Acute renal failure

OR
ACUTE KIDNEY
DISEASE(AKD)
OR
ACUTE KIDNEY
INJURY(AKI)
BY: DR.ZEEL NAIK

DEFINITION OF ACUTE RENAL
FAILURE
 ARF is defined as a decrease in glomerular filtration rate
(GFR), generally occurring over hours to days, sometimes
over week that is associated with an accumulation of
waste products, including urea and creatinine.
 Presence of proteinuria/albuminuria for at least 3 months
 Decrease in urine output.
 Normal urine output of ≥1,200 ml/day
 Patients with ARF are often categorized as being anuric
(urine output <50 ml/day), oliguric (urine output <500
ml/day), or nonoliguric (urine output >500 ml/day).
 Clinician use a combination of the serum creatinine(Scr)
value with change in either Scr or urine output(UOP) as
the primary criteria for diagnosing ARF.

ACUTE RENAL FAILURE
 It is one of the most common and serious problem.
 It is characterized by abrupt reduction(usually within a
48 hour period) in kidney function.
 Acute kidney injury has replaced the previously used
term acute renal failure.
 The first signal in the detection of ARF is a change is
serum creatinine, a surrogate marker of solute
clearance by the kidneys.
 A wide range of factors can precipitate AKI, including
trauma, obstruction of urine flow, including surgery
and medical conditions, for example sepsis, SLE ,
diabetes, acute liver disease and rapidly progressive
Glomerulonephritis.
 Drug involvement in the development of AKI is

ACUTE RENAL FAILURE
 In non-hospitalized patient, dehydration, exposure to selected
pharmacologic agents such as contrast media(used in
imaging techniques such as CT scan, MRI and USG to
enhance the difference between body tissues on images),
and presence of heart failure are associated with ARF.
 Additionally trauma, rhabdomyolysis , vessel thrombosis and
drugs are common culprits in development of ARF.
 The pharmacological agents commonly associated with ARF
includes chemotherapeutic agents, NSAIDs, ACE inhibitors,
ARB and anti-viral medication.

EPIDEMIOLOGY
 AKI is common among hospitalized patients.
 It affects some 3%-7% of patients admitted to the hospital and
approximately 25-30% of patients in the ICU.
 Most cases are caused by pre-renal AKI and are reversed with
appropriate intervention.
 Pre-renal AKI represents the most common
form of kidney injury and often leads to intrinsic AKI if it is
not promptly corrected.
 Severe AKI, may include a requirement for dialysis treatment, is
often associated with failure of one or more non-renal organs(multi-
organ failure); in this setting there is a mortality rate of 70% in
patient with sepsis and 45% in patients without sepsis.
 AKI that occurs in the community is responsible for around 1% of all
hospital admissions.

KDIGO CLASSIFICATION
CRITERIA FOR AKD STAGING

CRITERIA FOR DEFINITION AND
STAGING OF CONDITION
 R-Risk
 I- Injury
 F-Failure
 L-Loss
 E- End-stage renal disease (ESRD)

RIFLE
 It is the criteria proposed by the ACUTE DIALYSIS QUALITY
INITIATIVE(ADQI) group, aid in the staging of patients with AKI.
 RISK: GFR decreases >25 %, serum creatinine increased 1.5 times
the normal or urine production of <0.5ml/kg/hr for 6 hours.
 INJURY: GFR decreases > 50% , serum creatinine increased 2
times the normal or urine production <0.5ml/kg/hr for 12 hours.
 FAILURE : GFR decrease>75 %, serum creatinine increased to 3
times the normal(>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.
 ESRD: Complete loss of kidney function for more than 3 months.

RISK FACTORS
 Severe Burns – 20-60%
 Rhabdomyolysis – 20-30%
 Aminoglycoside Use – 10-30%
 Chemotherapy – 15-25%
 Open Heart Surgery – 5-20%
 ICU – 25-30%

Etiology And Classification
 The causes of ARF have been categorized as:
 (a) Pre-Renal(Decreased Blood Flow to
Kidney), which results from decreased renal
perfusion in the setting of undamaged
parenchyma tissue.
 (b) Intrinsic or Renal or Intra-Renal
(Nephrotoxicity), the result of structural
damage to the kidney, most commonly the
tubule from a ischemic or toxic insult.
 (c) Post-Renal(Obstructive), caused by
obstruction of urine flow downstream from the

 The most common cause of hospital-acquired
ARF is prerenal ischemia as the result of
reduced renal perfusion secondary to sepsis,
reduced cardiac output, and/or surgery.
 Drug-induced ARF may account for 18% to
33% of in-hospital occurrences.
 Other risk factors for developing ARF while
hospitalized include advanced age(>60 years of
age), Male gender, Acute infection, and pre-
existing chronic diseases of the respiratory or
cardiovascular systems.
Etiology

COMMON CAUSES OF THE
CATEGORIES OF AKI
PRE- RENAL RENAL POST-RENAL
SEPSIS Prolonged Pre- Renal AKI
and ATN
Tumors ( Pelvic or
retroperitoneal)
Hypovolaemia Rapidly progressive
glomerulonephritis
Prostate Disease (in men)
Vaso-active drugs (e.g.
NSAIDs and ACEi/ARBs)
Acute interstitial nephritis Renal Calculi (obstructing
the ureter)

1.PRE-RENAL AKI
 Pre-renal causes of AKI( also known as pre-renal Azotemia) are
those that decrease effective blood flow to the kidney.
 These include systemic causes, such as low blood volume
(hypovolaemia) , low blood pressure (hypotension) , and heart
failure , as well as local changes to the blood vessels supplying the
kidney(renal artery stenosis and embolus).
 The latter include renal artery stenosis , which is narrowing of the
renal artery that supplies the kidney , and renal vein thrombosis ,
which is the formation of a blood clot in the renal vein that drains
blood from the kidney.
 When the systolic blood pressure drops below 80mmHg, AKI may
develop.
 In individual with CKD or in the elderly , AKI may occur at higher
levels of systolic BP.
 Drugs that inhibits the RAAS, such as ACEi and ARBs ,or block the
production of prostaglandins , such as NSAIDs , can predispose to
the development of pre-renal AKI.

1.PRE-RENAL AKI
 HYPOVOLAEMIA:
 It results from any condition that causes intravascular fluid
depletion , either directly by hemorrhage or indirectly to
compensate for extra vascular loss.
 Examples of this include diarrhea and vomiting, burns and
excessive use of diuretics.
 Hypotension is a secondary effect of significant
hypovolaemia.
 HYPOTENSION:
 In addition to hypovolaemia, hypotension can result from
cardiac failure, of which there are number of causes, but the
most common is IHD.
 Another important cause is septic shock, where there is
peripheral vasodilation and low peripheral resistance which
leads to profound hypotension despite a high cardiac output.

PATHOPHYSIOLOGY OF PRE-
RENAL AKI

RENAL AKI
 Blood gets into the kidney through the renal artery into tiny clumps
of arterioles called glomerular where it is initially filtered. The filtrate
then moves into renal tubule.
 Sometimes the fluid or electrolytes can move back from the filtrate
into the blood called tubular re-absorption and sometimes more fluid
or electrolytes can move from the blood to the filtrate called renal
secretion.
 Along with fluid and electrolyte , waste compounds are also filtered
such as urea and creatinine.
 Some urea is reabsorbed back into the blood, whereas little bit of
creatinine is reabsorbed.
 The fact is, in the blood the normal ratio of BUN to creatinine is 5-
20:1 and it is very good diagnostic for looking at kidney function.
 Now PRE-RENAL AKI occurs because of decreased blood flow to
the kidney.

RENAL AKI
 1.Absolute loss of blood where actually fluid leaves the body.
 This could be due to major hemorrhage or blood loss, vomiting , diarrhea or
with severe burns where the body fluid evaporates quickly without the
protective skin layer.
 2. Relative loss of blood is one where fluid stays same.
 Sepsis shock or distributive shock where fluid moves from the blood
vessels into the tissues which keeps the total body fluid same but relatively
decreases blood volume.
 Another example is CHF where the heart cant pump blood to the tissues ,
so a portion of blood just pools in the venous side and isn't pumped into the
body, meaning less blood is seen in the kidney.
 3. Complication localized to renal artery itself, for example renal artery
can become narrowed as in Renal Artery Stenosis or blocked by an
embolus which is a blood clot from somewhere else in the body.

RENAL AKI
 Less blood going to the glomeruli , which means less blood being filtered , so there
is a decrease in GFR.
 If less blood is filtered, that means less urea and creatinine are filtered out, and
more stays in the blood, which is called azotemia – high level of nitrogen containing
compounds in the blood, this will also tend to cause oligouria, an abnormally low
amount of urine production.
 Also with less blood being filtered , the kidneys activate the RAAS system, which
causes aldosterone release by the adrenal glands, which tells the kidney to
reabsorb sodium(Na+).
 When sodium gets reabsorbed, water gets reabsorbed as well.
 Water and sodium reabsorption is also tied to urea reabsorption, so in pre-renal
situation, urea gets reabsorbed and so even more urea gets into the blood, resulting
in a BUN to creatinine ratio of greater than 20:1.
 There is a decrease in urine sodium level usually less than 20 mEq/L.
 The urine is more concentrated because less water is excreted, so typically the
urine has greater amount of urea which is why our urine smells so nitrogen, when
we are dehydrated.
 Tachycardia, hypotension , reduced skin turgor and cool extremities is commonly

2. Intrinsic AKI or Intra-Renal AKI or
Renal AKI
 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.
 Most common cause of intrinsic AKI (>80% cases) is ATN.
 ATN usually occurs in patients with sustained pre-renal AKI
leading to tubular injury; this is caused by hypotension and
hypovolaemia, often in the setting of sepsis and nephrotoxic
agents including drugs.
 Other endogenous sources can cause direct tubular damage,
including myoglobin , hemoglobin and immunoglobin light
chains in multiple myeloma.

PATHOPHYSIOLOGY of Intrinsic AKI-
Acute Tubular Necrosis

GLOMERULONEPHRITIS

PATHOPHYSIOLOGY of Intrinsic AKI- Acute Interstitial
Nephritis(AIN)

PATHOPHYSIOLOGY of Intrinsic AKI- Renal Artery
Stenosis

PATHOPHYSIOLOGY of Intrinsic AKI- Acute Tubular
Necrosis
 ATN is a diagnosis made by renal biopsy; the finding can include the damage to the
proximal tubule and the ascending loop of Henle, interstitial edema and sparse
infiltrating inflammatory cells.
 Although severe and sustained hypoperfusion (ischemia) can lead to ATN, it usually
develops when there is a combination of factors including the presence of one or
more range of nephrotoxins.
 These may arise exogenously from drugs or chemical poisons, or from endogenous
sources such as hemoglobin, myoglobin , crystals(uric acid, phosphate),
immunoglobulin light chains and toxic products from sepsis or tumor (tumor lysis
syndrome).
 Some endogenous toxins may be released (rhabdomyolysis) following muscle injury
or necrosis, hypoxia, infection or after drug treatment , for example , with fibrates and
statins , particularly when both are used in combination.
 Due to combination of factors including hypoperfusion, haem-catalysed free radical
tubular cytotoxicity and haem cast formation and precipitation leads to tubular injury.
 The likelihood of ATN is increased by underlying conditions that predispose to
ischaemia such as pre-existing CKD of any cause, atheromatous renovascular
disease and cholesterol embolisation from upward athemromatous plaque rupture.

Glomerulonephritis
 The kidney is vulnerable to a range of
immunological processes that can cause AKI.
 These are divided into glomerular
causes(glomerulonephritis) and interstitial
causes (acute interstitial necrosis or interstitial
nephritis).
 Rarely acute pyelonephritis (APN) can cause
AKI.

Pathophysiology -
Glomerulonephritis
 Glomerulonephritis refers to an inflammatory process within the
glomerulus.
 If the process causes AKI , it is called rapidly progressive
glomerulonephritis (RPGN).
 Most cases of RPGN are caused by a small-vessel vasculitis (SVV);
this gives patter of injury in the glomerular that is called a focal
segmental necrotising glomerulonephritis(FSNGN) with cresent
proliferation; cresents are presence of cells and extracelluar matrix
in Bowman’s spaces.
 Most cases of FSNGN are caused by anti-neutrophil cytoplasmic
antibody(ANCA)-associated SVV.
 The 2 main types of ANCA-associated SVV are granulomatosis with
polyangiitis, prevously known as Wegener’s granulomatosis , and
microscopic polyangiitis.
 Other important cause of RPGN include Goodpasture’s disease,
which is caused by antibodies against glomerular basement
membrane (anti-GBN antibodies)

Pathophysiology -
Glomerulonephritis
 SLE is one of the major reason for causing lupus nephritis or lupus
Glomerulonephritis.
 It majorly targets Nephron.
 It is auto immune which causes formation of antigen-antibody complex and
this complex gets deposited to glomerulus.
 There it activates complementary system and activates neutrophils and
macrophages and releases lysosomal enzyme which leads to inflammation.
 This will lead to necrosis of podocytes and will cause selective cell wall
destruction.
 Due to this there will be leakage of plasma proteins(albumin and globulin
and RBC.
 This situation leads to albuminuria and haemtouria.
 Also there will be decrease in GFR which will lead to Azotemia , oligouria
and edema and ultimately edema will lead to hypertension.
 Also there are many drug triggers for causing glomerulonephritis such as
aminoglycosides, amphotericin-B, cisplatin, beta lactam, quinolones,
rifampin, sulfonamides,vancomycin etc.

Pathophysiology – Interstitial
Nephritis
 Interstitial nephritis is nephrotoxin induced
hypersensitivity reaction associated with
infiltration of inflammatory cells into the
interstitium with secondary involvement of the
tubules.
 The nephrotoxins involved are usually drugs
and/or the toxic products of infection.
 Drugs that have been most commonly shown to
be responsible include NSAIDs, antibiotics
(especially penicillins, cephalosporins and
quinolones), PPI such as omeprazole,
furosemide, allopurinol and azathioprine.

PATHOPHYSIOLOGY- POST-RENAL
AKI

AKI
 Post renal AKI is a consequence of urinary tract obstruction.
 This may be related to benign prostatic hyperplasia, kidney stones , obstructed
urinary catheter, bladder stone, utereral or renal malignancy.
 Any mechanical obstruction from the renal pelvis to the urethra can cause post-renal
AKI; these can be divided into causes within ureter( e.g. calculi or clots), a problem
within the wall of ureter (e.g. malignancies or benign strictures) and external
compression(e.g. retroperitoneal tumours).
 It is extremely unusual for drugs to be responsible for post-renal AKI.
 Practolol-induced retroperitoneal fibrosis resulting in bilateral ureteric obstruction is a
rare example.
 It is useful to perform a bladder scan or 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.
 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 ARF, the use of IV contrast is contraindicated.

AKI
 1. Neurogenic bladder leads to peripheral
nueropathy which ultimately causes cholinergic
neuron damage which causes contraction of
bladder and increase the resistance and
decreases the GFR.
 The problem is known as cystopathy which
causes decreased bladder sensation, increased
bladder capacity and impaired contractility.
 The reason for this type of pathophysiology can
be cholecystitis ( gallbladder inflammation) ,
diabetes mellitus and anti-cholinergic medication,
all this can lead to neurogenic bladder.

AKI
2. BPH( Benign Prostatic Hyperplasia)and
prostate cancer leads to increase in size of
prostate gland which causes obstruction in
urethra.
 Benign prostatic hyperplasia (BPH), also
called prostate enlargement, is a
noncancerous increase in size of the prostate
gland.
 Symptoms may include trouble starting to
urinate, weak stream, inability to urinate, or
loss of bladder control.
 BPH+ Prostate Cancer = Prostate Process.

AKI
3. Nephrolithiasis in ureter, urethra and bladder
can lead to direct obstruction.
 Most common stones seen are calcium
oxalate , monosodium urate crystals (MSU).
 Also retroperitoneal fibrosis , colon cancer and
renal abscess(accumulation of pus cells) in
ureter can lead to post-renal AKI.
 Certain drugs such as Indinavir(anti-viral) ,
sulfonamide antibiotic and acyclovir are
common culprit for causing post-renal AKI.

Signs & symptoms
Symptoms
 Bloody stools
 Breath odour
 Changes in mental status or mood
 Decreased appetite
 Decreased sensation, especially in the hands or feet
 Fatigue
 Flank pain (between the ribs and hips)
 Hand tremor
 High blood pressure
 Metallic taste in mouth
 Nausea or vomiting, may last for days
 Nosebleeds
 Persistent hiccups
 Prolonged bleeding
 Seizures
 Slow, sluggish movements
 Swelling - generalized(fluid retention)
 Swelling of the ankle, foot, and leg
 Urination changes:
 Decrease in amount of urine
 Excessive urination at night
 Urination stops completely

 Signs
■ Patient may have edema; urine may be colored or foamy; orthostatic
hypotension in volume-depleted patients, hypertension in the fluid-
overloaded patient or in the presence of acute or chronic
hypertensive kidney disease.
Pre- Renal Renal Post-Renal
 High urine specific gravity
 Little or no proteinuria
 Elevated BUN: CR ratio
 Fixed urine specific gravity
 High sodium concentration in
urine
 Proteinuria
 Weight gain
 Edema
 Haemoptysis'
 Anaemia
 Hypertension
 Fixed urine specific gravity
 Elevated sodium concentration in
urine
 Little or no proteinuria

Diagnosis
 Laboratory Tests
 Elevations in the serum potassium, BUN, creatinine, and
phosphorous, or a reduction in calcium and the pH (acidosis), may
be present. The clinical findings are different based on the cause of
the ARF.
 An increased serum white blood cell count may be present in those
with sepsis-associated ARF, and eosinophilia suggests acute
interstitial nephritis.
 Urine microscopy can reveal cells, casts, or crystals that help
distinguish among the possible etiologies and/or severities of ARF.
 On microscopy there are muddy brown granular epithelial cell casts
along with renal tubular epithelial cells in ATN when kidney tissue
biopsy is done.

Other Diagnostic Tests
 An elevated urine specific gravity suggests prerenal ARF, as the tubules are concentrating the
urine.
 Urine chemistry also indicates the presence of protein, which suggests glomerular injury, and
blood, which can result from damage to virtually any kidney structure.
 Renal ultrasonography or cystoscopy may be needed to rule out obstruction; renal biopsy is rarely
used, and is reserved for difficult diagnoses.

MONITORING PARAMETERS IN AKD
 1. Measurement of BP, which needs to be interpreted in respect of
the baseline for the affected patient together with patient’s heart
rate.
 2. Auscultation of the heart for the presence of 3rd and 4th heart
sounds, the presence of which indicate cardiac strain associated
with fluid overload.
 3. Presence of added sounds in chest, in particular fine inspiratory
crackles that are found in some patients with pulmonary edema.
 4. A chest X-ray for the presence of pulmonary edema.
 5. Pulse oximetry to assess arterial oxygen saturation.
 6. Edema of legs indicates long-term fluid overload.
 7. Evaluation of decreased skin turgor , which is a sign of fluid loss.
 8. Serum electrolytes including potassium, bicarbonate, calcium,
phosphate and acid-base balance , should be measured on a daily
basis.
 9. Patient should be weighed daily as this is an important measure
of fluid balance.

Treatment
GENERAL APPROACH TO PREVENTION
 The patient should receive guidance regarding their optimal
daily fluid intake (approximately 2 L/day) to avoid dehydration.
 The patient’s fluid balance can be evaluated by measuring acute
changes in weight and blood pressure.
 If the patient has a history of nephrolithiasis, they may benefit
from dietary restrictions, depending on the type of stones that
were present in the past.
 If a patient has a Foley catheter in place, proper care and
monitoring needs to be performed to ensure that post
obstructive ARF does not develop.
 Potentially nephrotoxic medications should be avoided,
particularly in high-risk patients, whenever possible.
 Avoidance or discontinuation of drugs that increase renal vaso-
constriction, such as NSAID and selective COX-2 inhibitors.

TREATMENT – PREVENTION OF
AKI.
 Risk factors for ARF include advanced age, acute infection, pre-existing
chronic respiratory or CVS disease, dehydration , CKD.
 Decreased renal perfusion secondary to abdominal or coronary bypass
surgery, acute blood loss in trauma , and uric acid nephropathy also
increase risk.
 Nephrotoxin administration (e.g. radio contrast dye) should be avoided
whenever possible.
 When patient require contrast dye and are at risk of contrast-dye induced
nephropathy , renal perfusion should be maximized through strategies
such as assuring adequate hydration with normal saline or sodium
bicarbonate solutions and administration of oral ACETYLCYSTEINE 600
mg every 12 hours doses.
 Strict glycemic control with insulin, Amphotericin B nephrotoxicity can
be reduced by slowing the infusion rate to 24 hours or , in at-risk patients,
substituting liposomal Amphotericin B.
 Mannitol, loop diuretics , dopamine and fenoldopam are popular in
treatment of AKI.

Management of Established
ARF.
 No drugs have been found to accelerate ARF
recovery.
 Therefore, patients with established ARF should
be supported with non-pharmacologic and
pharmacologic approaches through the period
of ARF.

TREATMENT- NON-
PHARMACOLOGICAL
 Supportive care goals include maintenance of adequate cardiac
output and blood pressure to optimize tissue perfusion while
restoring renal function to pre-AKI baseline.
 Medications associated with diminished renal blood flow should be
stopped.
 Appropriate fluid replacement therapy should be initiated.
 Avoidance of nephrotoxins is essential in the management of
patients with ARF.
 RRT(Renal Replacement Therapy) , such as haemodialysis and
peritoneal dialysis , maintain fluid and electrolyte balance while
removing waste products. Intermittent and continuous options have
different advantages and disadvantages but, after correcting for
severity of illness, have similar outcomes.
 Consequently hybrid approaches (e.g. sustained low-efficiency
dialysis and extended daily dialysis) are being developed to provide
the advantage of both.

TREATMENT- NON-
PHARMACOLOGICAL
 Intermittent RRT (e.g. Hemodialysis) has the advantage of
widespread availability and the convenience of widespread
availability and convenience of lasting only 3-4 hours.
Disadvantages include difficult venous dialysis access in
hypotensive patients and hypotension due to rapid removal of
large amount of fluids.
 Several continuous renal replacement therapy (CRRT)
variants have been developed.
 CRRT, performed as continuous Hemodialysis ,
continuous haemofiltration , or both is becoming
increasingly popular.
 CRRT gradually removes solute resulting in better tolerability
by critically ill patients.
 Disadvantages include limited availability , need for 24 hours
nursing care , high expense and incomplete guidelines for
drug dosing.

TREATMENT-
PHARMACOLOGIC
 Loop diuretics have not shown to accelerate
ARF recovery or improve patient outcome;
however , diuretics can facilitate management of
fluid overload.
 The most effective diuretics are Mannitol and loop
diuretics.
 Mannitol 20% is typically started at a dose of 12.5
to 25 g IV over 3-5 minutes. Disadvantages
include IV administration , hyperosmolality risk,
need for monitoring because mannitol can
contribute to ARF.

TREATMENT-
PHARMACOLOGIC
 Equipotent doses of loop diuretics ( furosemide ,
bumetanide , torsemide , ethacrynic acid) have
similar efficacy.
 Ethacrynic acid is reserved for sulpha allergic
patients.
 Continuous infusions of loop diuretics appear to
be more effective and to have fewer adverse
effects than intermittent boluses.
 An initial IV loading dose (equivalent to
furosemide 40-80 mg) should be administered
before starting a continuous infusion (equivalent
to furosemide 10-20 mg/hour).

TREATMENT-
PHARMACOLOGIC
 Agents from different pharmacologic classes,
such as diuretics that work at the distal
convoluted tubule (thiazide) or the collecting
tubule (amiloride , triamterene,
spironolactone) , may be synergistic when
combined with loop diurerics.
 Metolazone is commonly used because ,
unlike other thiazides , it produces effective
Diuresis at GFR less than 20 ml/min.

Electrolyte management and Nutrition
Therapy
 Hyperkalaemia is the most common and serious electrolyte
abnormality in ARF.
 Typically, potassium must be restricted to less than 3g/day
and monitored daily.
 Hypernatremia and fluid retention commonly occur,
necessitating restricting daily sodium intake to no more than
3 g.
 All sources of sodium , including antibiotics , need to be
considered when calculating daily sodium intake.
 Phosphorous and magnesium should be monitored; neither is
efficiently removed by dialysis.
 Enteral , but not parenteral , nutrition has been shown to
improve patient outcomes.

DRUG-DOSING
CONSIDERATION
 Drug therapy optimization in ARF is a challenge.
 Confounding variables include residual drug
clearance , fluid accumulation, and use of RRTs.
 Volume of distribution for water soluble drugs is
significantly increased due to edema.
 Use of dosing guidelines for CKD does not reflect
the clearance and volume of distribution in
critically ill ARF patients.
 ARF patients may have a higher residual nonrenal
clearance than CKD patients with similar
creatinine clearances; this complicates drug
therapy individualization , especially with RRTs.

PHARMACOLOGIC Treatment
Low doses of dopamine
Loop diuretics
Osmotic diuretics
Prostaglandins
Calcium channel blockers

NON-Dialysis Treatment OF
AKI
 UREMIA AND INTRAVASCULAR VOLUME OVERLOAD
 In AKI and CKD, the symptoms of uremia include nausea,
vomiting and anorexia , and result principally from
accumulation of toxic products of protein metabolism
including urea.
 Unfortunately, because uremia causes anorexia , nausea and
vomiting , many severely ill patients are unable to tolerate
any kind of diet.
 In these patients and those who are catabolic, the use of
Enteral or parenteral nutrition should be considered at an
early stage.
 Intravascular fluid overload must be managed by restricting
NACL intake to about 1-2 g/day if the patient is not
hyponatraemic and total fluid intake to less than 1L/day.
 Care should be taken with the so-called low salt products,
because these usually contain KCL, which will exacerbate
hyperkalaemia.

AKI
 HYPERKALAEMIA
 Hyperkalaemia is a particular problem in AKI not only because urinary excretion
is reduced but also because intracellular potassium may be released.
 Rapid rises in extracellular potassium are to be expected when there is tissue
damage, as in burns , crush injuries and sepsis.
 Acidosis also aggravates Hyperkalaemia by provoking potassium leakage from
healthy cells.
 This condition may be life threatening , causing cardiac arrhythmias , and if
untreated, can result in asystolic cardiac arrest.
 Dietary potassium should be restricted to less than 40 mmol/day , and
potassium supplements and potassium sparing diuretics removed from the
treatment schedule.
 Emergency treatment is necessary if the serum potassium level reached 7
mmol/L (normal range 3.5-5.5 mmol/L) or if there are the progressive changes
in ECG associated with Hyperkalaemia.
 These include tall, peaked T waves , reduced P waves with increased QRS
complexes that often leads to cardiac arrest.

AKI
 TREATMENT OF HYPERKALAEMIA
1. 10-30 ml of calcium gluconate 10% intravenously over
5-10 minutes : This improves myocardial stability but
has no effect on the serum potassium levels.
2. 50 ml of 50 % glucose together with 8-12 units of
soluble insulin over 10 minutes : Endogenous insulin ,
stimulated by a glucose load or administered
intravenously stimulates intracellular potassium uptake
, thus removing it from the serum. The effect becomes
apparent after 15-30 minutes, peaks after about 1 hr,
and last for 2-3 hours and will decrease serum
potassium levels by around 1 mmol/L.

AKI
 ACIDOSIS
 The inability of the kidney to excrete hydrogen ions may
result in a metabolic acidosis.
 This may contribute to Hyperkalaemia.
 It may be treated with sodium bicarbonate 1-6 g/day in
divided doses or 50-100 mmol of bicarbonate ions
preferably as isotonic sodium bicarbonate 1.4% OR
1.26%, 250-500 over intravenously may be used.
 The administration of bicarbonate will also tend to
reduce serum potassium concentration.

AKI
 HYPOCALCAEMIA
 Calcium malabsorption , probably secondary to
disordered Vitamin D metabolism, can occur in AKI.
 Hypocalcaemia usually remains asymptomatic, as
tetany of skeletal muscles or convulsions does not occur
until serum concentrations are as low as 1.6-1.7
mmol/L( normal range 2.20 – 2.55 mmol/L).
 Oral calcium supplementation with calcium carbonate is
usually adequate , and although Vitamin D may be used
to treat hypocalcaemia of AKI, it rarely has to be added.
 Effervescent calcium tablets should be avoided because
they contain a high sodium or potassium load.

AKI
 INFECTIONS
 Patient with AKI are prone to infection and septicemia, which
can ultimately cause death.
 Bladder catheters , central catheters and even peripheral
intravenous lines should be used with care to reduce the
chance of bacterial invasion.
 Leucocytosis is sometimes seen in AKI and does not
necessarily imply infection.
 However, pyrexia must be immediately investigated and
treated with appropriate antibiotic therapy if accompanied by
toxic symptoms such as disorientation or hypotensive
episodes.
 Antibiotic therapy should be broad spectrum until a causative
organism is identified.

AKI
 Uremic GI Erosions
 Uremic GI erosions are a recognized consequence of
AKI, probably as a result of reduced mucosal cell
turnover owing to high circulating levels of uremic toxins.
 Proton pump inhibitors and H2 antagonists are effective,
 However, PPI should be used with cautions in hospitals
where there are significant rates of CLOSTRIDIUM
DIFFICILE diarrhea, because they may predispose to
the development of this organism.
 H2 antagonists are an appropriate alternative.
 Also PPI also causes AKI.

AKI
 NUTRITION
 There are 2 major constraints concerning the nutrition of
patients with AKI:
1. Patients may be anorexic, vomiting and too ill to eat.
2. Oligouria associated with renal failure limits the volume
of Enteral or parenteral nutrition that can be safely
given.
 Patients with AKI on RRT should receive a
basic intake of at least 1.5 g/kg/day of protein with an
additional 0.2 g/kg/day to compensate for amino
acid/protein loss during RRT, especially when daily
treatments and/or high efficiecy modalities are used.

Acute renal failure

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