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Maybelle Tipon-Beltran RN., MD.

•Describes several disease process that results in


glomerular injury
•Result of antigen-antibody deposits within the glomeruli
•School-aged children, more common in boys
 Antibiotics
 Mostly symptomatic; most patients
recovers spontaneously.
 Salt and fluid intake restriction
 Diuretics
 Renal biopsy – if patient does not
recover
 Hypertensiveencephalopathy
 Congestive heart failure
 Uremia
 Anemia
 Obtain history of streptococcal infection
 Obtain culture
 Measure UO and degree of hematuria
and proteinuria
 Weigh child and document areas and
extent of edema
 Obtain baseline BP
 Altered urinary elimination
 Fluid volume excess
 Diversional activity deficit related to
focus on fluid restriction
 Knowledge deficit
•Heavy proteinuria, hypoalbuminemia, and edema with
hyperlipidemia
• More frequent in asian children and in girls than in boys
• Mean age of onset is 21/2 years old
 Loss of charge selectivity of GBM, permits
negatively charged proteins (albumin) to pass
easily through capillary walls into urine
 Excessive urinary loss of protein and
catabolization by kidney of albumin 
hypoalbuminemia
 Osmotic pressure is reduced  edema
 Reduce vascular fluid volume  Hypovolemia
 stimulates RAS
 Tubular reabsorption of Na+ and water 
increase intravascular volume
 Loss of protein (Ig)  prone to infection
 Onset is insiduous – occurs after a mild URTI
 Edema
 First apparent around the eyes
 Dependent edema
 Ascites and/or pleural effusion
 Striae on the skin
 Profound weight gain caused by edema
(double normal weight)
 Decreased UO – concentrated and frothy
 Pallor, irritability, lethargy, fatigue
 GI disturbances – n/v, diarrhea or anorexia
 Urinalysis
Protein – 2+ or greater
Blood – absent or transient
 24 hour urine protein - >2g/m2 per day
 Blood
Total protein – reduced
Albumin - <2g/dl
Cholesterol - >200mg/dl with edema
 Renal biopsy if steroid resistant (no
remission after 28 days of steroid therapy)
 Obtain history of onset
 PE
Vital signs
Auscultation of breath sounds
Areas and extent of edema
Peripheral perfusion (pulse, color, warmth of
extremities)
 Fluid volume excess
 Risk for infection
 Altered nutrition: Less than body
requirements
 Altered family processes
•Bacteria that exist anywhere between the renal cortex
and the urethral meatus
 Causative organisms – E.coli (80%)
 Route of entry:
 Ascent from urethra (most common)
 Circulating blood
 Contributing causes:
 Urinary stasis
 Obstruction, usually congenital
 Vesicoureteral reflux
 Infection elsewhere
 Poor perineal hygiene
 Short female urethra
 Catheterization and instrumentation
 Antimicrobial use
 Congenital renal anomalies
 May be asymptomatic
 Fever – may be accompanied by chills
 Anorexia and general malaise
 Urinary frequency, urgency, dysuria, dribbling
 Daytime or nocturnal enuresis
 Foul odor or change in appearance of urine
 Abdominal or suprapubic pain
 Tenderness over both kidneys
 Irritability
 Vomiting
 Urine culture
>100,000 bacteria/ml – bacteriuria
Catheterized urine specimen: >100 colonies of
bacteria/ml
 Urinalysis
Leukocytes
Casts
Hematuria
 Renal concentrating ability – decreased
 Ultrasound, IVP
 Oral antibiotic for uncomplicated UTI
 Repeat culture before discontinuing
treatment
 Obtainhistory
 Focus assessment on identifying clinical
manifestations
Urethral discharge
High grade fever (upper UTI)
Low grade fever (lower UTI)
 Determine urinary pattern
 Altered urinary elimination
 Pain
 Self-esteem disturbance
Malposition of the urethral opening that may be
associated with other urogenital tract abnromalities; more
common in boys
 Decreased testosterone production in early
gestation
 In males, the urethra opens on the ventral
aspect of the penis
 In females, urethra opens into the vagina
 Undescended testes or inguinal hernia may
be associated
 Increase incidence with future male
siblings
 Inability
to void with the penis in the
normal elevated position
 In females, urine dribbling from vagina
 Not difficult to diagnose. Assess glans
penis for possible hypospadias before
circumcision.
 Genotypic/phenotypic sex
determination, chromosomal, and
hormonal studies
 Renal ultrasound, IVP
 Surgical reconstruction before 1 year of
age
Failure of one or both testes to descend through the
inguinal canal to the normal position in the scrotum.
More common in premature infants.
 Mechanical lesion or endocrine disorder
(rare)
 Testicular and ductal development are
abnormal.
 Degeneration of the sperm forming cells
occurs after puberty
 Testicle non-palpable within the scrotum
 Ultrasound – undescended
 Serum testosterone measurements –
decreased
 Orchiopexy/ orchidopexy surgery –
between ages 1-3 y/o
 Plastic surgery in patients with 1 testicle
 Administration of human chorionic
gonadotropin (hcg)
 Some testicle have descended
spontaneously
•Sudden, usually reversible deterioration in normal renal
function
•Results in fluid and electrolyte imbalance and accumulation
of metabolic toxins.
 n/v
 Diarrhea
 Decreased skin turgor
 Dry mucous membranes
 Lethargy
 Difficulty in voiding, changes in urine flow
 Steady rise in serum creatinine
 Fever
 edema
 Serum creatinine level – most reliable
measure of the GFR; rising
 Radionuclide studies – to evaluate GFR
and renal blood flow
 Urinalysis – proteinuria, hematuria,
casts
 Ultrasonography
 75% - complete recovery
 Correction of any reversible cause (surgery
for obstruction)
 Correction and control of fluid and
electrolyte imbalances
 Restoration and maintenance of stable v/s
 Low sodium, low potassium, moderate
protein diet
 Life threatening complications - Dialysis
 F/E imbalance – hyperkalemia
 Metabolic acidosis – caused by
decrease excretion and HCO3
regeneration
 Insufficient nutritional intake – because
of n/v
 Obtain hx of all medications, recent and
past illnesses or injuries, allergies and
potential exposure to toxic substances
 Measure I/O. Insert indwelling catheter
urinary catheter as indicated
 Monitor v/s.
 Monitor urine specific gravity; fixed
1.010 – inability to concentrate or dilute
urine
 Risk for fluid volume imbalance related
to inability of the kidneys to maintain
fluid balance
 Risk for injury related to hyperkalemia
•Irreversible
destruction of nephrons, so that they are no
longer capable of maintaining normal F/E balance
 Congenital renal and urinary tract
abnormalities (<5y/o)
 Most common causes from 5-15 y/o:
Glomerular disease
Hereditary renal disease
Renal vascular disorders
 GFR – indicates severity of CRF
Lower GFR  greater the loss of renal
function
 Correction of calcium-phosphorus
imbalance
Vitamin D and Calcium phosphate binders
 Correction of acidosis with buffers
 Adequate protein and calories in the diet
 Correction of anemia – erythropoietin SC at
home
 Evaluate growth retardation – give GH
 Hemodialysis, peritoneal dialysis and
transplantation
 Growth retardation
 Delayed or absent sexual maturation
 Severe anemia
 HPN – stimulates RAS
 CHF
 Azotemia/uremia
 Metabolic acidosis
 Electrolyte imbalance – hypocalcemia,
hyperkalemia
 Perform comprehensive, multisystem
assessment to help in planning care
 Assess growth and development status
 Assess coping, support systems, and
other resources
 Risk for injury related to hypocalcemia
 Risk for fluid volume imbalance related to
renal failure and dialysis
 Altered nutrition: Less than body
requirements r/t GI disturbances and diet
restrictions
 Activity intolerance r/t fatigue and anemia
 Coping, ineffective, related to changes in
lifestyle and body image on dialysis
•Dialysis– passage of a solute through a semipermeable
membrane
•Purpose: Preserve life by replacing some of the normal
kidney functions

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