Acute kidney injury (AKI), previously called
acute renal failure (ARF),is an abrupt loss of kidney function that develops within 7 days.
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 on other organ systems, including death. People who have
experienced AKI may have an increased risk of 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 clinical picture is often dominated by the underlying cause, eg
postoperative state. 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 blood pressure can be high, low or normal.
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 (or vasculitis) and a palpable bladder in
obstructive nephropathy.
Causes
AKI can be caused by systemic disease (such as a manifestation of an
autoimmune disease, e.g. lupus nephritis), crush injury, contrast
agents, some antibiotics, and more. It is often multifactorial. The most
common cause is dehydration and sepsis combined with nephrotoxic drugs,
especially following surgery or contrast agents.
The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.
Classic laboratory findings in AKI
Type UOsm UNa FeNa BUN/Cr
Prerenal >500 <10 <1% >20
Intrinsic <350 >20 >2% <15[citation needed]
Postrenal <350 >40 >4% >15
Prerenal
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 can result in depression of GFR. Causes include
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.
Intrinsic
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. Other causes of intrinsic AKI are rhabdomyolysis and tumor
lysis syndrome.
Postrenal
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
AKI, the use of IV contrast is contraindicated as the contrast agent
used is nephrotoxic. On the basic metabolic panel, the ratio of BUN to
creatinine may indicate post renal failure.
Diagnosis
Detection
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.
Further testing
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 renal biopsy. Indications for renal
biopsy in the setting of AKI include:
Unexplained AKI, in a patient with two non-obstructed normal sized kidneys
AKI in the presence of the nephritic syndrome
Systemic disease associated with AKI
Renal transplant dysfunction
Classification
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 (less than 400 mls of urine
per 24 hours).
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; 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.
Staging
The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:
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: Two-fold increase in the serum creatinine, or GFR decrease by 50
percent, 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 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
Treatment
The management of AKI hinges on identification and treatment of the
underlying cause. The main objectives of initial management are: (1) to
prevent cardiovascular collapse and death; and, (2) to call for
specialist advice. 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.
Specific therapies
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 vasculitis or glomerulonephritis may
respond to steroid medication, cyclosphosphamide 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.
If the cause is obstruction of the urinary tract, relief of the
obstruction (with a nephrostomy or urinary catheter) may be necessary.
Diuretic agents
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.
