Acute kidney injury
|Acute kidney injury|
Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.
|Classification and external resources|
|Patient UK||Acute kidney injury|
Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased renal blood flow (renal ischemia) from any cause (e.g. low blood pressure), exposure to substances harmful to the kidney, an inflammatory process in the kidney, or an obstruction of the urinary tract which impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine.
AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects to other organ systems. Management includes supportive care, such as renal replacement therapy, as well as treatment of the underlying disorder.
- 1 Signs and symptoms
- 2 Causes
- 3 Diagnosis
- 4 Classification
- 5 Treatment
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 See also
- 10 References
Signs and symptoms
The symptoms of acute kidney injury result from the various disturbances of 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 irregularities in the heartbeat, which can be severe and life-threatening. Fluid balance is frequently affected, though hypertension is rare. The construct of renal angina has been developed to assist with detection of early signs of kidney injury.
Pain in the flanks may be encountered in some conditions (such as thrombosis of the renal 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, there may be thirst as well as evidence of fluid depletion 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 and a palpable bladder.
Inability to excrete sufficient fluid from the body can cause accumulation of fluid in the limbs (peripheral edema) and the lungs (pulmonary edema), as well as cardiac tamponade as a result of fluid effusions.
The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.
Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney. These include systemic causes, such as low blood volume, low blood pressure, heart failure, liver cirrhosis and local changes to the blood vessels supplying the kidney. The latter include 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.
Renal ischaemia ultimately results in functional disorder, depression of GFR, or both. These causes stem from the inadequate cardiac output and hypovolemia or vascular diseases causing reduced perfusion of both kidneys. Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function.
Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. A cause of intrinsic acute renal failure is tumor lysis syndrome.
Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted immediately after urinating to measure fluid still in the bladder. 50-100 ml suggests neurogenic bladder dysfunction. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis, however, in case of acute renal failure, the use of IV contrast is contraindicated. On the basic metabolic panel, the ratio of BUN to creatinine may indicate post renal failure.
The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none are currently established enough to replace creatinine as a marker of renal function. Use of the renal angina index, a composite of risk factors and early signs of injury, has been used to detect fulfillment of renal angina in children.
Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include urine sediment analysis, renal ultrasound and/or kidney biopsy. Indications for renal biopsy in the setting of AKI include:
- Unexplained AKI
- AKI in the presence of the nephritic syndrome
- Systemic disease associated with AKI
Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria.
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; or
- Increase in SCr to ≥1.5 times baseline, which have occurred within the prior 7 days; or
- Urine volume < 0.5 ml/kg/h for 6 hours.
- Risk: 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output <0.5 mL/kg per hour for six hours.
- Injury: Twofold increase in the serum creatinine, or GFR decrease by 50 percent, or urine output <0.5 mL/kg per hour for 12 hours
- Failure: Threefold increase in the serum creatinine, or GFR decrease by 75 percent, or urine output of <0.3 mL/kg per hour for 24 hours, or anuria for 12 hours
- Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than four weeks
- End-stage renal disease: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than three months
The management of AKI hinges on identification and treatment of the underlying cause. 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, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.
Monitoring of renal function, by 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 relieves possible bladder outlet obstruction, such as with an enlarged prostate.
In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.
Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit, and may be harmful.
The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to Wegener's granulomatosis may respond to steroid medication. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as aminoglycoside, penicillin, NSAIDs, or paracetamol.
The use of diuretics such as furosemide, is widespread and sometimes convenient in ameliorating 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.
Renal replacement therapy
Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH). Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.
Depending on the cause, a proportion of patients will never regain full renal function, thus entering end-stage renal failure and requiring lifelong dialysis or a kidney transplant. Patients with AKI are more likely to die prematurely after being discharged from hospital, even if their kidney function has recovered.
New cases of AKI are unusual but not rare, affecting approximately 0.1% of the UK population per year (2000 ppm/year), 20x incidence of new ESRD. AKI requiring dialysis (10% of these) is rare (200 ppm/year), 2x incidence of new ESRD.
Acute renal failure was one of the most expensive conditions seen in U.S. hospitals in 2011, with an aggregated cost of nearly $4.7 billion for approximately 498,000 hospital stays. This was a 346% increase in hospitalizations from 1997, when there were 98,000 acute renal failure stays. According to a review article of 2015, there has been an increase in cases of acute kidney injury in the last 20 years which cannot be explained solely by changes to the manner of reporting.
Before the advancement of modern medicine, acute kidney injury was referred to as uremic poisoning while uremia was contamination of the blood with urine. Starting around 1847, uremia came to be used for reduced urine output, a condition now called oliguria, which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra.
Acute kidney injury due to acute tubular necrosis (ATN) was recognised in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function. During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids.
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