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RENAL FAILURE IN CHILDREN Dr. Mai Mohamed Elhassan Assistant Professor Jazan University
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OBJECTIVES
By the end of this lecture each student should be able
to:
Define acute & chronic kidney disease(CKD)
Classify causes of ARF
Discuss the clinical presentation of ARF & CRD.
Discuss the pathophysiology of anemia & renal
osteodystrophy in CKD.
List the clinical & biochemical indicators of dialysis.
List the complications of Acute & CKD
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Acute renal failure(ARF)
It is a clinical syndrome in which a
sudden deterioration in renal function
results in the inability of the kidneys to
maintain fluid & electrolytes
homeostasis.
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Pathogenesis
Classified into:
1. Prerenal
2. Intrinsic renal
3. Post renal
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PRERENAL ARF
Due to inadequate renal perfusion &decreased GFR, common causes include:
Dehydration
Sepsis
Hemorrhage
Severe hypoalbuminemia
Heart failure
If hypo perfusion is sustained intrinsic renal parenchyma damage may occur.
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Intrinsic Renal ARF
Characterized by renal parenchymal damage including
sustained hypo perfusion.
Post infectious glomerulonephritis
Membranoproliferative GN
Lupus Nephritis
Henoch Schonlein purpura
Hemolytic Uremic Syndrome
Acute Tubular Necrosis(nephrotoxic /ischemic insults)
Tumor Lysis syndrome ????
Acute Interstitial Nephritis
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Postrenal ARF
Posterior urethral valve
Bilateral uteropelvic obstruction
Stones
Tumor
others
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Clinical Manifestations
Accurate detailed history
Thorough physical examination(volume status)
Signs of dehydration
Edema
Skin rash
Arthritis
Flank masses
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Laboratory diagnosis
CBC
Urine analysis
Blood urea, K, phosphate & calcium
Serum creatinine
C3 level—SLE--GN
How to differentiate between prerenal & intrinsic renal failure?
o CXR
o Renal US
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Treatment---ARF
Pediatric ICU management
1-conservative treatment
2-Dialysis
Treat the hypovolemia adequately.
Emergency fluid management.
Usually patients void within 2 hours, failure to do so points towards intrinsic or post renal ARF.
if no urine output do diuretic challenge (single iv frusemide)
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Treatment---ARF
Normal intravascular volume give fluids (urine
output plus insensible loss)
Hyper volemic patients treated by fluid restriction.
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Treatment--ARF
Monitor urine output and other outputs and daily weight.
Careful restoration of caloric, fluid and electrolyte losses.
Administer frusemide.
Potassium restriction
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Hyperkalemia
K more than 6 mEq/l requires treatment by:
-Albuterol
-insulin and glucose.
-kayexalate cation exchange resin.
-Restrict potassium
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Hyperkalemia & ECG
Tall, peaked T’s
Wide QRS
Prolong PR
Diminished P
Prolonged QT
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Hyperkalemia
More severe elevation in serum potassium >7
mEq/l requires emergency treatment:
IV Calcium gluconate 10%
Sodium bicarbonate
Insulin with glucose
If no improvement dialysis.
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Treatment ---ARF
Treat metabolic acidosis
Treat other electrolyte disturbance
Treat hypertension
Peritoneal dialysis
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Indications for dialysis in ARF
Volume overload(HF, pulmonary
edema)
Severe metabolic acidosis
Neurologic
symptoms(convulsion,
encephalopathy)
Pericarditis
Anuria
Persistent hyperkalemia
Urea> 150 mg/dl or rapidly rising
Creatinine>10 mg/dl
Calcium/phosphorus imbalance with
hypocalcaemia tetany.
k more than 6.5mEq/l with ECG
changes
Clinical indicators Biochemical indicators
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Chronic Kidney Disease (CKD)
Defined as renal injury (proteinuria) and/or a glomerular filtration rate
<60 mL/min/1.73 m2 for >3 mo
The normal GFR in children is 90 - 130 ml/min/1.73m2
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CKD is divided into 5 stages according to GFR:
GFR
mL/min/1.73 m2 Description Stage
More than 90 Slight kidney damage with
normal or increased filtration 1
60-89 Mild decrease in kidney
function 2
30-59 Moderate decrease in kidney
function 3
15-29 Severe decrease in kidney
function 4
Less than 15 Kidney failure; requiring
dialysis or transplantation 5
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:
- Congenital
- Acquired
- Inherited
- Metabolic
The age of presentation of CKD correlates closely with the underlying cause
☻ < 5 years → congenital
☻ > 5 years → acquired glomerular diseases.
☻CKD related to metabolic disorders and certain inherited disorders (may
present throughout the childhood years.
Etiology– CKD--CRF
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progressive injury with ongoing structural or
metabolic genetic diseases.
Hyper filtration injury
Proteinuria
hypertension
Hyperphosphatemia
Hyperlipidemia
Pathogenesis
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CLINICAL MANIFESTATIONS
Depends on the underlying renal disease.
Anemia
Acidosis
Fluid overload
Hypertension
Renal osteodystrophy
Stunted Growth
Bleeding
Edema
Neurological manifestations
immunodeficiency
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#Anorexia
# vomiting
#bone pain
#headache
#malaise
#Poluuria&polydipsia
#recurrent urinary tract infections
#paler
#Acidotic breathing
#Edema
# irritability
#poor muscle tone
#change in mental alertness
#stunted growth
Signs and Symptoms--CRF
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Other systemic disorders--CRF
Impaired immunologic defense mechanisms.
Neurological complication &uremic encephalopathy.
Duodenal ulcers.
Pericardial effusion & pericarditis.
Pulmonary edema.
Pruritis .
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Investigations
♥ Blood urea nitrogen ↑↑
♥ Serum creatinine ↑↑
♥ S. K + ↑↑
♥ S. Na +↓↓(if volume overloaded)
♥ Arterial pH ↓ (acidosis)
♥ S. Ca++ ↓↓
♥ S. Phosphorus ↑↑
♥ S. uric acid ↑↑
♥ Patients with heavy proteinuria can have hypoalbuminemia
♥ CBC: normochromic, normocytic anemia
♥ Serum cholesterol and triglyceride levels may be elevated
♥Bone x ray (signs of Rickets ,renal osteodystrophy)
♥ Urinalysis:
☻ GN → hematuria and proteinuria
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Treatment of CKD
The treatment of CKD aimed at:
1-replacing absent/diminished renal function
2-slowing the progression of renal dysfunction
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Slowing the progression of kidney
dysfunction
1) Optimum Control of Hypertension
2) Control of proteinuria
3) Maintain Serum Phosphorus within normal range
4) Prompt treatment of infectious complications and
dehydration
5) Correction of anemia
6) Control of hyperlipidemia
7) Dietary Protein restriction
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Multidisciplinary service
Medical
► Nursing
► Social service
► Nutritional
► Psychological
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fluid & electrolyte management
Acidosis
– Sodium bicarbonate is used to maintain the serum bicarbonate level above 22
mEq/L.
Anemia-what are the causes?
– Erythropoietin
– erythropoietin therapy plus iron supplementation.
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Renal osteodystrophy
It is spectrum of bone disorders seen in patients with
CKD.(Bone pain,fractures,muscle weakness,bone deformities)
– The goals of treatment are to prevent bone deformity and normalize growth
velocity
low phosphorus diet
Phosphate binders are used to enhance fecal phosphate excretion.
Ca carbonate and Ca acetate are the most commonly used phosphate binder,.
The cornerstone of therapy for renal osteodystrophy is vitamin D
administration.
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Growth problems
– Growth problems (especially short stature) are very common in
CKD children why?
– CKD children have an apparent growth hormone resistant state
with elevated GH levels but decreased insulin-like growth factor-I
(IGF-I).
– Treatment may be initiated with recombinant human GH- rHuGH
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Nutrition
– Sufficient energy should be provided in the diet
– Proteins of high biological value or ‘good quality’ are preferred.
– Dietary phosphorus, potassium, and sodium should be restricted
according to the individual patient's laboratory studies and fluid balance.
Treat hypertension
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End stage Renal disease--ESRD
ESRD represents the state in which homeostasis &
survival can no longer be sustained without dialysis
& the ultimate goal is renal transplantation.
Plans for renal replacement when a child reaches
stage 4.
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Thanks