echogenicity of the renal structures, delineation of the kidney, renal vascularity, kidney size, and focal abnormalities are observed.Content initially copied from: (CC-BY 4.0) CT is preferred in renal traumas, but US is used for follow-up, especially in the patients suspected for the formation of urinomas. A CT scan of the abdomen can also demonstrate bladder distension or hydronephrosis.
Classification Acute kidney injury is diagnosed based on clinical history and laboratory data. A diagnosis is made when a rapid reduction in kidney function occurs, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria (less than 0.5 mL/kg/h for at least 6 hours).
+ Classic laboratory findings in AKI Type UOsm UNa FeNa BUN/Cr Prerenal >500 <10 <1% >20 Intrinsic <350 >20 >2% <10-15 Postrenal <350 >40 >4% >20 AKI can be caused by systemic disease, e.g., autoimmune conditions, such as lupus nephritis), as well as other conditions, such as crush injury, contrast agents, some antibiotics, and more. AKI is often due to multiple factors.
AKI occurs in up to 30% of patients following cardiac surgery. Mortality increases by 60-80% in postcardiopulmonary bypass patients who go on to require renal replacement therapy. Preoperative creatinine levels greater than 1.2 mg/dL, combined valve and bypass procedures, emergency surgery, and preoperative intra-aortic balloon pump are risk factors most strongly correlated with postcardiopulmonary bypass acute kidney injury. Other well-known minor risk factors include female gender, congestive heart failure, chronic obstructive pulmonary disease, insulin-requiring diabetes, and depressed left ventricular ejection fraction. Volatile anesthetic agents have been shown to increase renal sympathetic nerve activity, which causes retention of salts and water, diminished renal blood flow, and an increase in serum renin levels, but not in antidiuretic hormone .
Postoperative acute kidney injury is defined as an AKI based on the KDIGO criteria occurring within 7 days of an operative intervention.
Pediatric AKI is defined using the KDIGO definition and the modified neonatal KDIGO criteria for neonates.
Treatment The management of AKI hinges on identifying the underlying cause and treating it. The main objectives of initial management are to prevent cardiovascular collapse and death and to call for specialist advice from a nephrologist. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen or naproxen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.
Monitoring of kidney function, using serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieve possible bladder outlet obstruction, such as with an enlarged prostate.
Prerenal In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improving kidney function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.
If low blood pressure persists despite providing a person with adequate amounts of intravenous fluid, medications that increase blood pressure (vasopressors) such as norepinephrine, and in certain circumstances medications that improve the heart's ability to pump (known as inotropes), such as dobutamine, may be given to improve blood flow to the kidney. While a useful vasopressor, no evidence suggests that dopamine is of any specific benefit and may in fact be harmful.
Intrinsic The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclophosphamide, and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol.
The use of diuretics such as furosemide is widespread and sometimes convenient in improving fluid overload. It is not associated with higher mortality (risk of death), nor with any reduced mortality or length of intensive care unit or hospital stay.
Postrenal