Renal System
Samah Suleiman
20/4/2006
Urinary tract infections
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is the inflammatory process resulting
from bacterial invasion into urinary
sterile urinary tract
Epithelial cells that line the urinary
tract respond quickly to bacterial
invasion, producing pathogendestroying leukocytes
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Diagnosis of UTI is confirmed by
pyuria-white blood cells, and
bacteriuria-bacteria in the urine
Prevalence: Childhood bacterial UTI is
the second after upper respiratory tract
infections
UTI affect 3-5% of all girls and 1% of
boys by the age 11years
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Escherichia coli which found in the GI
tract is the responsible bacteria for
80% of pediatric UTI
Risk factors
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Anatomic factors such as short and
strait female urethra, situated close to
rectum
Female infants are specially vulnerable
as a result from fecal soiling
Congenital anomalies
In male: UTI is associated with
prostate problems
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UTI is also documented with bowel
dysfunction: this believed to be due to
pressure of the distended rectal
segment and colonic seeding bacteria
via the heamatogenic route
Host factors include reduced immune
response, bacterial adherence
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male found to have greater immune
system immaturity and decreased
resistance to pyelonephritis and
septicemia
uncircumcised male infants has
elevated colonization, more risk for
UTI for the first 6 months of age
breast feeding offer protective benefits
against UTI
Pathophysiology
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The kidneys are essentially regulatory
organs which maintain the volume and
composition of body fluid by filtration of
the blood and selective reabsorption or
secretion of filtered solutes.
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the kidneys are retroperitoneal organs
(ie located behind the peritoneum)
situated on the posterior wall of the
abdomen on each side of the vertebral
column, at about the level of the
twelfth rib. The left kidney is lightly
higher in the abdomen than the right,
due to the presence of the liver
pushing the right kidney down.
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The kidneys take their blood supply
directly from the aorta via the renal
arteries; blood is returned to the
inferior vena cava via the renal veins.
Urine (the filtered product containing
waste materials and water) excreted
from the kidneys passes down the
fibro muscular ureters and collects in
the bladder
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The bladder muscle (the detrusor
muscle) is capable of distending to
accept urine without increasing the
pressure inside; this means that large
volumes can be collected (7001000ml) without high-pressure
damage to the renal system occuring.
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When urine is passed, the urethral
sphincter at the base of the bladder
relaxes, the detrusor contracts, and
urine is voided via the urethra.
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urinary tract is a sterile system, the
slightly acidic urine creates hostile
environment for most alkaline
microorganisms
first line of defense is expulsion via
bladder flushing or voiding-increase
frequent voiding
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immune response start and leukocytes
flood the area
affected tissue become inflamed and
edematous
bacteria release toxin that is alkaline in
nature
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nerve endings responds with painful
bladder spasm to flush out the
pathogen
mucosal infiltration produce
hemorrhagic areas
ureterovesicle junction (UVJ) may be
become incompetent
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transient reflux permits the infection to
ascend into the kidneys- pyelonephritis
result and may cause irreversible renal
involvement (renal parenchymal
scarring with loss of glomeruli)
infants acquire pyelonephritis have
mote extensive renal damage than
children older than 4 years old- have
30% UTI recurrence after the first
infection
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risk of future hypertension or renal
compromise in adulthood
gram-negative septic shock may result
from the pyelonephritis due to bacterial
endotoxins-life threatening condition
child may experience seizures,
hypertension, fever and loss of
consciousness
Assessments
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Lower tract infections usually
presented by increase urinary
frequency, urgency, dysuria,
hematuria, starngeuria (stopping and
starting the urinary stream)
Urine may appear cloudy, blood-tinged
Incontinence, mild fever, and
suprapupic pain are common
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High fever->39C, flank pain, vomiting,
lethargy, and genaralised malaise point
to pyelonephritis
Vomiting, diarrhea, irritable cry, poor
feeding, slow weight gain or weight
loss, diaper rash should raise
suspicion of UTI
Diagnostic tests
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Collecting urine sample:
Midstream urine sample: depends on
the child ability to void
Adhesive urine-collection bag: from
non-toilet trained child
High incidence of contamination
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Recover urine from diaper via
aspiration technique: do not recover
urine from diapers containing gelling
materials for specific gravidity, pH, or
protein
Catheterization: inserting polyurethane
catheter into the bladder by sterile
technique
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Suprapupic aspiration: with a syringe
withdraw urine directly from the
bladder
Blood and protein in the urine confirm
UTI
Leukocyte esterase is an enzyme
released during WBC destruction
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Leukocyte esterase and nitrate testing
are often negative because of frequent
voiding and lower levels of esterase in
the child’s blood
Interventions
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Symptomatic relief
Arrest the spread of infections
Eliminate systemic infiltration of
bacteria
Combined antibiotic therapy, increased
fluid intake, and frequent voiding
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Urinary evaluation and monitoring for
recurrence
Antibiotic therapy for lower UTI include
combined sulfamethoxazole,
nitrofurantoin, penicillins, and
cephalosporins orally for 7-10 days
These may altered after culture results
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Repeated urine specimen should be
collected 48-72hours after initiation of
medication
Increased fluid intake: up to 1000 cc
for the older child to dilute and washed
out endotoxins and tissue debris
Bladder irritants such as chocolate and
caffeine rich should be avoided
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Give mild analgesic such as
acetaminophen
IV therapy: nursing care directed
toward V/S, level of discomfort, intake
and output monitoring
Child and family teaching include
aspects of disease progression and
management, handling of medication
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Discuss the risk factors for reinfection
and recommended prevention
technique
Females whose first UTI before age 5
years and all males should have renal
ultrasound, voiding cystourethrogram
(VCUG), and intravenous pyelogram
(IVP)
Glomerulonephritis
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The glomeruli are the structures of the
kidneys that supply blood flow to the
small units (nephrons) in the kidneys
that filter urine.
In glomerulonephritis, the glomeruli
become inflamed and impair the
kidney's ability to filter urine.
Causes
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systemic immune disease such as
systemic lupus erythematosus (SLE,
or lupus)
Henoch-Schönlein purpura - A disease
usually seen in children that is
associated with purpura (small or large
purple lesions on the skin and
internally on the organs) and involves
multiple organ systems.
Anti-Glomerular Basement
Membrane Disease (Goodpasture's
syndrome)
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Is a clinical group of glomerulonephritis
and pulmonary hemorrhage, mediated
by an anti-glomerular basement
membrane antibody which also reacts
with the basement membrane of
pulmonary capillaries.
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Antibody response is directed toward a
normal antigen present in the GBM
Goodpasture's syndrome and antiGBM disease are classic examples of
autoimmune disorders.
Clinical Course
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Goodpasture's syndrome may occur at
any time, but peaks in the spring and
summer months are common.
It frequently begins with a flu-like
illness with evidence of pulmonary
compromise. Progressive dyspnea,
hemoptysis and occasionally
ventilatory failure occur.
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Urinalysis reveals hematuria with red
blood cell casts and variable
proteinuria.
Patients with Goodpasture's syndrome
require immediate institution of plasma
exchange and immunosuppressive
therapy.
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Patients with an initial serum creatinine
less than 7 mg/dl have a greater
responding favorably to therapy.
Post-Infectious
Glomerulonephritis
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It is the most common form of
glomerulonephritis in children
A common cause is from a
streptococcal infection, such as upper
respiratory infection. Usually from
group A beta-hemolytic streptococci.
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usually occurs more than one week
after an infection and referred to as
acute post-streptococcal
glomerulonephritis, APSGN
The post-streptococcal
glomerulonephritis is primarily a
disease of children, 6 to 7 years of age
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The onset is usually abrupt, with a
latent period of 7 to 21 days between
infection and the development of
nephritis
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Common initial clinical
manifestations of poststreptococcal
glomerulonephritis
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Hematuria
Edema
Hypertension
Oliguria
In most patients hematuria disappears
by 6 months but proteinuria may
persist for two years in a third of
patients
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The prognosis for complete recovery is
excellent in children even
accompanied by initial impairment in
renal function, persistent proteinuria
and the nephrotic syndrome
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Children prostacycline and
prostaglandin E promote the
maintenance of glomerular filtration
It is evidenced that they reduced by
the reduction of their output in the
stage of chronic renal failure.
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The growth of renin and antidiuretic
hormone synthesis in children suffering
from nephrotic glomerulonephritis is
not accompanied by the increase of
the output of prostaglandin E, their
renal antagonist,
This lead to the development of the
edematous syndrome
Generally, Symptoms may
include
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Dark browncolored urine
(from blood and
protein)
Sore throat
Diminished urine
output
Fatigue
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Lethargy
Increased
breathing effort
Headache
High blood
pressure
Joint pain
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Seizures (may
occur as a result
of high blood
pressure)
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Pale skin color
Fluid
accumulation in
the tissues
(edema)
Diagnosis
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Thorough
physical
examination
Complete
medical history
Throat culture
Urine tests
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Blood tests
Electrocardiogra
m (ECG) - to
detects heart
muscle damage.
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Renal ultrasound - to determine the
size and shape of the kidney, and to
detect a mass, kidney stone, cyst, or
other obstruction or abnormalities.
Chest x-ray - to produce images of
internal tissues, and organs onto film.
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Renal biopsy - kidney tissue is sent for
special testing to determine the
specific disease.
Treatment
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Specific treatment will be determined
based on:
Child's age, overall health, and
medical history
The extent of the disease
Child's tolerance for specific
medications, procedures, or therapies
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Expectations for the course of the
disease
Family preference
If glomerulonephritis is caused by a
streptococcal infection, then treatment
will be focused on curing the infection
and treating the symptoms associated
with the infection.
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Other different reason cannot be
cured, so treatments focus on slowing
the progression of the disease and
preventing complications.
Treatment
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Fluid restriction
Decreased protein diet
Decreased salt and potassium diet
Medication, such as diuretics, blood
pressure medications, phosphate
binders - medications to decrease the
amount of the mineral phosphorus in
the blood. immunosuppressive agents
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Dialysis: used for short-term or longterm therapy to remove wastes and
additional fluid from the blood after the
kidneys have stopped functioning.
If glomerulonephritis does not resolve,
long-term kidney failure may need to
be addressed.
Acute renal failure
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Develop rapidly over days or weeks
and classified according to the site of
injury to the kidney:
Prerenal: result from impared blood
flow to or oxygenation of the kidneys
Usuallu cured with early supportive
treatment
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Renal or parenchymal: injury or
malformation of the kidney tissueNeed dialysis
Postrenal: obstruction of the urinary
flow at some level between the kidney
and the urinary meatus –require
surgical removal of the obstruction