Renal Failure

• Acute Kidney Injury has been traditionally defined as

an abrupt loss of kidney function leading to;
 a rapid decline in the glomerular filtration rate (GFR),
 accumulation of waste products such as blood urea
nitrogen (BUN) and creatinine, and
 dysregulation of extracellular volume and electrolyte
homeostasis.
• ranges from a small increase in serum creatinine to
complete anuric renal failure.
• The incidence of AKI varies from 2–5% of all
hospitalizations to > 25% in critically ill infants and
children.
• The etiology of AKI varies widely according to age,
geographic region, and clinical setting.
• Functional AKI induced by dehydration is usually
reversible with early fluid therapy.
• However, the prognosis for patients with structural
AKI in the intensive care setting with multiorgan
failure remains guarded.
..cont
 Pathogenesis
• AKI has been conventionally classified into
three categories:
• prerenal,
• intrinsic renal, and
• post renal
 PRERENAL

• Dehydration
• Gastroenteritis
• Hemorrhage
• Burns
• Sepsis
• Capillary leak
• Hypoalbuminemia
• Cirrhosis
• Abdominal compartment syndrome
• Cardiac failure
• Anaphylaxis
 INTRINSIC RENAL

• Glomerulonephritis
• -Postinfectious/poststreptococcal
• -Lupus erythematosus
• -Henoch-Schönlein purpura
• -Membranoproliferative
• -Anti–glomerular basement membrane
• Hemolytic-uremic syndrome
• Acute tubular necrosis
• Cortical necrosis
• Renal vein thrombosis
• Rhabdomyolysis
• Acute interstitial nephritis
• Tumor infiltration
• Toxin and drugs
 POSTRENAL

• Posterior urethral valves

• Ureteropelvic junction obstruction
• Ureterovesicular junction obstruction
• Ureterocele
• Tumors
• Urolithiasis
• Urethral strictures
• Hemorrhagic cystitis
• Neurogenic bladder
• Anticholinergic drugs
• Prerenal AKI is characterized by a diminished
effective circulating arterial volume, which leads
to inadequate renal perfusion &a decreased GFR.
• Evidence of structural kidney damage is absent.
• If the underlying cause is reversed promptly, renal
function returns to normal.
• If hypo perfusion is sustained, intrinsic renal
parenchymal damage can develop.
• Intrinsic renal AKI - includes a variety of disorders
characterized by renal parenchymal damage.
• The typical pathologic feature of ATN is tubular cell
necrosis, although significant histologic changes are
not consistently seen in patients with clinical ATN.
• The mechanisms of injury in ATN can include
alterations in intrarenal hemodynamics, tubular
obstruction, and passive backleak of the glomerular
filtrate across injured tubular cells into the
peritubular capillaries.
• Tumor lysis syndrome is a specific form of AKI related
to spontaneous or chemotherapy-induced cell lysis in
patients with lymphoproliferative
• malignancies.
• This disorder is primarily caused by obstruction of
the tubules by uric acid crystals
• Acute interstitial nephritis is another common cause
of AKI and is usually a result of a hypersensitivity
reaction to a therapeutic agent or various infectious
agents
• Post renal AKI includes a variety of disorders
characterized by obstruction of the urinary tract.
• In a patient with two functioning kidneys,
obstruction must be bilateral to result in AKI.
• Relief of the obstruction usually results in recovery of
renal function, except in patients with associated
renal dysplasia or prolonged urinary tract
obstruction.
 CLINICAL MANIFESTATIONS
• Most children come very late/advanced ARF
• Depends on the cause
• Decreased UOP
• Body swelling
• Flank mass

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 Diagnosis
History of
• Fluid loss
• A recent pharyngitis
• Periorbital edema
• Redish discoloration of urine
• Exposure to nephrotoxic medications
• Hematuria
• Oligohydramnios/polyhydramnios
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 Family history
• Family history of renal disease
• Oligohydramnios/polyhydramnios
• Maternal diabetes
• Parental consanguinity
• Previous spontaneous abortions

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 Birth & neonatal history
• Duration of gestation
• Birth weight
• APGAR score
• Duration passage of urine
• Pattern of urine stream
• Umbilical catheterization

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 Infancy & childhood
• Symptoms of UTI
• Hematuria
• Urinary stream
• Enuresis
• Feeding difficulties
• Salt cramming
• Skin/ throat infection

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 Physical examination
• Vital sign
• Anthropometry
• Coloboma & Scleral calcification
• Compression deformities in neonates
• Preauricular pits, ear lobe abnormalities and branchial clefts
• Abdominal examination
• Imperforate anus or abnormal position
• Flank mass
• Feel also for distended bladder
• Sign of GUT anomalies

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• Sign of vertebral anomaly
• Rash , arthritis or skin infection
• Look for edema
• Signs of anemia
• Evidence of rickets or bony deformity
• Level of consciousness
• Motor & sensory examination

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 LABORATORY FINDINGS

• CBC • Antibodies
• Serum electrolyte • Renal U/S
• Serum pH • CXR
• RFT • Serum C3 level
• U/A • Renal biopsy
• Uric acid • Urine pH & specific
gravity

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 Urinary indices
Prerenal AKI Intrinsic AKI

Specific gravity >1.020 <1.010

Urine osmolality > 500 mOsm/kg < 350 mOsm/kg
(UOsm)

Urine sodium (UNa) < 20 mEq/L > 40 mEq/L

Fractional excretion <1% (<2.5% in >2% (>10% in

of sodium neonates neonates)

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 TREATMENT
Medical Management
• Catheterization
• Treating the underlying cause
• Prevention of progression
• Treatment of complications
• Removal of the offending agents

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 Fluid
• Expansion of intravascular volume
Isotonic saline
• in edematous pt
• Fluid restriction to 400 mL/m2/24 hr plus
replacement with ml for ml
• Markedly hypervolemic fluid restriction &
omitting the replacement
• Input & output should monitored daily
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 Diuretics

• Furosemide (2-4 mg/kg)

• Continuous diuretic infusion
• Mannitol (0.5 g/kg) as a single IV dose
• Bumetanide (0.1 mg/kg)
• Dopamine (2-3 μg/kg/min) in conjunction
with diuretic therapy
• Atrial natriuretic peptide
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 hyperkalemia

• Act when K+>6.0 mEq/L

• Eliminated exogenous sources of potassium
• If serum K+>7 mEq/L &/or ECG change
-Calcium gluconate 10% solution, 1.0 mL/kg
IV, over 3-5 min
-Regular insulin, 0.1 units/kg, with glucose
50% solution, 1 mL/kg, over 1 hr

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 Metabolic acidosis
• Due to retention of hydrogen ions, phosphate
& sulfate
• If acidosis is severe (arterial pH < 7.15)
• Serum bicarbonate < 8 mEq/L
• Contributes to significant hyperkalemia
 Acidosis should be corrected partially IV
bicarbonate

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 Hypocalcemia
• PO calcium to avoid deposition of calcium
salts into tissues
• IV calcium only if there is tetany
• low-phosphorus diet
• Phosphate binders (sevelamer, calcium
carbonate, and calcium acetate )
• Aluminum-based binders should be avoided

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 Hyponatremia
• Fluid restriction
• hypertonic (3%) saline
 if symtomatic (seizures, lethargy)
 serum sodium level <120 mEq/L

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GI bleeding
• Oral or intravenous H2 blockers such as
ranitidine are
Hypertension
• Salt and water restriction
• Diuretics
• Antihypertensives

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 Seizures
• Headache, seizures, lethargy, and confusion
(encephalopathy)
• Benzodiazepams are the most effective
agents
• Treating the precipitating cause

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 Anemia
• Transfusion of packed RBCs if Hgb <7 g/dL
• Slow (4-6 hr) transfusion with packed RBCs
(10 mL/kg)
• Use fresh, washed red blood cells
• In severe hypervolemia or hyperkalemia,
tranfuse during dialysis or ultrafiltration

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 Nutrition
• Is of critical importance
• Restrict sodium, potassium, and phosphorus
• Protein intake should be moderately
restricted
• Maximize caloric intake
• In critically ill patients, parenteral
hyperalimentation with essential amino acids

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 Dialysis
Indications
• Anuria/oliguria
• Volume overload refractory to diuretic
therapy
• Persistent hyperkalemia
• Severe metabolic acidosis unresponsive to
medical management

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• Uremia (encephalopathy, pericarditis, neuropathy)
• BUN>100-150 mg/dL (or lower if rapidly rising)
• Calcium:phosphorus imbalance, with hypocalcemic
tetany that cannot be controlled by other measures
• Inability to provide adequate nutritional intake because
of the need for severe fluid restriction
Types
 Hemodialysis
 Peritoneal dialysis
 CRRT
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 PROGNOSIS

Rate depends entirely on the underlying disease

Good prognosis in
• Postinfectious glomerulonephritis (mortality rate <1%)
• Recovery from prerenal causes ATN, acute interstitial
nephritis, TLS
Poor prognosis from
• AKI related to multiorgan failure (mortality rate >90%)
• RPGN
• Bilateral renal vein thrombosis
• Bilateral cortical necrosis
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