ACUTE RENAL FAILURE

DR. NAGARAJU TANNERU

M.D.S
ORAL & MAXILLOFACIAL SURGEON; LECTURER
COLLEGE OF DENTISTRY, UNIVERSITY OF DAMMAM
Acute kidney injury (AKI), previously called acute
renal failure (ARF), is an abrupt loss of kidney
function that develops within 7 days.
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 recognized 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.

Causes
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.
CAUSES:

AKI can be caused by disease, crush injury, contrast
agents, some antibiotics, and more.

The causes of acute kidney injury are commonly
categorized into prerenal, intrinsic, and postrenal.

Pre-renal 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.

Renal causes:

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.

Post-renal causes

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.

SIGNS & 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, lossofappetite, headache, nausea and vomi
ting.
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),

DIAGNOSIS
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.
Elevated blood urea nitrogen [BUN] and creatinine,
or inability of the kidneys to produce sufficient
amounts of urine.
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.

Advanced 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

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.
AKI can be diagnosed if any one of the following is
present:
Increase in SCr by 0.3 mg/dl (26.5 mol/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: 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

Treatment

Management includes supportive care, such
as renal replacement therapy, as well as treatment
of the underlying disorder.

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 pre-renal 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.


Diuretic agents

The use of diuretics such as furosemide, is
widespread and sometimes convenient in 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. Among
critically ill patients, intensive renal replacement
therapy does not appear to improve outcomes
compared to less intensive intermittent hemodialysis.

Complications

Metabolic acidosis, hyperkalemia, uremia and changes in
body fluid balances like pulmonary edema, which may
require medical treatment with sodium bicarbonate, anti-
hyperkalemic 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 being discharged from
hospital, even if their kidney function has recovered.

Further reading/references: