Dr.

Vineet Chaturvedi
Acute Kidney Injury
Abrupt increase in the blood concentration of
creatinine and nitrogenous waste products and
by the inability to regulate fluid and electrolyte
homeostasis appropriately
A Common, Serious Problem

 Present in 5% of all hospitalized patients, &

up to 30% of ICU patients
 Incidence is increasing at an alarming rate
 Mortality rate >50% in dialyzed ICU patients
 25% of ICU dialysis survivors progress to
ESKD within 3 years
Terminology
 More than 30 different definitions

 Change in nomenclature of this condition to acute kidney

injury (AKI), acknowledging that acute renal dysfunction
occurs due to injurious endogenous or exogenous disease
processes

 Recently, a group of pediatric and adult nephrologists and

intensivists founded the Acute Dialysis Quality Initiative and
proposed a consensus definition called the RIFLE classification
 In 2004, a consensus definition for AKI was
proposed by the Acute Dialysis Quality Initiative:
the RIFLE criteria
- R = risk for renal dysfunction
- I = injury to the kidney
- F = failure of kidney function
- L = loss of kidney function
- E = end-stage renal disease
 Pediatric RIFLE criteria

 The adult-derived RIFLE definition was modified, and then

applied and validated in pediatric patients and renamed as
the pediatric RIFLE (pRIFLE) criteria.
 pRIFLE stratifies AKI from mild (RIFLE R, risk) to severe
(RIFLE F, failure) based on changes in the SCR or estimated
creatinine clearance (eCCl)
 Estimated creatinine clearance (ml/min/1.73 m2) is
calculated using the Schwartz formula:

eCCl = k × height / SCR

 pRIFLE R –
eCCl decrease by 25%
OR urine output is < 0.5 ml/kg/hr for 8 hr
 pRIFLE I –
eCCl decrease by 50%
OR urine output < 0.5 ml/kg/hr for 16 hr
 pRIFLE F –
eCCL decrease by 75% or eCCl < 35 ml/min/1.73 m2
OR urine output < 0.3 ml/kg/hr for 24 hr or anuric for 12 hr
 pRIFLE L –
persistent failure > 4 weeks
 pRIFLE E –
persistent failure > 3 months (ESRD)
 Pediatric RIFLE criteria definition and classifications of AKI

Pediatric RIFLE criteria

Urine Output Estimated CCl (eCCl)
ml/kg/hr for 8 h 0.5 < eCCl decrease by 25% Risk
ml/kg/hr for 16 h 0.5 < eCCl decrease by 50% Injury
ml/kg/hr for 24 h 0.3 < eCCl decrease by 75% or eCCl Failure
or anuric for 12 h <35 ml/min/1.73 m2
Persistent failure > 4 weeks Loss
Persistent failure > 3 months End stage
 Aetiologic Classification
 Pre-renal

 Renal (intrinsic)

 Postrenal (obstructive)
 Prerenal failure
Decreased true intravascular volume
1. Dehydration
2. GIT losses
3. Salt-wasting renal or adrenal diseases.
4. Central or nephrogenic diabetes inipidus
5. Third space losses:
sepsis
trauma
nephrotic syndrome
Decreased effective intravascular volume
1. congestive heart failure
2. Pericarditis
3. cardiac tamponade
4. hepatorenal syndrome
Prerenal Azotemia
Pathophysiology
Renal
Renal Autoregulation
Autoregulation
myogenic
myogenic reflex
reflex
glomerulotubular
glomerulotubular feedback
feedback
angiotensin
angiotensin IIII

Sodium
Sodium and
and water
water reabsorption
reabsorption
aldosterone
aldosterone
vasopressin
vasopressin
 Mechanisms of Intrarenal Autoregulation
Afferent
Arteriolar Maintenance of
Resistance RBF

Reduced Myogenic Reflex

Renal and Tubuloglomerular Maintenance
Perfusion Feedback of
Pressure Angiotensin II
GFR

Efferent
Maintenance of
Arteriolar
GHP
Resistance
 Mechanisms of Sodium and Water
Conservation in Prerenal Azotemia
Decreased Renal Perfusion
Renin
Vasopressin

Angiotensin II

Aldosterone

Renal Tubular Na
Renal Tubular H2O
Reabsorption
Reabsorption
Urine Volume

Concentrated Urine

Urine Sodium
 Intrinsic ARF

Intrinsic
Intrinsic ARF
ARF may
may be
be due
due to
to the
the following
following broad
broad
categories:
categories:
ischemic
ischemic
acute tubular necrosis
nephrotoxic
nephrotoxic

vascular - glomerular changes

vascular // glomerular
glomerular - minimal tubular involvement

other
other
 Acute Tubular Necrosis

Hypoxic / ischemic ATN

₪ Prolonged prerenal injury OR severe hypoxic insults

₪ Urinalysis → Casts + Epithelial cells

Casts ± low grade proteinuria
₪ Urinary indices: inability to conserve Na+ and water
₪ Serum creatinine ↑↑ 0.5 – 2 mg/dl/day
₪ U/S : Normal sized-kidneys with loss of C.M. differentiation
₪ Prognosis ?? → CKD
₪ Recovery + diuretic phase → attention to fluid and electrolyte balance
 Acute Tubular Necrosis

Nephrotoxic AKI

- Antibiotics
Acyclovir, Cidofovir, Indinavir, Foscarnet, Pentamidine, Aminoglycosides
and amphotericine B
- Organic solvents
Ethylene glycol, Toluene
- Poisons
Paraquat, Snake bites
- Chemotherapeutic agents
Cisplatin, Ifosphamide
- Anti-inflammatory and immunosuppressive agents
NSAIDs, Cyclosporin, Tacrolimus, IVIG, Radiocontrast agents
 Acute Interstitial Nephritis

☻ Reaction to drug OR idiopathic

☻ Presentation:
Fever, Arthralgia, Rash, Uveitis, Eosinophilia,Pyuria
☻ Pathogenesis: Hypersensitivity reaction with the
development of antitubular basement membrane
antibodies
☻Urine microscopy-eosinophils will be present
☻ U/S: large echogenic kidneys
☻ Biopsy: Interstitial infiltrates with many eosinophils
☻ Specific therapy → withdrawal of the drug and
corticosteroid
Etiology of AIN
 Hemolytic Uremic Syndrome
 One of the most common causes of community-acquired
AKI in young children
 Triad of microangiopathic hemolytic anemia,
thrombocytopenia, and renal insufficiency
 HUS has clinical features in common with thrombotic
thrombocytopenic purpura (TTP) which is also characterized
by these features but can include central nervous system
(CNS) involvement and fever and can have a more gradual
onset
 A low platelet count can usually, but not always, be
detected early in the illness, but it can then become normal or
even high. If a platelet count obtained within 7 days after onset
of the acute gastrointestinal illness is not <150,000/mm3, other
diagnoses should be considered
Microangiophathic hemolytic anemia with fragmented
erythrocytes (schistocytes)
Pre-Renal vs. Renal Failure

Renal Prerenal
<20 >20 BUN/Cr
>2% <1% FENa
>1% <1% Renal Failure Index
>40 mEq/L <20 mEq/L UNa
<1.010 >1.020 Specific Gravity
<350 mOsm/L >500 mOsm/L Uosm
<1.3 >1.3 Uosm/Posm
Renal Lecture Required Picture #3
 Postrenal AKI

۩ Obstructive cause
- Solitary kidney
- Ureters bilaterally
- Urethra
۩ Congenital OR Acquired
۩ Rx: promptly relieve the obstruction
ARF - Pathophysiology

 Damage is caused mostly by renal perfusion

problems and tubular dysfunction
 Usual causes
 Hypo-perfusion and ischemia
 Toxin mediated
 Inflammation
ARF – Pathophysiology

 Hypo-perfusion
 Well perfused kidney – 90% of blood to cortex
 Ischemia – increased blood flow to medulla
 Outcome may be able to be influenced by
restoration of energy/supply demands
 Leads to tubular damage
ARF - Pathophysiology

 Oxidative damage
 Especially during reperfusion injuries
 Main players
 Super-oxide anion, hydroxyl radical – highly ionizing
 Hydrogen peroxide, hypochlorous acid – not as
reactive, but because of that have a longer half life
and can travel farther and cause injury distal to the
site of production
ARF - Pathophysiology

 Ischemia
 Damage to mitochondrial membrane and change
of xanthine dehydrogenase (NAD carrier) to
xanthine oxidase (produces O2 radicals)
 Profound utilization of ATP  5-10 minutes of
ischemia you use ~90% of your ATP
 Make lots of adenosine, inosine, hypoxanthine
 ATP

ADP

AMP

Adenylosuccinate Adenosine

IMP Hypoxanthine Inosine

H20 ∙ O2 H2O2

Xanthine

H20 ∙ O2 H2O2

Uric Acid

H20 ∙ O2 CO2

Allantoin
ARF - Pathophysiology

 Once you get reperfusion, the hypoxanthine gets

metabolized to xanthine and uric acid – each
creating one H2O2 and one super-oxide radical
intermediate
 Reactive oxygen species oxidize cellular proteins
resulting in:
 Change in function/inactivation/activation
 Loss of structural integrity
 Lipid peroxidation (leads to more radical formation)
 Direct DNA damage
ARF Pathophysiology

 Amount of damage depends on ability to

replete ATP stores
 Continued low ATP leads to disruption of cell
cytoskeleton, increased intracellular Ca, activation
of phospholipases and subsequently the apoptotic
pathways
ARF Pathophysiology

 Amount of damage depends on ability to

replete ATP stores
 Continued low ATP leads to disruption of cell
cytoskeleton, increased intracellular Ca, activation
of phospholipases and subsequently the apoptotic
pathways
 This endothelial cell injury sparks an immune
response….that can’t be good….
Clinical Approach to AKI:
Pre-, Intra-, and Post-Renal
History
Volume status
Ultrasound
Urinalysis US shows
Urinalysis Normal Hydronephrosis

Urinalysis
Abnormal

Post-Renal
Pre-renal

Tubulointerstial Glomerular and

Disorders Vascular Disorders
 Nephrologists Clinical Approach to AKI
History
Volume Status
Normal Urinalysis Ultrasound Hydronephrosis
Urinalysis

Pre-Renal Vascular Disorders Post-Renal

Abnormal urinalysis

Low ECF Volume Altered renal blood flow

GI losses or hemodynamics
Hemorrhage Sepsis Arterial Prostate disease
Diuretics Heart failure Renal artery stenosis BPH
Osmotic diuresis Cirrhosis/Hepatorenal syndrome Renal artery thromboembolism Cancer
Medications Renal parenchymal disorders Fibromuscular dysplasia
NSAIDs/Cox-2 inhibitors Pelvic malignancy
Takayasu arteritis
ACE inhibitors Stones
Medium vessel
Angiotensin II receptor blockers Polyarteritis nodosa Stricture
Vascular disease Kawasaki disease Retroperitoneal fibrosis
Small vessel
Glomerular Glomerulonephritis
Tubulointerstitial
Disorders Thrombotic microangiopathies
Disorders Cholesterol emboli
Renal vein
Renal vein thrombosis
Abdominal compartment syndrome

Tubular obstruction Acute interstitial nephritis

Crystals Acute tubular necrosis Medication-induced
Calcium oxalate Ischemic Autoimmune
(Ethylene glycol, Nephrotoxic Sjogren syndrome
orlistat) Contrast-induced Sarcoidosis
Indinivir Rhabdomyolysis Infection-related
Acyclovir
Methotrexate
Tumor lysis syndrome
Myeloma cast
nephropathy
Acute Renal Failure -
Diagnosis
 Diagnosis
 Ultrasound
 Structural anomalies – polycystic, obstruction, etc.
 ATN –
 poor corticomedullary differentiation
 Increased Doppler resistive index
 (Systolic Peak – Diastolic peak) / systolic peak
 Nuclear medicine scans
 DMSA – Static - anatomy and scarring
 DTPA/MAG3 – Dynamic – renal function, urinary
excretion, and upper tract outflow
New Biomarkers in AKI
Alternatives to Serum Creatinine
 Urinary Neutrophil Gelatinase-Associated
Lipocalin (NGAL)
 Ann Intern Med 2008;148:810-819
 Urinary Interleukin 18
 Am J Kidney Dis 2004;43:405-414
 Urinary Kidney Injury Molecule 1 (KIM-1)
 J Am Soc Nephrol 2007;18:904-912
 NGAL:
◦ Expressed in proximal and distal nephron
◦ Binds and transports iron-carrying molecules
◦ Role in injury and repair
◦ Rises very early (hours) after injury in animals, confirmed in children having aki

 IL-18:
◦ Role in inflammation, activating macrophages and mediates ischemic renal injury
◦ IL-18 antiserum to animals protects against ischemic AKI
◦ Studied in several human models

 KIM-1:
◦ Epithelial transmembrane protein, ?cell-cell interaction.
◦ Appears to have strong relationship with severity of renal injury
Urine analysis

 Unremarkable in pre and post renal causes

 Differentiates ATN vs. AIN. vs. AGN
 Muddy brown casts in ATN
 WBC casts in AIN
 RBC casts in AGN
 Treatment of AKI

Aims of treatment:

1.Maintenance of Fluid and Electrolyte Homeostasis

2.Preventing Life-threatening Complications
3.Avoiding Further Kidney Injury
4.Providing Apprpriate Nutrition
5.RRT in most severe forms of AKI
 The treatment of AKI divided into:
nondialytic therapy (supportive therapy and medical
management)
dialytic therapy .
 The nondialytic therapy:
to date the only effective nondialytic treatment of AKI entails:

1. Restoration of adequate renal blood flow

2. Avoidance of nephrotoxic medications or those that interfere
with renal compensatory mechanisms
3. Assurance that renal perfusion has been maximized before
exposure to nephrotoxic agents.
 1- Vasoactive agents:

a- dopamine :
 . the use of “renal dose” dopamine(0.5-5 μg / kg / min) to
improve renal perfusion after an ischemic insult has become
very common in ICU(in the absence of hypertension).
 . dopamine increases renal blood flow by promoting
vasodilatation and may improve urine output by promoting
natriuresis.
b- ANP:
an atrial natriuretic peptide, it increases the GFR by dilating
afferent arterioles while constricting efferent arterioles and so
improve GFR , urinary out put .
 : Diuretics therapy -2

 Stimulating urine output eases management of AKI, but the

conversion of oliguric to nonoliguric AKI has not been shown
to alter the course of the disorder.
 Diuretics therapy have no value in patient with established
anuria.
 These agents act by altering tubular function but it should be
recognized that the increase in urine flow does not represent
an improvement in renal function nor does it affect the natural
history of the disease that precipitated the AKI.
1. Mannitol (0.5-1 g/kg delivered over 30 minutes) may increase
intratubular urine flow to limit tubular obstruction and may limit cell
damage by preventing swelling or by acting as a scavenger of free
radicals or reactive oxygen molecules.
 S.E. of mannitol

a. Lack of response to therapy can precipitate congestive heart

failure, particularly if the child’s intravascular volume is expanded
before mannitol
b. Lack of excretion may result in hyperosmolarity.

2. Furosemide (Lasix) (1-5 mg / kg / dose)

 . increases urine flow rate to decrease intratubular obstruction
 . inhibits Na-K ATP ase, which limits oxygen consumption in already
damaged tubules with a low oxygen supply .
 S.E. of Furosemide is ototoxicity. Continuous in fusions may be more
effective and may be associated with less toxicity than bolus
administration.
 :Fluid Balance -3

 Depending on the cause of AKI and the presence or absence

of associated symptoms such as vomiting or diarrhea, children
with AKI may present with hypovolemia, euvolemia, or fluid over
load and pulmonary edema.
 Patients with salt-wasting renal disease, diarrhea or vomiting
may present with fluid deficits that need correction to a euvolemic
state, whereas patients with oliguria or anuria more commonly
present with hypervolemia and need fluid restriction and/or acute
fluid removal to achieve a euvolemic state.
 In some oliguric patients it may be imposible to distinguish
whether oliguria is due to hypoperfusion (hypovolemia) or
impending ATN . so evaluation of the urine may prove helpful in
this regard

. in patient with hypovolemia

 1- urine is concentrated (urine osmolality >500mOsm / kg) because increase

reabsorption of water
 2- urinary Na conc. < 20 m Eq / L because Na reabsorption increase
 3- Fractional excretion of sodium (F.E.Na) is usually <1%

urine / plasma..Na..concentrat ion

 100
urine / plasma..creatinine ..concentration

 4- increase serum BUN to creatinine ratio due to increase tubular reabsorption

of urea.
 5- Increase urine to plasma creatinine ratio because the creatinine is not
reabsorbed.
by contrast in patient with ATN

1- Dilute urine is (osmolality<350mOsm / kg)

2- urine Na conc.>40 mEq / L
3- FE Na > 1%
4- Urine creatinine to plasma creatinine ratio dose not increase
above 20:1 ratio.
5- The serum BUN to creatinine ratio does not increase
 Assessment of the patient for fluid balance
 . Weight, BP, heart rate, skin turgor and capillary refill are each
used to assess the intravascular volume.
 1- in children who are intravascularly volume depleted, 10-20 ml / kg
of normal saline can be infused to reestablish intravascular volume
(dehydrated pt. generally void with in 2 hours) .
 If U.O.P. does not increase and azotemia does not improve after
fluid resuscitation, then catheterization of the bladeler and central
venous pressure monitoring may be necessary to further guide fluid
therapy. This achieved through the use of central venous catheter
that positioned in the central venous area of the right heart is
satisfactory guide to the speed of fluid administration; the CVP
normally between 2 and 12 cm H2O. If clinical and laboratory
evaluations show that the patient is adequately hydrated, then
aggressive diuretic therapy may be considered.
 2- for fluid overload, fluid restriction and/or fluid removal with
dialysis or hemofiltration may be instituted if the child does not
respond to diuretic therapy.
 . when intravascular volume normalized, euvolemia can be
maintained by providing the child with fluid to replace normal
water losses from the skin, respiratory tract, and GIT (insensible
losses, 400 ml / m2 / 24hr. + UOP)
 . excess losses need to be accounted for as well and replaced
with the appropriate fluid.
 In general, glucose containing solutions (10-30%)with out
electrolytes are used as maintance fluids . the composition of
the fluid may be modified in accordance with the state of
electrolyte balance.
 . daily weight measurements, BP, accurate fluid input & output
records, physical examination and nutritional needs of the child
guide ongoing fluid therapy.
 4-Electrolyte and Acid-Base Balance:
 1. Na+ Balance

 . mild hyponatremia is very common in AKI due to hyponatremic dehydration

but fluid overload with dillutional hyponatremic is much more common.
 . if the serum Na level is >120 m Eq / L , fluid restriction or removal by dialytic
therapy corrects the serum Na.
 . However, if the serum Na level is <120 m Eq / L , the child is at higher risk for
seizures due to hyponatremia and correction to a Na level of approximately
125m Eq / L with hypertonic saline should be considered.
 The amount of Na required can be calculated by the following formula:(125-
PNa ) (wt. in kg) (0.6) = mEq Na
 The required amount is usually infused over several hours to ovoid rapid
correction of serum Na level .
 Rapid correction of the serum Na conc. In adults with chronic hyponatermia
has been associated with Neurologic injury, particularly central pontine
myelinolysis althongh the incidence of such injury in children is unknoun .
 2. K+ balance:
 Common and potentially life threatening.
 . kidney tightly regulates K+ balance and excretes approximately 90% of dietary
K+ intake.
 a. decrease filtration
b. impaired tubular secretion.
c. altered distribution of K+ by acidosis, which shifts potassium from the
intracellular to the extracellular compartment
d. release of intracellular K+ due to the associated catabolic state.
 True hyperkalemia results in disturbances of cardiac rhythm by its depolarizing
effect on the cardiac conduction pathways .
 ECG: → Tall, peaked T waves are the first manifestation of cardiotoxicity, and
prolongation of the PR interval, flattening of P waves & widening of QRS
complexes are later abnormalities. Severe hyperkalemia leads to ventricular
tachycardia and fibrillation.
 . symptoms of hyperkalemia include malaise, nausea & progressive muscle
weakness.
 . Treatment of hyperkalemia is indicated if cardiac conduction abnormalities
are noted or if the K+ levels are higher than 6 to 7 mEq/L.
 Table : Treatment of Hyperkalemia

Complications Onset of effect Dose Mechanism Agent

Hypernatremia Change in .min 15-30 mEq/kg IV over 0.5-1 Shifts K+ into cells Sodium bicarbonate
ionized calcium level .10-30 min

Bradycardia Arrhythmias Immediate mL/kg over 5-15 0.5-1 Stabilizes membrane Calcium gluconate
Hypercalcemia .min potential (10%)

Hypoglycemia .min 30-120 Glucose 0.5 g/kg Stimulates cellular Glucose and insulin
insulin 0.1 U/kg IV +
uptake of K
.over 30 min

Tachycardia .min 30 mg nebulizer 5-10 Stimulates cellular β – Agonists

Hypertension (adult dose) +
uptake of K (albuterol)a

Hypernatremia .min 30-60 1g/kg PO or PR in Exchanges Na+ for K+ Sodium polystyrene

Constipation sorbitol across colonic mucosa sulfonate (Kayexalate)
 3. acidosis:
 . as long as the Child’s CNS is intact, respiratory compensation provides partial
correction of the acidosis. But if the child is obtunded, respiratory
compensation may be compromised, which results in severe acidosis.
 . severe acidosis (arterial pH <7.15, serum Hco3 <8 mEq / L “m.mol. / kg”) may
increase myocardial irritability and requires treatment to raise the PH to 7.20
which approximates a serum Hco3 level to 12 mEq / L.
 . severe acidosis can be treated with intravenous or oral NaHCO 3 , oral sodium
citrate solutions, and/or dialysis .
 . it is important to consider the serum total and ionized Ca level
 . because of the risks involved in the rapid infusion of alkali, the acidosis should
be corrected only partially by the IV route according to the correction formula :
 mEq NaHCO3 required =0.3×wt(kg)×(12-serum HCO3 {mEq/L})
 . the remainder of the correction should be accomplished only after
normalization of the serum Ca and phosphorus level may be made by oral
administration of NaHCO3 tablets or Na citrate solution.
 4. Ca + phosphate Balance:
 Hyperphosphatemia treated with dietary phosphorus restriction and with
oral CaCo3 or other Ca compounds
 Dialysis therapy also effectively removes phosphorus, but it cross the
dialysis membranes less readily than uncharged molecules such urea or K+

 . The causes of hypocalcemia in AKI is multifactorial

 a. hyperphosphatemia .
 b. inadequate GI Ca absorption due to in adequate 1,25-dihydroxy vitamin
D production by the kidney .
 c. Skeletal resistance to the action of PTH
 . If hypocalcemia is severe and/or if HCo3 therapy is necessary for
hyperkalemia , treatment with 10% calcium gluconate (100mg/kg up to
aminimum of 1g , or 1ml/kg up to a maximum of 10 ml) should be given
over 30-60 minutes with continuous ECG monitoring .
 . hypocalcemia may also be treated by oral administration of CaCo3 or
other Ca salts.
 5- Medications:
 . when medications are prescribed in AKI, the mechanism of drug
elimination and the metabolic pathway of the drug must be
considered and adjustments made for renal impairment .
 . many drug adjustment tables are based on the level of Renal
function (GFR>50ml/min/1.73m2 ,GFR of 20-50ml/min/1.73m2 , or
GFR<20ml/min/1.73m2) and it is important to estimate the Child’s
level of RF appropriately and to consider the rate of increase in the
serum creatinine level rather than the absolute creatinine level .
 . To prevent further insults to the kidney it is best to avoid
nephrotoxic drugs in ARF , if potentially nephrotoxic drugs are
needed it is appropriate to use them while monitoring drug levels
and potential adverse effects.
 6- Hypertension:
 . HT in AKI is commonly related to volume overload and/or to alterations in vascular tone.
 . if HT is releated to volume overload → diuretic therapy if no response then dialysis or
hemofiltration.
 . antihypertensive drugs may also indicated depending on the degree of BP elevation &
the cause of HT
 . The choice of antihypertension therapy depends on
 a. degree of BP elevation.
 b. presence of CNS symptoms of HT
 c. presence of associated conditions
 d. the cause of AKI
 . For the child who has sever HT and/or is encephalopathic IV therapy with Na
nitroprusside (beginning dose 0.5-1μg/kg/min) is indicated with monitoring of the serum
levels of thiocyanate, a metabolic product of nitroprusside that is excreted by the kidney .
 Alternative therapies include IV labetalol (0.5-3.0 mg/kg/h) also diazoxide (1-5mg/kg/dose),
enalaprilat (0.005-0.01mg/kg/day) and nicardipine (1-3μg/kg/min) .
 . for less sever HT IV hydralazine or sublingual nifedipine can be used , sever hypotension
and tissue ischemia after sublingual administration of Nifedipine, which has been observed
in adult pts, is uncommon in pediatric patients .
 . once the BP is controlled treatment with oral long-acting agents can be initiated.
 7- Nutritional support

 . AKI is associated with marked catabolism & malnutrition leading to delayed

recovery from AKI
 . if GIT is intact and functional, enteral feedings with formula (similac PM 60/40
for Newborns & infants) should be instituted .
 . Dilute formula should be given initially and then feedings can be increase and
concentrated to achieve optimal calories intake.
 . in older children a diet of high-biologic-value protein, low-phosphorus& low-
potassium foods can be used.
 . infants should receive maintenance calories (120 Kcal/kg/day) and older children
appropriate maintenance calories or higher if needed due to the catabolic state
and malnutrition.
 . if enteral feeding are not possible, then hyperalimentation, usually through a
central line, with high concentration of dextrose (25%), lipids (10-20%), and
protein (1-2g/kg/day) should be instituted .
 . if the child is oliguric or anuric and sufficient caloric intake cannot be achieved
while appropriate fluid balance is maintained, dialysis should be initiated earlier
than in the usual case.
 Dialytic therapy (Renal Replacement therapy)

 . The purpose of acute Renal replacement therapy is to remove endogenous and

exogenous toxins and to maintain fluid, electrolyte and acid-base balance until
renal function return
 Indications for RRT
 Still evolving….Generally accepted
 Oliguria/Anuria
 Hyperammonemia
 Hyperkalemia
 Severe acidemia
 Severe azotemia
 Pulmonary Edema
 Uremic complications
 Severe electrolyte abnormalities
 Drug overdose with a filterable toxin
 Anasarca
 Rhabdomyolysis
Renal Replacement Therapy

 Peritoneal Dialysis
 Acute Intermittent Hemodialysis
 Continuous Hemofiltration
 CAV
 CVVH, CVVHD
 And others….
 Peritoneal dialysis
Advantages
 Simple to set up & perform
 Easy to use in infants
 Hemodynamic stability
 No anti-coagulation
 Bedside peritoneal access
 Treat severe hypothermia
or hyperthermia
Disadvantages
 Unreliable ultrafiltration
 Slow fluid & solute removal
 Drainage failure & leakage
 Catheter obstruction
 Respiratory compromise
 Hyperglycemia
 Peritonitis
 Not good for
hyperammonemia or
intoxication with dialyzable
poisons
Intermittent Hemodialysis
Advantages Disadvantages

 Maximum solute  Hemodynamic instability

clearance of 3 modalities  Hypoxemia
 Best therapy for severe  Rapid fluid and
hyperkalemia electrolyte shifts
 Limited anti-coagulation  Complex equipment
time
 Specialized personnel
 Bedside vascular access
 Difficult in small infants
can be used
Continuous Hemofiltration
Advantages Disadvantages

 Easy to use in PICU  Systemic

 Rapid electrolyte correction
 Excellent solute clearances
 Rapid acid/base correction
 Controllable fluid balance
 Tolerated by unstable pts.
 Early use of TPN
 Bedside vascular access
routine
anticoagulation (except
citrate)
 Frequent filter clotting
 Vascular access in
infants
 Therapy to Decrease injury and promote Recovery

 Recovery of Renal function after ATN requires a complex and not fully
understood set of events that leads to restoration of renal blood flow and
regeneration of renal tubular epithelial cells
 a- post-ischmic infusion of growth factors including IGF-1, epidermal GF,
hepatocyte GF →accelerate recovery of rena impairment .
 b- administration of melatonin-stimulating hormone, thyroxine, C5a receptor
antagonist, selective inhibitors of inducible nitric oxide synthase, statins &
novel inhibitor of the Na / H exchange subtype 3 as well as inhibition of
monocyte chemoattractant protein 1 by gene therapy has been shown to
ameliorate AKI
 c- other studies demonstrate that anti-adhesion molecule therapy markedly
decrease ischemic renal injury by preventing adhesion of activated
neutrophils to renal cells.