Acute renal failure in children

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outline
 Objective
 Etiologies and pathogenesis of ARF
 Classification
 Diagnosis and management

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Objectives
 Understand the etiology and
pathogenesis of ARF
 Request appropriate investigations
 Manage a child with acute renal
failure

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 Acute renal failure or AKI
Definition :
 Loss of renal function measured by a decline in
GFR that develops over a period of hours to days
 Manifested by :
 Oliguria :decreased urine amount. In children <
0.5ml/kg/h, in infants < 1ml/kg/h
 Anuria : no urine production for over 24 hours.

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Pathophysiology
 Three phases in the development of
ARF
 Initiation phase: ischemia or a toxin
sets in motion a sequence of events
which produce an injury to tubular
epithelial cells

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Pathophysiology../2
 Maintenance phase: GFR remains
relatively low for several days
 Recovery phase: characterized by
gradual and progressive restoration
of GFR and tubular function

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Pathophysiology…/3
Three major factors that may account
for the development of ARF:
 Renal hemodynamics, nephronal
factors, metabolic/cellular factors

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Renal hemodynamics
tubular injury
Decreased cortical BF
altered reabsorption of solute & water

release of vasoactive compounds

Increased cortical VR
diminished GF dynamics

decreased GFR

ARF

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Nephronal factors in ARF
proximal tubule injury

epithelial cell necrosis

Loss of tubule integrity impacted cellular debris

Back leak of solute/fluid tubule obstruction

diminished GFR
diminished tubule flow

ARF

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Cellular and metabolic mechanisms
 Oxygen free radical production
contributing to an ischemic insult
 Calcium accumulation in tissues who
have undergone necrosis contributing
to renal cell injury:
- uncouples oxidative phosphorilation
- activation of membrane bound
phospholipases
- activation of intracellular proteases
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Cellular …/2
- Inhibition of Na/K-ATPase
- Direct effect on intracellular pH.
 Depletion of tissue adenine nucleotide
levels which is a source of energy and
concomitant increase in nucleosides,
adenosine, and inosine. These are
responsible for renal vasoconstriction
following an ischemic insult.

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Etiology of ARF
 Pre renal Etiology: oliguria due to
inadequate perfusion of the kidneys
 Renal Etiology: renal parenchymal
cell injury or disease
 Post renal Etiology: results from
mechanical obstruction to urine flow

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Etiology of ARF

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Pre renal ARF
Etiology:
 Hypo perfusion of kidneys. Renal
function (GFR) falls when BP falls
below auto regulatory range. Readily
reversible with prompt correction of
hypo perfusion.
 Decreased cardiac out

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Pathophysiology
Neuro-hormonal:
 Renin Angiotensin II Aldosterone

 ADH

 Catecholamines

 Renal nerves activation

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 glomerular
RBF= Afferent Arteriole flow
Efferent Arteriole constriction
Filtration Fraction=GFR/RBF
GFR= RBF * FF = * =

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tubular
In the Peri-Tubular Capillaries;

Oncotic Pressure

Hydrostatic pressure

Na Absorption

FeNa= u/p Na *100

u/p cre
<1%

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tubular
Water Absorption in Proximal Tubule

Urea Absorption in Proximal Tubule

FeUre= u/pUrea *100

u/p Cre
<30%

Plasma Urea/ creatinine

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Diagnosis
1. P/E: signs of volume depletion, CHF
2. Rise in BUN>Cr (BUN:Cr>20)
3. U-Na<10 mEq/lit (neonates<20
mEq/lit)
4. U-osm>500 mOsm/L (neonates
>400 mOsm/L)
5. FE Na<1%(neonates <2.5%) before
diuretics FENa=(UNa x PCr)
(PNa xUCr)
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Diagnosis…/2
6. Urine sediment normal or granular
casts
7. Response to trial bolus of isotonic
fluid (10-20ml/kg)

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Therapy
 Prompt correction of hypo-perfusion
to prevent renal cell injury
1. Isotonic fluid (RL, NS)
2. Blood transfusion
3. IV albumin, 1g/kg in severe
hypo-albuminemia
4. correct cardiac failure, inotrops

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Intrinsic renal injury
Etiology
1. Ischemia
2. Renal vascular insult: thrombosis,
HUS
3. Toxins: drugs, venoms
4. Endogenous substances: tumor lysis
syndrome, Hg, Rhabdomyolysis
5. Immune mediated, AGN
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diagnosis
1. Sediment : hematuria, proteinuria,
RBC casts, renal tubular epithelial
cells
2. U-Na > 40 mEq/l
3. U-osm < 350 mOsm/L
4. FeNa > 2%

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Therapy
 Use of manitol and diuretics
controversial, may help at the
initiation phase. Manitol 0.5g/kg,
frusemide 1-5mg/kg
1. Fluid balance
If patient euvolemic replace losses:
IWL+UOP+other losses, fluid could
be replaced as 5% DW or ¼ NS

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Therapy…/2
2. Hyperkalemia : Calcium gluconate 10% 0.5
ml/kg IV over 2-4 min with ECG monitoring
- 7.5% sodium bicarbonate, 2-3 mEq/kg
over 30-60 min
- glucose 0.5g/kg, with 0.3u of insulin per
gram of glucose
- cation exchange resin (Kayexalate), 1g/kg
PO or rectally with 1-2 ml/kg sorbitol or 5%
glucose
- Dialysis

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Therapy …/3
3. Hyperphosphatemia and hypercalcemia
seldom need therapy
4. Calories: 400cal/m2 after first 2-3 days to
decrease catabolism
5. Hypertension: fluid and salt restriction,
antihypertensives,
6. Dialysis: In severe fluid overload, severe
hyperkalemia, intractable acidosis,
dialysable toxins, massive tumor lysis

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Postrenal ARF
 Only bilateral obstruction leads to ARF
Etiology :
1. Internal ureteral or bladder obstruction
2. External compression: abdominal mass
3. Bladder paralysis: spinal cord injury
4. Neurogenic bladder dysfunction
5. Vesico-uretheral reflux

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Obstruction of urinary tract
Important to rule out early:
potential for recovery
inversely related to duration

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Diagnosis
1. Palpation of the bladder
2. Bladder catheterization
3. U/S: large distended bladder,
hydronephrosis

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Therapy
 Remove the obstruction
 Bladder decompression by indwelling
catheter
 surgery

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Summary of etiology of ARF
ARF

Pre-Renal Intra-Renal Post-Renal

Vascular Glomerular Tubular Interstitial

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Renal replacement therapy
1. Urgent- uncontrolled hyperkalemia,
metabolic acidosis and volume overload,
pericarditis and significant encephalopathy

2. Uremic symptoms- vomiting, nausea and

anorexia, pruritus and bleeding tendency

3. Laboratory parameters- GFR, creatinine,

urea

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RRT
• Therapy which partially replaces the
kidneys’ functions
• RRT is started when renal function is
severely compromised.
Volume, GFR- uremia, K- acidosis

• Only partial replacement of kidney

functions
• Hopefully, additional to residual renal
function

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 RRT
RENAL
REPLACEM ENT
THERAPY

DIALYSIS TRANSPLANTATION

HEM ODIALYSIS PERITONEAL LIVING CADAVERIC

DIALYSIS DONOR RENAL
TRANSPLANT

INT ENSIVE C C PD
REL A T ED UNREL A T RD K ID NEY K ID NEY-
D O NO R D O NO R PA NC REA S
C O NVENT IO NA L C A PD

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