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Acute kidney injury


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, exposure to toxins, and prostate
enlargement. AKI is diagnosed on the basis of clinical history, such
as decreased urine production, and characteristic laboratory
findings, such as elevated blood urea nitrogen and creatinine.
Depending on its severity, AKI may lead to a number of
complications, including metabolic acidosis, high potassium levels,
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.

Definition :
Introduced by the Acute Kidney Injury Network (AKIN), specific criteria
exist for the diagnosis of AKI:

1. Rapid time course (less than 48 hours)

2. Reduction of kidney function :

Rise in serum creatinine

Absolute increase in serum creatinine of 0.3 mg/dl (26.4 mol/l)

Percentage increase in serum creatinine of 50%

Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours

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.


The causes of AKI traditionally are divided into 3 main categories:

prerenal, intrinsic, and postrenal.
Prerenal AKI
o Volume depletion

Renal losses (diuretics, polyuria)

GI losses (vomiting, diarrhea)
Cutaneous losses (burns, Stevens-Johnson syndrome)
o Decreased cardiac output
Heart failure
Pulmonary embolus
Acute myocardial infarction
Severe valvular disease
Abdominal compartment syndrome (tense ascites)
o Systemic vasodilation
Drug overdose
o Afferent arteriolar vasoconstriction
Drugs (NSAIDs, amphotericin B, calcineurin
inhibitors, norepinephrine, radiocontrast agents)
Hepatorenal syndrome
o Efferent arteriolar vasodilation ACEIs or ARBs
o Renal artery occlusion
Intrinsic AKI
o Vascular (large and small vessel)
Renal artery obstruction (thrombosis, emboli,
dissection, vasculitis)
Renal vein obstruction (thrombosis)
Microangiopathy (TTP, hemolytic uremic syndrome
[HUS], DIC, preeclampsia)
Malignant hypertension
Scleroderma renal crisis
Transplant rejection
Atheroembolic disease
o Glomerular
Antiglomerular basement membrane (GBM) disease
(Goodpasture syndrome)
Antineutrophil cytoplasmic antibody-associated
glomerulonephritis (ANCA-associated GN) (Wegener
granulomatosis, Churg-Strauss syndrome, microscopic
Immune complex GN (lupus, postinfectious,
cryoglobulinemia, primary membranoproliferative
o Tubular
Heme pigment (rhabdomyolysis, intravascular
Crystals (tumor lysis syndrome, seizures,
ethylene glycol poisoning, megadose vitamin C,
acyclovir, indinavir, methotrexate)
Drugs (aminoglycosides, lithium, amphotericin
B, pentamidine, cisplatin, ifosfamide,
radiocontrast agents)
o Interstitial
Drugs (penicillins, cephalosporins, NSAIDs, proton-
pump inhibitors, allopurinol, rifampin, indinavir,
mesalamine, sulfonamides)
Infection (pyelonephritis, viral nephritides)
Systemic disease (Sj gren syndrome, sarcoid, lupus,
lymphoma, leukemia, tubulonephritis, uveitis)
Postrenal AKI
o Ureteric obstruction (stone disease, tumor, fibrosis, ligation
during pelvic surgery)
o Bladder neck obstruction (benign prostatic hypertrophy
[BPH], cancer of the prostate [CA prostate or prostatic CA],
neurogenic bladder, tricyclic antidepressants, ganglion
blockers, bladder tumor, stone disease, hemorrhage/clot)
o Urethral obstruction (strictures, tumor, phimosis)
o Intra-abdominal hypertension (tense ascites)
o Renal vein thrombosis


The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative

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

Clinical :

A detailed and accurate history is crucial to aid in diagnosing the type of
AKI and in determining its subsequent treatment. A detailed history and a
physical examination in combination with routine laboratory tests are
useful in making a correct diagnosis
Distinguishing AKI from chronic renal failure is important, yet making
the distinction can be difficult. A history of chronic symptoms fatigue,
weight loss, anorexia, nocturia, and pruritus suggests chronic renal

Obtaining a thorough physical examination is extremely important when
collecting evidence about the etiology of AKI.
o Petechiae, purpura, ecchymosis, and livedo reticularis
provide clues to inflammatory and vascular causes of AK
o Infectious diseases, thrombotic thrombocytopenic purpura
(TTP), disseminated intravascular coagulation (DIC), and
embolic phenomena can produce typical cutaneous changes.
o Evidence of uveitis may indicate interstitial nephritis and
necrotizing vasculitis.
o Ocular palsy may indicate ethylene glycol poisoning or
necrotizing vasculitis.
o Findings suggestive of severe hypertension, atheroembolic
disease, and endocarditis may be observed on careful
examination of the eyes.
Cardiovascular system
o The most important part of the physical examination is the
assessment of cardiovascular and volume status.
o The physical examination must include pulse rate and blood
pressure recordings measured in both the supine position and
the standing position; close inspection of the jugular venous
pulse; careful examination of the heart, lungs, skin turgor,
and mucous membranes; and assessment for the presence of
peripheral edema.
o In hospitalized patients, accurate daily records of fluid intake
and urine output and daily measurements of patient weight
are important.
o Blood pressure recordings can be important diagnostic tools.
o Hypovolemia leads to hypotension; however, hypotension
may not necessarily indicate hypovolemia.
o Severe congestive cardiac failure (CHF) may also cause
hypotension. Although patients with CHF may have low
blood pressure, volume expansion is present and effective
renal perfusion is poor, which can result in AKI.
o Severe hypertension with renal failure suggests renovascular
disease, glomerulonephritis, vasculitis, or atheroembolic
o Abdominal examination findings can be useful to help detect
obstruction at the bladder outlet as the cause of renal failure,
which may be due to cancer or an enlarged prostate.
o The presence of tense ascites can indicate elevated intra-
abdominal pressure that can retard renal venous return and
result in AKI.
o The presence of an epigastric bruit suggests renal vascular
hypertension, which may predispose to AKI

Take note of the following findings during the physical


o Hypotension

o Volume contraction

o Congestive heart failure

o Nephrotoxic drug ingestion

o History of trauma or unaccustomed exertion

o Blood loss or transfusions

o Evidence of connective tissue disorders or autoimmune diseases

o Exposure to toxic substances, such as ethyl alcohol or ethylene


o Exposure to mercury vapors, lead, cadmium, or other heavy metals,

which can be encountered in welders and miners

People with the following comorbid conditions are at a higher risk

for developing AKI:

o Hypertension

o Congestive cardiac failure

o Diabetes

o Multiple myeloma

o Chronic infection

o Myeloproliferative disorder

Urine output history can be useful. Oliguria generally favors AKI.

Abrupt anuria suggests acute urinary obstruction, acute and severe
glomerulonephritis, or embolic renal artery occlusion. A gradually
diminishing urine output may indicate a urethral stricture or bladder
outlet obstruction due to prostate enlargement.

Because of a decrease in functioning nephrons, even a trivial

nephrotoxic insult may cause AKI to be superimposed on chronic renal


Metabolic acidosis, hyperkalemia, and pulmonary edema[12] 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. Depending on
the cause, a proportion of patients will never regain full renal function,
thus having end-stage renal failure requiring lifelong dialysis or a kidney

1. Significance of the fractional excretion of urea


Fractional excretion of sodium (FENa) has been used in the

diagnosis of acute renal failure (ARF) to distinguish between the
two main causes of ARF, prerenal state and acute tubular
necrosis (ATN). However, many patients with prerenal disorders
receive diuretics, which decrease sodium reabsorption and thus
increase FENa. In contrast, the fractional excretion of urea
nitrogen (FEUN) is primarily dependent on passive forces and is
therefore less influenced by diuretic therapy.


To test the hypothesis that FEUN might be more useful in

evaluating ARF, we prospectively compared FEUN with FENa
during 102 episodes of ARF due to either prerenal azotemia or


Patients were divided into three groups: those with prerenal

azotemia (N = 50), those with prerenal azotemia treated with
diuretics (N = 27), and those with ATN (N = 25). FENa was low
only in the patients with untreated plain prerenal azotemia while
it was high in both the prerenal with diuretics and the ATN
groups. FEUN was essentially identical in the two pre-renal
groups (27.9 2.4% vs. 24.5 2.3%), and very different from the
FEUN found in ATN (58.6 3.6%, P < 0.0001). While 92% of the
patients with prerenal azotemia had a FENa <1%, only 48% of
those patients with prerenal and diuretic therapy had such a low
FENa. By contrast 89% of this latter group had a FEUN <35%.

Low FEUN ( 35%) was found to be a more sensitive and

specific index than FENa in differentiating between ARF due
to prerenal azotemia and that due to ATN, especially if
diuretics have been administered.

2. Acute post-transplantation renal failure: differential

diagnosis by ultrasound.

Sonograms of 35 patients with cadaveric renal allografts were

reviewed. The patients included five with successful renal
transplantations, seven with acute tubular necrosis, 19 with
acute rejection, one with complete occlusion of the renal artery,
and three with stenosis of a renal artery. During the course of
acute tubular necrosis, the renal anatomy remained
sonographically unaltered. During the course of acute rejection,
there was a spectrum of sonographic findings including increase
in renal volume, decreased amplitude of the renal sinus echoes,
enlarged medullary pyramids, indistinct corticomedullary
boundary, increased echogenicity of the renal cortex, areas of
decreased parenchymal echogenicity, sparse cortical echoes, and
perirenal fluid collections as a result of hematoma or crescentic
collection of fluid around the kidney. In both arterial occlusion
and stenosis, no sonographic abnormalities of renal anatomy
were seen and the only finding was lack of normal post-
transplantation hypertrophy. Our study encourages the use of
sonography in acute post-transplantation renal failure. If serial
ultrasound studies are available and correlation with clinical and
laboratory data and nuclear medicine studies are obtained, the
correct diagnosis may be reached without the use of invasive

Clinical approach to the patient with acute renal
History and examination in acute renal failuregeneral points

Treat any life threatening features firstshock, respiratory

failure, hyperkalaemia
Is this acute or chronic renal impairment?

Identify the cause of acute renal failure that warrants

specific treatment
A full drug history (current, recent, and alternative
medication) is vital and any other clues from history

Is there a prerenal cause? What is the patient's current

fluid status?

Could this be obstruction?

Is intrinsic renal disease probablewhat does urine

analysis show ?

(1) Treat any life threatening features.

Hypotension, shock and respiratory failure should be

immediately apparent when assessing the patient, and clearly
these demand urgent treatment. Hyperkalaemia is less likely to
be immediately obvious. Unless changes are evident on ECG or
cardiac monitoring, it will only become apparent when
chemistry is

(2) Is this acute or chronic renal failure?

Previous laboratory data, information from case notes or GP

may provide the answer, but in many cases such information
will not be available., hypocalcaemia, and hyperphosphataemia
are not good indicators of chronicity. Renal ultrasonography
may show small (<9cm) kidneys, often with cortical scarring
and possibly cyst formation, in which case chronic disease is
probable. The converse is not always truethe presence of two
normal sized (914cm) kidneys does not always indicate acute

(3) Identify any cause of ARF that warrants specific


Many patients with ARF present with other diagnoses.

Dehydration secondary to gastrointestinal losses, pneumonia,
bowel obstruction, and new impairment of functional capacity in
the elderly patient are often the initial diagnoses, and a diagnosis
of renal failure is only made when laboratory parameters are
available later. The clinician should then ask themselves the
following questions

(4) Are there other clues from the history?

Additional targeted history will often be necessary. Has there

been a recent throat infection (possible poststreptococcal
glomerulonephritis) and, if so, a course of amoxicillin (possible
AIN)? A detailed drug history is important, and should include
current and recent medications, and also over the counter
preparations (especially NSAIDs),. Box 2 lists drugs commonly
linked with AIN. Rash, fever, and arthralgia are also suggestive
of AIN. Bone pain is a feature of myeloma.

Common drug causes of acute interstitial nephritis

Antimicrobial agents







NSAIDs and salicylates





Antiulcer agents



Thiazide diuretics



Constitutional symptoms may point to systemic vasculitis.

These frequently precede the acute presentation by many
months, have often been dismissed by patients and clinicians
and for example, nasal stuffiness and epistaxis as the initial
symptoms of Wegener's granulomatosis), and only come to light
during a detailed review of the history. Haemoptysis could show
a pulmonaryrenal syndrome.

In currentlyor recentlyhospitalised patients, nephrotoxic

agents such as

aminoglycosides and radiocontrast media must be rigorously

excluded. After angiography renal function tends to reach its
nadir a few days after the contrast dose. Cholesterol emboli may
occur weeks or months later.

(4) Is a prerenal cause probable?

Assessing the haemodynamic status of the patient is an essential

part of the initial assessment and correction of hypovolaemia
and hypotension may form part of the initial, lifesaving,
management. Hypotension is usually easy to spotbut can be
relative. A systolic pressure of 110mm Hg in the hypertensive
patient whose normal value is around 160mm Hg can
compromise renal perfusion. Postural hypotension (a decrease in
systolic blood pressure of 2030mm Hg from the lying to the
upright position) and the jugular venous pressure (JVP),
measured with the patient at 45 to the horizontal, are invaluable
markers of volume status. A significant postural decrease with
the JVP not visible shows volume depletion and the need for
fluid replacement, best carried out by rapid, repeated, infusions
of small volumes (250ml), through secure venous access, with
regular clinical reassessment. Once the patient is considered
euvolaemic, replacement should be stopped or pulmonary
oedema may occur. If fluid assessment is difficult ultrasound
guided placement of an internal jugular catheter to measure
central venous pressure may be necessary. The procedure is not
without risks. These are exacerbated in patients with ARF who
may have collapsed veins, and increased risks of bleeding
because of coagulopathy and platelet dysfunction. The time
taken to perform the task must not delay fluid resuscitation.
Evidence of currentor a history suggestive of recentvolume
depletion implies a prerenal cause or ATN, and response to
treatment differentiates between the two.

(5) Could this obstruction be post renal?

ARF is usually reversible with rapid relief of obstruction, but

the longer the delay the more the long term damage. Obstruction
should be sought by history and examination, before proceeding
to urgent ultrasonography of the urinary tract. Prostatic disease
is a common cause of ARF in men. Obstructive urinary
symptoms may be elicited, a palpable bladder or hypertrophied
prostate found on examination, and/or urethral catheterisation
may yield a significant residual volume. In women, carcinoma
of the cervix may be detectable on vaginal examination. There
may be a history of renal stone disease.

Ultrasonography is an excellent tool for detecting obstruction;

noninvasive, relatively simple, fast to perform, and portable. It
also gives information on renal size. However, it is not perfect,
and will fail to show hydronephrosis in about 5% of cases.
Encasement of the renal pelvices and ureters by malignant tissue
or retroperitoneal fibrosis may result in a failure to dilate even
when obstructed, and dilatation may not be observed if there is
an additional prerenal element (with reduced GFR),
immediately after acute obstruction (<24hours), or if the renal
pelvis is abnormally small (an anatomical variant). The
diagnosis should be performed in those patients where
obstruction seems likely on the basis of the clinical picture
computed tomography, cystoscopy with retrograde
ureteropyelography and antegrade pyelography are alternative
means of confirming the diagnosis. Occasionally a trial of
ureteric stenting or percutaneous nephrostomy is required.
(6) Is intrinsic renal disease likely?

We need to exclude renal inflammation that requires urgent

diagnosis and treatment to prevent further lossand aid
recoveryof renal function. History and examination may
provide clues (for example, vasculitic rash). Urine analysis is
important and must be performed in all patients presenting with
ARF. Haematuria or proteinuria suggest intrinsic renal disease.
Urine should be microscoped and cultured. Red cell casts are
highly suggestive of glomerulonephritis although only present in
30% of cases. If intrinsic renal disease is considered probable,
further urgent investigation is essential, as is urgent referral to a


Management is directed at treating any life threatening features,

attempting to decrease or reverse the decline in renal function,
and if unsuccessful providing support by renal replacement
anticipating renal recovery. Hyperkalaemia, pulmonary oedema,
and severe acidosis require immediate attention. Fluid
balance,the use of diuretics and dopamine, as well as the relief
of obstruction are all issues in the further management of the
1. Hyperkalaemia

Severe hyperkalaemia (plasma potassium ([K+]p) >6.5mmol/l)

is a medical emergency because of the risk of life threatening
cardiac arrhythmias.. As [K+]p rises, a typical pattern of ECG
changes shows: peaked/tented T waves ([K+]p>6.5mmol/l);
flattening of the P wave and prolongati); on of the QRS complex
([K+]p 78mmol/land ventricular fibrillation or asystole ([K+]p
>9mmol/l) (These changes are not always consistent, however,
and patients with a normal baseline ECG may also develop
arrhythmias. Urgent treatment of hyperkalaemia should be
started if the serum potassium is >6.5mmol/l, or if any ECG
changes are present.

An ECG from a haemodialysis patient with a

serum potassium of 8.0mmol/l, showing the classic
changes of significant hyperkalaemia: tented T
waves, flattening of the P wave, and prolongation
of the QRS complex.

The treatment of hyperkalaemia can be divided into four steps

(1)Stabilization of cardiac myocyte

Calcium antagonises the effects of hyperkalaemia, stabilising
the myocardium within a few minutes of infusion and producing
a more normal ECG trace without affecting serum potassium. It
should be given immediately if P wave or QRS changes are
present. A bolus of 1020ml of 10% calcium gluconate or
chloride is given intravenously over two to five minutes

(2) Reduction in plasma potassium concentration

Treatment with calcium is a temporising measure buying time

while measures are started to reduce the serum potassium
through increasing cellular uptake. Various options exist:

.Insulin with glucose

Insulin acts rapidly to indirectly activate the cell membrane

Na+/K+ATPase and thus increase cellular potassium uptake,
probably via activation of Na+/H+ channels and an increase in
intracellular [Na+]. The addition of glucose to the insulin bolus
is necessary to prevent hypoglycaemia. Ten units of fast acting
soluble insulin should be added to 50ml of 50% dextrose and
infused over 1020minutes. A reduction in [K+]p is seen after

.2 adrenergic agonists

Salbutamol binds to 2 receptors and through cytosolic second

messengers activates the Na+/K+ATPase, thus promoting
cellular potassium uptake. Nebulised and intravenous
salbutamol produce a similar effect to insulin, but at higher
doses than used for bronchospasm (1020mg via nebuliser, or
0.5mg intravenously). insulin and dextrose plus salbutamol may
be more effective than either treatment alone.

.Sodium bicarbonate

The infusion of sodium bicarbonate has little immediate effect

on hyperkalaemia, but may be used to correct acidosis

.Removal of potassium from the body

(Ion exchange resins )

These bind potassium in the gastrointestinal tract, in exchange

for calcium or sodium, and result in increased potassium
excretion in the stool. Calcium resonium (calcium polystyrene
sulphonate) and Resonium A (sodium polystyrene sulphate) are
the most commonly used, given at an oral dose of 15 g up to
thrity daily, together with an osmotic laxative (for example,
lactulose 10ml) to prevent constipation. They can also be given
rectally. An effect takes two to three hours.


this is the definitive means by which potassium can be removed

from the body, and is indicated in refractory severe
(Prevention of further potassium accumulation).

This can be achieved through a low potassium diet.

(2) Pulmonary oedema

The oligoanuric patient with pulmonary oedema resulting from

fluid overload (with/without underlying cardiac disease)
represents a clinical challenge., if significant ventilatory failure
is present, this must be dealt with first, through supplementary
oxygen, noninvasive ventilation, or intubation and ventilation,
depending on the state of the patient. While these measures are
being undertaken, pharmacological treatment to offload the
decompensated heart can be startedintravenous opioids
(diamorphine 2.55mg, with care taken depending on the
degree of respiratory distress) and an intravenous infusion of
nitrate (for example, glyceryl trinitrate 50mg in 50ml 0.9%
saline, at a rate of 220ml/h keeping the systolic blood pressure
>95mm Hg)and attempts made to provoke a diuresis. Much
larger doses of diuretics are required in renal failure, for
example, furosemide 250mg in 50ml 0.9% saline over one
hour, with an effect seen within one to two hours, if at all, and
which can be repeated if effective.

If these interventions are not successful, or if the patient is in

extremis such that they seem unlikely to prove effective, then
fluid removal by renal replacement therapy is the definitive
answer. Either haemodialysis or haemofiltration can be used,
(3) Acidosis

Severe metabolic acidosis (blood pH <7.2) often accompanies

ARF and arises through a variety of mechanisms, related both to
reduced renal function and the underlying cause of the patient's
illness. Systemic acidosis impairs cardiac contractility, induces
bradycardia, produces vasodilatation, and augments
hyperkalaemia, among other effects. Reversing acidosis through
administration of an alkaline solutionsodium bicarbonate.

(4) Fluid balance :

The approach to the hypovolaemic patient with prerenal failure

has been described earlier. Which is the optimal resuscitation
fluid is still debated. Normal saline and 4% albumin have
clinical equivalence, shown by the recent SAFE study of
patients admitted to intensive care units in Australia and New
Zealand, and which overturns previous studies showing that
albumin use may be associated with a higher mortality. Once the
patient is considered euvolaemic (normotensive, no postural
drop, JVP and/or central venous pressure (CVP) normal), care
should be taken to avoid fluid overload and a maintenance
regimen started, which takes account of renal and insensible
losses, aiming for a positive balance of 500ml/day (hourly input
= previous hour's output plus 25ml). This requires accurate
observation and record keeping by nursing staff, and regular re
assessment by the clinician.

(5) Dopamine

The use of low dose (13g/kg/min) dopamine has been

advocated to increase renal perfusion in critically ill patients.
Recent studies, including a large randomised controlled trial,
have shown it to lack efficacy on renal outcome or overall
mortality. Use of dopamine may also reduce splanchnic
perfusion, depress respiration, suppress anterior pituitary
hormone release and function, and worsen renal function in
hypovolaemic or normovolaemic patients. Its routine use in
ARF is not currently justifiable.

(6) Diuretisc

There is a theoretical rationale for the use of loop diuretics in

ARFinhibition of the Na+/K+/2Cl pump in the thick
ascending limb of the loop of Henle, with subsequent decrease
in Na+/K+ATPase activity, should reduce the oxygen
requirements of these cells, and thus their susceptibility to
ischaemic damage. There are scarce clinical data to support this,
and recent studies have either correlated the use of diuretics with
increased mortality, or shown no benefit. It seems reasonable to
use diuretics only in adequately resuscitatedbut oliguric
patients, at a dose suitable to the degree of renal impairment
(250mg furosemide intravenously over one hour is a standard
regimen), and to stop diuretic treatment if oliguria persists.
Converting oliguric to nonoliguric renal failure may help with
fluid and electrolyte management, but does not seem to affect
eventual need for dialysis or overall mortality, and should not
delay the start of renal replacement therapy when otherwise

(7) Relief of obstruction

It is important to relieve urinary tract obstruction promptly.

Bladder outflow obstruction can be relieved by passage of a
urethral catheterwhich should be considered in all patients
with ARF to accurately measure urine output ;referal to

(8) General measures

Patients with ARF may suffer from excessive bleeding, because

of uraemia induced platelet dysfunction and coagulopathies (for
example, sepsis associated disseminated intravascular
coagulation). Correction of coagulopathy may be necessary with
blood products and vitamin K. Renal replacement therapy (RRT)
may improve platelet function. ARF is associated with
numerous metabolic disturbances but energy expenditure is not
increased significantly.
Associated conditions such as sepsis and burns, however, often
lead to hypercatabolic states. Carbohydrate and protein
requirements should be tailored individually and ideally
delivered via the enteral route.protiens arenot prevented to avoid
catabolism but at the same time it shoudnot be increased to
aviode urea ecacerbation and this achieved by daily protein level
of 40 gm.citrus food shoud be avoided .water isnot allowed in
the 1st 24hs as the patient is hypervolemic

Parenteral administration may be necessary in some cases..

Additional water soluble vitamins may be required, as these are
removed by RRT. There is an increased susceptibility to
infection. Good infection control practices and a low threshold
for considering an infectious aetiology for any clinical
deterioration may minimise the risk. prophylaxis against deep
venous thrombosis can avoid some of the problems of prolonged

Replacement Therapy
As a broad generalisation, patients with ARF as part of a
systemic illnessoften with failure of multiple organ systems
require intensive care unit admission, given their probable needs
for intensive monitoring, nursing and support of other organ
systems. Patients with single organ renal failure can usually be
managed on a renal ward, and nephrologists will often support
the role of the intensivist on the intensive care unit. The severity
of the ARF will determine the urgency for nephrology referral
but this should be the same day if intrinsic renal disease is

Guidelines for the start of RRT

It must be emphasised that the patient should be viewed as a

whole, and dialysis neither started nor withheld on the basis of a
single variable. It is common practice to start RRT at an
earlier stage in patients with multiorgan failure because of
their potential for further deterioration and the benefits that RRT
may bring

Who needs dialysis? Guidelines for the initiation of renal

replacement therapy

Severe hyperkalaemia, unresponsive to medical therapy

Fluid overload with pulmonary oedema (in the context of
acute renal failure)

Uraemia (blood urea >3050 mmol/l)

Complications of severe uraemia: encephalopathy,

pericarditis, neuropathy/myopathy

Severe acidosis (pH <7.1)

Drug overdose
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