Acute Kidney Injury 2

DR. Dr. Mirza Zoebir, Sp.PD,Sp.PP

Acute Kidney Injury (AKI)

Previously called acute renal failure (ARF),is a rapid loss of

kidney function .
Its causes are numerous and include low blood volume from
any cause, exposure to substances harmful to the kidney , and
obstruction of the urinary tract . 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.

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.
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.

Causes

Prerenal
Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney.
kidney. These include
systemic causes, such as low blood volume,
volume, low blood pressure,
pressure, heart failure,
failure, and local changes to the blood vessels
supplying the kidney. The latter include renal artery stenosis,
stenosis, or the narrowing of the renal artery which supplies the
kidney with blood, and renal vein thrombosis,
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,
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.

Intrinsic
Sources of damage to the kidney itself are dubbed intrinsic.
intrinsic. Intrinsic AKI can be due to damage to the glomeruli,
glomeruli,
renal tubules,
,
or
interstitium.
.
Common
causes
of
each
are
glomerulonephritis,
,
acute
tubular
necrosis
(ATN),
and
tubules
interstitium
glomerulonephritis
acute interstitial nephritis (AIN), respectively. A cause of intrinsic acute renal failure is tumor lysis syndrome.
syndrome.

Postrenal
Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia,
hyperplasia,
kidney stones,
stones, obstructed urinary catheter,
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. 50-100ml suggests neurogenic bladder. 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.

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.
Sodium and potassium, two electrolytes that are commonly deranged in people with
acute kidney injury, are typically measured together with urea and creatinine.

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 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

Classification (1/3)

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.

Classification (2/3) :Definition

Introduced by the (AKIN), specific criteria exist
for the diagnosis of AKI:
Rapid time course (less than 48 hours)
Reduction of kidney function
Reduction in urine output, defined as <0.5
ml/kg/hr for more than 6 hours

Classification (3/3) : Staging

The RIFLE criteria, proposed by the (ADQI)
group, aid in the staging of patients with AKI:
Risk: GFR decrease >25%, serum creatinine increased
1.5 times or urine production of <0.5 ml/kg/hr for 6
hours
Injury: GFR decrease >50%, doubling of creatinine or
urine production <0.5 ml/kg/hr for 12 hours
Failure: GFR decrease >75%, tripling of creatinine or
creatinine >355 mol/l (with a rise of >44) (>4 mg/dl)
OR urine output below 0.3 ml/kg/hr for 24 hours
Loss: persistent AKI or complete loss of kidney function
for more than 4 weeks
End-stage renal disease: need for renal replacement
therapy (RRT) for more than 3 months

Treatment (1/5)

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.

Treatment (2/5) : 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 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.
If the cause is obstruction of the urinary tract, relief of the obstruction
(with a nephrostomy or urinary catheter) may be necessary.

Treatment (3/5) :Diuretic agents

The use of diuretics such as furosemide, is
widespread and sometimes convenient in
ameliorating fluid overload, and is not
associated with higher mortality (risk of
death).

Treatment (4/5) :

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.

Treatment (5/5) :

Metabolic acidosis, hyperkalemia, and

pulmonary edema may require medical treatment
with sodium bicarbonate, antihyperkalemic
measures, and diuretics.
Lack of improvement with fluid resuscitation,
therapy-resistant hyperkalemia, metabolic
acidosis, or fluid overload may necessitate
artificial support in the form of dialysis or
hemofiltration.

Prognosis

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 they were discharged from
hospital even if their kidney function has
recovered.

Epidemiology

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 kidney injury is common among
hospitalized patients. It affects some 3-7% of
patients admitted to the hospital and
approximately 25-30% of patients in the
intensive care unit.

History

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
.