Renal/Genitourinary Disorders: Ncm-104 Pediatric Nursing

NCM-104 PEDIATRIC NURSING
RENAL/GENITOURINARY DISORDERS
CARE OF CHILD SUMMARY OF FINAL TOPICS:
WITH
1. GENITOURINARY
GENITOURINARY
2. CNS
DYSFUNCTION 3. MUSCULOSKELETAL
4. ENDOCRINE
5. INTEGUMENTARY
21. Anatomy and A. Renal Physiology
Physiology of the 1. Glomerular filtration
Renal system 2. Tubular function
3. Renal development and
function in early infant
B. Renal Pelvis and Ureters:
Structure and function
C. Urethrovesical unit: structure
and function
A. Signs and Symptoms of
Urinary tract Disorders in

22. Assessment and Different Ages
Diagnostic 1. neonatal period

evaluation
2. infancy
3. childhood
B. Physical test
C. Chemical test
D. Microscopic test
E. Radiologic and other test of
the urinary system function
F. Blood test of the renal function
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A. Phimosis
B. Hydrocele
C. Crytorchydism
D. Hypospadias
23.Congenital E. Epispadias / Extrophy complex
Abnormality/ F. Renal Dysplasia/Hypoplasia
Autoimmune G. Polycystic Kidney Disease
Disorders H. Systemic Lupus Erythematosus
I. Nephrotic Syndrome
A. Urinary Tract Infection
B. Acute Glomerulonephritis
C. Interstitial Nephritis
A. Wilms Tumor
24. Infectious Diseases A. Acute Renal Failure
B. Chronic Renal Failure
C. Dialysis
D. Renal Transplant
25. Renal Tumor
26. Renal Failure
GUS -ADPIE
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Assessment:
• -physical examination
• -history taking
• -radiology
CLINICAL MANIFESTATION:
-the incidence and type of kidney or urinary tract dysfunction changes w/ the age and
maturation of the child. eg. Enuresis has greater significance at age 8 than at age 4.
-in new born, urinary tract disorder are associated w/ number of obvious malformation of
other body system.
Laboratory test:
• urine culture sensitivity.

• Determine presence of pathogen.
• Renal/bladder ultrasound (allows vision of renal parenchyma)
• Testicular (scrotal) ultrasound (allows vision visualization of scrotal content including
testis.)
NURSING CONSIDERATION:
• Observation of any manifestation

• Maintain intake and output measurement.
• Check blood pressure.
• Clinical estimation of creatinine.
• Urine collection (12 or 24 hours)
URINARY TRACT INFECTION:
-10% will have a febrile UTI. During first 2 year of life.
-impossible to localize the infection.
-UTI is applied to the presence micro organism of the urinary tract
-peak incidence of UTI not caused by structural anomalies occurs bet. 2 and 6 years of age.
-females have higher risk for developing UTI.
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CLASSIFICATION:
• Bacteriuria-presence of bacteria in urine.

• Asymptomatic bacteriuria- significant bacteriuria with no evidence of clinical infection.
• Symptomatic bacteriuria- bacteriuria accompanied by physical sign of urinary infection.
• Recurrent UTI-repeated episode of bacteriuria
• Persistent UTI-persistent bacteriuria despite antibiotic treatment.
• Febrile UTI- bacteriuria accompanied by fever
• Cystitis – inflammation of the bladder
• Urethritis – inflammation of the urethra
• Pyelonephritis – inflammation of the urinary tract and kidney
• Urosepsis- febrile urinary tract infection coexisting with systemic signs of bacterial illness
ETIOLOGY:
Escherichia coli organism can be responsible for UTI.
-80% cases
-found in the anal and perineal region.
Other organisms are PROTEUS,PSEUDOMONAS,
KLEBSIELLA,STAPHYLOCOCCUS AUREUS,
HAEMOPHILUS.
ANATOMIC and PHYSICAL FACTORS:
 -lower urinary tract is believed to account for the increased incidence of bacteriuria in females.
 -short urethra which measures about 2 cm. (0.75inch.) in young girls.
 -4 cm in mature women provides a ready pathway for invasion of organism.
 -closure of urethra at the end of micturation may return contaminated bacteria to the bladder.
 -longer male urethra 20cm (8 inch) in an adult. Antibacterial properties of prostatic secretions
 inhibit entry and growth of pathogens.
 -fewer UTI among male infants.
ALTERED URINE AND BLADDER CHEMISTRY
-mechanical and chemical characteristics of the urine and bladder mucosa help urinary sterility.
-increased fluid intake promotes flushing and lower the concentration of organisms.
-Diuresis enhance the anti bacterial properties of the renal medulla
-Most pathogens favor on alkaline medium
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-urine pH of about 5 hampers bacterial multiplication
DIAGNOSTIC EVALUATION:
- Manifestation of UTI depends on the age of the child.

- Diagnosis of UTI is confirmed by detection of bacteriuria.
- Infants and very small children are often difficult for
Urine collection.
• Perineal flora in bag specimen is most frequent cause
Of false positive result.
- should be first thing in the morning
• Suprapubic aspiration (most accurate in 2years of age)
• Dipstick test (quick and in expensive)
• Percutaneous kidney tap
• Ultrasonography
• voiding cystourethrogram (VCUG)
SIGNS AND SYMPTOMS:
Neonatal period (birth to 1 month.)
• Poor feeding
• Vomiting
• Failure to gain weight
• Rapid respiration
• Respiratory distress
• Screaming on urination
INFANCY (1 TO 24 MONTH)
• Excessive thirst
• Frequent urination
• Foul smelling urine
• Pallor
• Fever
CHILDHOOD (2 TO 14 YRS)
• Poor appetite
• Vomiting
• Growth failure
• Swelling of face
• Blood in urine
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Therapeutic management
• To eliminate current infection

• Identify contributing factors
• prevent systemic spread of infection
• preserve renal function
o defects such as primary reflux or bladder neck obstruction
• Surgical correction is necessary
VESICOURETERAL REFLUX
Abnormal retro grade flow of the urine into the
Ureters.
• urine is swept up into the ureters then flows back into the empty bladder, where its
serve as reservoir for the bacteria.
• more likely to be associated with recurring kidney infection
• bacteria from urine has access to bladder going to kidney results to kidney infection
• associated w/ UTI most common cause of renal scarring to children
MANAGEMENT:
• Prevention of bacteria
• Daily dose of anti-biotic
• Urine culture (2to3 months)
• voiding cystourethrogram
PROGNOSIS:
• Progressive renal injury is greatest when infection

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Occurs (2 yrs)
• Early diagnosis of children at risk is important
N. CONSIDERATION:
• instruct patient to observe symptoms of UTI
• Infants, young children not able to express their
Feelings
• Unexplained irritability may assist suspected UTI
• collect appropriate specimen.
• Acceptable clean-voided specimen
• suprapubic aspiration of urine
• 3 to 4 yrs explain w/ doll
• older may use simple diagram
PREVENTION:
•hygienic habits
-females wipe from front to back after voiding/defecating
-void as soon as possible after intercourse
-reccurent UTI frequently maintain low-dose of antibiotics
OBSTRUCTIVE UROPATHY
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Functional abnormalities of urinary system that obstruct
Normal urine flow
-congenital or aquired, unilateral or bilateral
-can occur at any level of the upper or lower urinary tract
-boys are more frequent than girls
MANAGEMENT:
-Early diagnosis & surgical correction
-divert the flow to bypass the obstruction
-placement of temporary nephrostomytube
NURSING CONSIDERATION:
-identify case
-assisting diagnostic
-parents & children needs counseling
-maintain adequate urine flow
NEPHROTIC SYNDROME
Includes massive proteinuria, hypoalbuminemia, Hyperlipemia and edema.
• Idiopathic nephrosis (primary)
• Glomerular damage
• Congenital form
- Glomerular membrane normally permeable to albumin
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Leaks through membrane and lost in urine (hyperalbuminuria)
- reduce the serum albumin (hypoalbuminuria)
CLINICAL MANIFESTATION:
Weight gain
Puffiness of face (facial edema)
Abdominal swelling (ascites)
Pleural effusion
Labial or scrotal swelling
Edema of intestinal mucosa
Poor intestinal absorption
THERAPEUTIC
- Reducing excretion of urinary protein
- reducing fluid retention in the tissue
- preventing infection
- Corticosteroid first line of therapy
ACUTE GLOMERULONEPHRITIS
Acute glomerulonephritis (AGN) is a primary event or a manifestation of a systemic disorder that

can range from minimal to severe. Common features this includes oliguria, edema, hypertension
and circulatory congestion, hematuria, and proteinuria. Most cases are postinfectious and have
been associated with pneumococcal, streptococcal, and viral infections. Acute poststreptoccocal
glomerulonephritis (APSGN) is the most common of the postinfectious renal diseases in
childhood. APSGN can occur at any age but affects primarily early school-age children, with peak
age of onset of 6 to 7 years. It is uncommon in children younger than 2 years of age, and males
outnumber females.
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ETIOLOGY
APSGN is an immune-complex disease that occurs after an antecedent streptococcal infection

with certain strains of the group A-B_hemolytic stertococcus. Most streptococcal infections do
not cause APSGN.the latent period is 10 to 21 days and occurs between the streptococcal
infection and the onset of clinical manifestations.
PATHOPHYSIOLOGY
The glomeruli becomes edematous and infiltrated with the polymorphonuclear leukocytes, which
occlude the capillary lumen. The decrease in plasma filtration results in an excessive
accumulation of water and retention of sodium that expands plasma and interstitial fluid
volumes, leading to circulatory congestion and edema.
DIAGNOSTIC EVALUATION
The onset of nephritis appears after an average latent period of about 10 days. The edema is
relatively moderate and may not be appreciated by someone unfamiliar with the child’s normal
appearance. The urinalysis during the acute phase characteristically shows hematuria and
proteinuria. Proteinuria generally parallels the hematuria and may be 3+ or 4+ in the presence
of gross hematuria.Gros discoloration of the urine reflects red blood cell and hemoglobin
content. Microscopic examination of the sediment shows many red blood cells, leukocytes,
epithelial cells, and granular nad red blodd cell casts. Bacteria are not seen.
CLINICAL MANIFESTATIONS
Edema:
Especially periorbital
Facial edema more prominent in the morning
Spreads during the day to involve extremities and abdomen
Anorexia
Urine:
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Cloudy, smoky brown
Severely reduced volume
Pallor
Irritability
Lethargy
Child appears ill
Child seldom expresses specific complaints
Older children may complain of:
Headaches
Abdominal discomfort
Dysuria
Vomiting possible
Mild to moderately elevated blood pressure
THERAPEUTIC MANAGEMENT
Management consists of general supportive measures and early recognition and treatment of
complications. Children can be treated at home if they have normal blood pressure and a
satisfactory urine output. Those with substantial edema, hypertension, gross hematuria, or
significant oliguria should be hospitalized because of the unpredictability of complications.
Dietary restrictions depend on the stage and severity of the disease, especially on the extent of
edema. During period of oliguria the substantial amounts of potassium are generally restricted.
The regular measurement of vital signs, body weight, and intake and output is essential to
monitor the progress of the disease and to detect complications that may appear at any time
during the course of the disease. Acute hypertension must be anticipated and identified early.
Blood pressure measurements are taken every 4 to 6 hours. Antihypertensive medications as
well as diuretics are given to conrol hypertension.
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HEMOLYTIC-UREMIC SYNDROME
Is an acute renal disease that occurs primarily in infants and small children between the ages of
6 months and 5 years. HUS is the most frequent cause of acquired acute renal failure in
children. The appearance of the disease has been associated with Rickettsia, E. coli,
pneumococci, shigella, and salmonella and may represent an unusual response to these
infections. Multiple cases of HUS caused by enteric infection of the E.coli . serotype have been
traced to undercooked meat, especially ground beef.
PATHOPHYSIOLOGY
The endothelial lining of the small glomerular arterioles are the primary site of injury,which
become swollen and occluded with deposits of platelets and fibrin clots. The Red blood cells are
damaged as they attempt to move through the occluded blood vessels. These damaged are
removed by the spleen, causing acute hemolytic anemia. The platelet aggregation within the
damaged blood vessels or the removal of platelets produce the thrombocytopenia.
The triad of anemia, thrombocytopenia, and renal failure is sufficient for diagnosis. Renal
involvement is evidenced by proteinuria, hematuria, and the presence of urinary casts. Blood
urea nitrogen and serum creatinine levels are elevated. A low hemoglobin and hematocrit and a
high reticulocyte count confirm the hemolytic nature of the anemia.
The most consistently effective treatment of HUS is hemodialysis or peritoneal dialysis ,which is
instituted in any child who has been anuric for 24 hours or who demonstrates oliguria with
uremia or hypertension and seizures.
NURSING CONSIDERATIONS
Nursing care is the same as that provided in the acute renal failure and, for children with
continued impairment, includes management of chronic disease. Because of the sudden and life
threatening nature of the disorder in a previously well child, parents are often ill-prepared for
the impact of hospitalization and treatment. Therefore support and understanding are especially
important aspects of care.
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WILMS TUMOR
Is the most common malignant renal and intraabdominal tumor of childhood. The peak age at
diagnosis is approximately 3 years, and occurrence is slightly more frequent in boys than girls.
ETIOLOGY
Wilms tumor probably arises from a malignant, undifferentiated cluster of primordial cells
capable of initiating the generation of an abnormal structure. Its occurrence slightly favors left
kidney, which is advantageous because surgically this kidney is easier to manipulate and
remove. Studies have shown that development of Wilms tumor is frequently associated with
aniridia, hemihypertrophy, Beckwith-Wiedemann syndrome, or genitourinary anomalies.
Most children with Wilms tumor are brought to the practitioner because of abdominal swelling or
an abdominal mass. Specific tests include radiographic studies, including abdominal and chest
computed tomography scan, hematologic studies, biochemical studies, and urinalysis.
Combined treatment of surgery and chemotherapy with or without radiation is based on the
histologic pattern and clinical stage. Surgery is scheduled as soon as possible after confirmation
of a renal mass, usually within 24 to 48 hours of admission.
Abdominal swelling or mass:
Firm
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Nontender
Confined to one side
Hematuria
• Fatigue
• Hypertension
• Weight loss
• Fever
RENAL FAILURE
is the inability of the kidneys to excrete wasted material, concentrate urine, and conserve
electrolytes. It can occur suddenly in response to inadequate perfusion , kidney disease, or
urinary tract obstruction, or it can develop slowly as a result of long-standing kidney disease or
an anomaly.
ACUTE RENAL FAILURE
ARF is said to exist when the kidneys suddenly are unable to regulate the volume and
composition of urine appropriately in response to food and fluid intake and the needs of the
organism. The principal features of ARF is oliguria. ARF is not common in childhood,but the
outcome depends on the cause, associated findings, and prompt recognition and treatment. The
most common cause in children is transient renal failure resulting from severe dehydration.
PATHOPHYSIOLOGY
ARF is usually reversible, but the deviations of physiologic function can be extreme, and
mortality in the pediatric age group remains high. There is severe reduction in the glomelular
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filtration rate, an elevated blood urea nitrogen level, and a significant reduction in renal blood
flow.
When a previously well child develops ARF without obvious cause, a careful history is taken to
reveal symptoms that may be related to glomerulonephritis, obstructive uropathy, or exposure
to nephrotoxic chemicals. Significant laboratory measurements during renal shutdown that serve
as a guide for therapy are blood uera nitrogen, serum creatinine, pH, sodium, potassium, and
calcium.
Treatment of poor perfusion resulting from dehydration consists of volume restoration. If oliguria
persists after restoration o fluid volume or if the renal failure is caused by intrinsic renal
damage, the physiologic and biochemical abnormalities that have resulted from kidney
dysfunction must be corrected or controlled.
The amount of exogenous water provided should not exceed the amount needed to maintain
zero water balance. When output begins to increase, either spontaneous or in response to
diuretic therapy, the intake of fluid, potassium, and sodium must be monitored and adequate
replacement provided to prevent depletion and its consequences.
Specific:
Oliguria
Anuria uncommon
Nonspecific (may develop)
Nausea
Vomiting
Drowsiness
Edema
Hypertension
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CHRONIC RENAL FAILURE
CRF begins when the diseased kidneys can no longer the normal chemical structure of body
fluids under normal conditions. Progressive deterioration over months or years produces a
variety of clinical and biochemical disturbances that eventually culminate in the clinical
syndrome known as uremia.
PATHOPHYSIOLOGY
Early in the progressive nephrotic destruction, the child remains asymptomatic with only minimal
biochemical abnormalities. Midway in the disease process, as increasing numbers of nephrons
are totally destroyed and most others are damaged to varying degrees, the few that remain
intact are hypertrophied but functional. As the disease progresses to the end stage, because of
severe reduction in the number of functioning nephrons, the kidneys are no longer able to
maintain fluid and electrolyte balance, and the features of uremic symdrome appear. Children
with CRF seem to be more susceptible to infection, especially pneumonia, urinary tract infection,
and septicemia, although the reason for this is unclear.
Laboratory and other diagnostic tools and tests are of value in assessing the extent of renal
damage, biochemical disturbances, and related physical dysfunction. Because the onset is
usually gradual, and the initial signs and symptoms are vague and nonspecific.
In irreversible renal failure the goals of medical management are to
1. promote maximum renal function

2. maintain body fluid and electrolyte balance within safe biochemical limits
3. treat systemic complications
4. promote as active and normal a life as possible for the child for as long as possible.
CLINICAL MANIFESTATION
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Child may complain of:
Headache
Muscle cramps
Nausea
Other signs and symptoms:
Weight loss
Facial edema
Malaise
Bone or joint pain
Growth retardation
Dryness or itching in the skin
Bruised skin
Sensory or motor loss
Amenorrhea
Uremic syndrome (untreated)
Gastrointestinal symptoms
Anorexia
Nausea and vomiting
Bleeding tendencies
Bruises
Bloody diarrheal stools
Stomatitis
Bleeding from lips and mouth
SUPPLEMENT
I. Glomerulonephritis (Acute Poststreptococcal Glomerulonephritis)
A. Description
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1. Glomerulonephritis is a term that includes a variety of disorders, most of which are caused by
an immunological reaction.
2. The disorder results in proliferative and inflammatory changes within the glomerular structure.
3. Destruction, inflammation, and sclerosis of the glomeruli of both kidneys occur.
4. Inflammation of the glomeruli results from an antigen-antibody reaction produced by an

infection elsewhere in the body.
5. Loss of kidney function develops.
B. Causes
1. Immunological diseases
2. Autoimmune diseases
3. Streptoccocal infection, group A, B-hemolytic
4. History of phryngitis or tonsiltis 2 to 3 weeks before symptoms
C. Types
1. Acute: Occurs 2 to 3 weeks after a streptococcal infection
2. Chronic: Can occur after the acute phase or slowly over time
D. Complications
1. Renal failure
2. Hypertensive encephalopathy
3. Pulmonary edema
4. Heart failure
E. Assessment
1. Periorbital and facial edema that is more prominent in the morning
2. Anorexia
3. Decreased urinary output
4. Cloudy, smoky, brown-colored urine
5. Pallor, irritability, lethargy
6. In the older child, headaches, abdominal or flank pain, dysuria
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7. Hypertension
8. Proteinuria that produces a persistent and excessive foam in the urine
9. Azotemia
10. Increased blood urea nitrogen and creatinine levels
11. Increased antistreptolysin O titer (used to diagnose disorders caused by streptococcal

infections)
F. Interventions
1. Monitor vital signs, weight, intake and output, and the characteristics of urine
2. Limit activity, provide safety measures
3. Nutrition
a. Restrictions depend on the stage and severity of the disease, especially the extent of the
edema
b. In uncomplicated cases, a regular diet is permitted but sodium is restricted to a no added salt
to foods diet.
c. Moderate sodium restriction is prescribed for the child with hypertension or edema
d. Foods high in potassium are restricted during periods of oliguria
e. Protein is restricted if the child has severe azotemia resulting from prolonged oliguria
4. Monitor for complications (renal failure, hypertensive encephalopathy, pulmonary edema, and
heart failure).
5. Administer diuretics (if significant edema and fluid overload are present), antihypertensives
(for hypertension), and antibiotics (to the child with evidence of persistent streptococcal
infections) as prescribed.
6. Initiate seizure precautions and administer anti-convulsants as prescribed for seizures

associated with hypertensive encephalopathy.
7. Instruct the parents to report signs of bloody urine, headache, or edema.
8. instruct the parents that the child needs to obtain treatment for infections, specially sore
throats and upper respiratory infections.
II. Nephrotic syndrome
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A. Description
1. Nephrotic syndrome is a kidney disorder charactererized by:
• massive proteinuria
• hypoalbuminemia
• edema
2. The primary objective of therapeutic management is:
- to reduce the excretion of urinary protein
- maintain protein free urine.
B. Assessment findings in nephrotic syndrome
1. Child gains weight
2. Periorbital and facial edema is most prominent in the morning
3. Leg, ankle, labial or scrotal edema occurs
4. Urine output decreases; urine is dark and frothy
5. Abdominal swelling occurs
6. Blood pressure is normal or slightly decreased
C. Interventions
1. Monitor vital signs, intake and output, and daily weights
2. Monitor urine for specific gravity and albumin
3. Monitor for edema
4. Nutrition: A regular diet without added salt is prescribed if the child is in remission; sodium is
restricted during periods of massive edema.
5. Corticosteriod therapy is prescribed as soon as the diagnosis has been determined (monitor
child closely for signs of infection).
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6. Immunosuppressant therapy may be prescribed to reduce the relapse rate and induce long
term remission; therapy may be administered along with the corticosteroid
7. Diuretics may be prescribed to reduced edema
8. Plasma expanders such as salt-poor human albumin may be prescribed for the severely
edematous child
9. Instruct the parents about testing the urine for albumin, medication administration, side
effects of medications, and general care of the child.
10. Instruct the parents regarding the signs of infection and the need to avoid contract with
other children who may be infectious.
III. Nephroblastoma (Wilms’ tumor)
A. Description
1. Wilm’s tumor is a tumor of the kidney that may present unilaterally and localized or bilaterally,
sometimes with metastasis to other organs.
2. Is the most common intra-abdominal tumor in children, and the most curable.
3. The peak incidence is at 3 years of age
4. The occurrence is associated with a genetic inheritance and with a several congenital
anomalies
5. Therapeutic management includes a combined treatment of surgery (partial to total

nephrectomy) and chemotherapy with or without radiation, depending on the clinical stage and
histologic pattern.
B. Etiology
- Unknown
- Siblings of children with Wilms’ tumor have a higher risk of developing the disorder.
C. Pathophysiology
1. The tumor originates from immature renoblast cells located in the renal parenchyma.
2. It is well encapsulated in early stages, but it may later extend into lymph nodes and the renal
vein or vena cava and metastasize to the lungs and other sites.
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3. It is classified into five stages:
a. Stage I - tumor is confined to one kidney
b. Stage II - tumor extends beyond kidney but can be resected
c. Stage III - tumor has residual nonhematogenous tumor cells confined to the abdomen
d. Stage IV - tumor is characterized by distant metastases involving lung, liver, bone, or brain
e. Stage V - tumor involves both kidneys.
D. Assessment findings:
1. Swelling or mass within the abdomen (mass is characteristically firm, nontender, confined to
one side,and deep within the flank
2. Abdominal apin
3. Urinary retention and/or hematuria
4. Anemia (caused by hemorrhage within the tumor)
5. Pallor,anorexia, lethargy (resulting from anemia)
6. Hypertension (caused by secretion of excess amounts of rennin by the tumor)
7.Weight loss and fever
8. Symptoms of lung involvement such as dyspnea, shortness of breath, and pain in the chest, if
metastasis has occurred
E. Interventions preoperatively
1. Monitor vital signs, particularly blood pressure.
2. Place a sign at the bedside: “Do not palpate abdomen.”
3. Palpation of the abdomen may rupture encapsulated tumor which may spread to distant sites.
4. Measure abdominal girth
F. Interventions postoperatively
1. Monitor temperature and blood pressure closely
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2. Monitor for signs of hemorrhage and infection
3. Monitor intake and output and urine output closely
4. Monitor for abdominal distention; monitor bowel sounds and for other signs of gastrointestinal
activity because of the risk for intestinal obstruction.
PHIMOSIS
HYDROCELE
CRYPTORCHIDISM
HYPOSPADIAS
EPISPADIAS
EXTROPHY
RENAL DYSPLASIA
RENAL HYPOPLASIA
POLYCYSTIC KIDNEY DISEASE
SLE
INTERSTITIAL NEPHRITIS
DIALYSIS
RENAL TRANSPLANT
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The Child with Renal

Dysfunction
The Child with Renal Dysfunction
Renal Structure and Function
The kidney’s primary responsibility is to maintain the composition and volume of the body fluids in equilibrium. To
maintain this constant internal environment, the kidney must respond appropriately to alterations in the internal
environment caused by variations in dietary intake and external losses of water and solutes. This is accomplished by
formation of urine (the product of glumerular filtration), tubular reabsorption, and tubular secretion. Reabsorption is
the transport of a substance from the tubular lumen to the blood in surrounding vessels. Secretion is the transport in
the blood in surrounding vessels.
A secondary function to the kidney is the production of certain humoral substances. One substance is an
enzyme, erythropoietin- stimulating factor (or erythrogenin), which acts on a plasma globulin to form erythropoietin,
which in turn stimulates erythropoiesis in the bone marrow. Its production increased in the presence of hypoxia and
androgens. Another enzyme, renin, is also secreted by the kidney in response to reduced blood volume, decreased
blood pressure, or increased secretion of catecholamines. Rennin stimulates the production of the angiotensins,
which produce arteriolar constriction and elevation in blood pressure and stimulate the production of aldosterone by
adrenal cortex.
Renal Physiology
The structural and functional unit of the kidney is the nephron, which is composed of complex system of tubules,
arterioles, venules, and capillaries. The nephron consists of the Bowman capsule, which encloses a tuft of capillaries
and is joined successively to the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule, and the
straight or collecting duct. Collecting tubules join larger ducts, and all the larger collecting ducts of one renal pyramid
join to form a single duct that opens into a minor calyx.
The blood supply to the kidneys constitutes approximately one fifth of the total cardiac output; therefore profuse
bleeding can accompany renal trauma. Because interstitial tissue is sparse, individual nephrons with their blood
vessel component are closely packed together. Each nephron is supplied by a sizable afferent arteriole, which
separates into capillary loops that constitute the glomerular tuft. Blood leaves by small efferent arteriole. From there
the efferent arterioles branch into peritubular capillary network and hairpin loops called the vasa recta, which parallel
the loops of Henle and collecting ducts. The total surface area of the renal capillaries air approximately equal to the
total surface of the tubules.
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The Bowman capsule is composed of two cellular layers that separate the blood from the glumerular filtrate-the
capillary endothelium and layer of tubular epithelial lining cells. Situated between these layers is the basal lamina, or
basement membrane.
Glomerular Filtration
Filtration through the glomerular capillaries is governed by the same mechanism as filtration across other capillaries
in the body. The filtration capacity of the gomerulus is product of permeability of glomerular capillaries and three
pressure forces: glomerular hydrostatic pressure, colloidal osmotic pressure, and intracapsular pressure.
Tubular Function
The function of renal tubules is to modify the glomerular filtrate. The absorption is selective and discriminating for
substances essential to body processes and equilibrium, whereas nonessential substances are eliminated as waste.
The substances are secreted or reabsorbed in the tubules by osmosis, passive movement down a chemical or
electric gradient, or are actively transported against these gradients. These processes operate throughout the length
of tubules, but there are variations in types, amounts, and mechanisms by which substances are secreted or
reabsorbed in the different tubular segments; these variations are caused in large part by cellular characteristics of
each segment.
Renal Development and Function in early Infancy
Development of the kidney begins with the first weeks of embryonic life but is not completed until about the end of
the first year after birth. The nephrons increase in number throughout gestation and reach their full complement by
birth. However, at this point they are immature and less efficient than at later ages. Many of the tubular sections are
not fully formed, and the glomeruli enlarge considerably after birth.
Glomerular Filtration and absorption are relatively low in the infant and do not reach adult values until between 1
and 2 years of age. This appears to be related to a barrier imposed by more cuboida- shaped glomerular epithelial
cells and higher afferent arteriole resistance. Consequently the newborn is unable to dispose of excess water and
solutes rapidly or efficiently.
Other characteristics of the newborn’s kidneys result in renal function that differs fro that old of older children and
adults. Because of some as yet undetermined cause, newborn infants are unable to excrete a water load at rates
similar to those of older persons. Hydrogen ion excretion is reduced, acid secretion is lower for the first year of life,
and plasma bicarbonate levels are low. Because of these inadequacies of the kidney and because of less efficient
blood buffers, the newborn is more liable to develop severe metabolic acidosis.
The kidney functions during fetal life and produces urine that contributes to the amniotic fluid volume. The 24
hour urine volume is low at birth, rapidly increases in the neonatal period, and steadily increases with normal growth.
The kidneys continue to grow in size until body growth is complete in adolescence.
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Renal Pelvis and Ureters: Structure and Function*
The renal pelvis is funnel-shaped structure that originates at the major calyces and terminates in the funnel- shaped
uteropelvic junction. The ureter is a thin mucomuscular tube that extends from uteropelvic to the uterovesical
junction in the base of the bladder. Three areas- the uteropelvic junction, the uterovesical junction, and the segment
nearest the sacroiliac junction – are particularly narrow and prone to obstruction when a solid body (such as
calculus) passes.
The principal function of the renal pelvis and ureter is transport of urine from the kidney to the bladder. Urine is
moved via a process called peristalsis, whereby muscular movements originating in the renal pelvis propel a bolus of
urine toward the urinary bladder for storage and eventual evacuation when the child urinates. The renal pelvis stores
only a relatively small volume of urine (approximately 15ml on adults) before contraction is triggered that pushes the
urine toward the bladder. The forward movement of urine from the kidney to the bladder is efflux, whereas abnormal
or backward urine movement is termed reflux.
The uterovesical junction joins the ureters and bladder. It is made up of three principal components: the lowest
segment of the ureter, the trigone muscle and the adjacent bladder wall. The ureters allow the passage of urine from
the upper urinary tracts while preventing regurgitation of urine from bladder to the ureters. During bladder filling,
intravesical pressure remains relatively low and the detrusor muscle remains in relaxed state. A peristaltic
contraction of the ureter propels urine into the bladder. During micturition, the intravesical pressure raises as the
detrusor muscle contracts; this raises the potential for harmful reflux into the upper urinary tracts.
Urethrovesical Unit: Structure and Function*
The Urethrovesical unit consists of the bladder, urethra, and pelvic muscles; it is also called the lower urinary tract.
The urinary bladder is a muscle- lined sac that stores and empties itself of urine. In the infant the bladder lies entirely
in the abdomen. The bladder assumes its place in true pelvis shortly before puberty. This change in position is
caused by maturation of pelvic bone rather than migration of the bladder and urethra.
The bladder is characterized by two inlets and single outlet. The base of the bladder is relatively fixed, triangular
area consisting of the bladder neck and trigone. In contrast the body of the bladder neck and trigone.
One of the four layers of the bladder wall consists of smooth muscles bundles that promote bladder evacuation
via micturition. Collectively this muscular tunic is called the detrusor. The muscular tunic of the bladder wall also
contains collagen, a tough, nonelastic substance that maintains the integrity of the bladder wall while also preventing
overdistention.
The urethra is a mucomuscular tube that connects the external meatus and the bladder. The male urethra
originates at the bladder neck, piercing the prostate and pelvic floor before tunnelling through the posterior portion of
the penis and terminating at the glans penis.
The female urethra follows a relatively short, straight course compared with the male. It originates at the bladder
base and terminates an external meatus located immediately superior to the vaginal orifice.
26
The primary responsibilities of the bladder are to store urine manufactured by the kidneys and to evacuate this
urine at regular intervals via the process of micturition. During infancy the bladder is expected to empty
spontaneously; by the fourth year of life the child is expected to gain control of detrusor and urethral sphincter
function. Control of the Urethrovesical unit is referred to as urinary continence.
Clinical manifestations
As in most disorders of childhood, the incidence and type of kidney or urinary tract dysfunction change with a child’s
age and maturation. In the newborn, urinary tract disorders are associated with a number of obvious malformations
of other body systems. Important signs and symptoms that suggest possible renal or genitourinary tract disease in
children at different ages are outlined below.
Signs and symptoms of Urinary Tract Disorders or Disease at Different Ages
NEONATAL PERIOD (BIRTH TO 1 MONTH)
Poor feeding
Vomiting
Failure to gain weight
Rapid respiration (acidosis)
Respiratory distress
Spontaneous pneumothorax or pneumomediastinum
Frequent urination
Screaming on urination
Poor urinary system
Jaundice
Seizures
Dehydration
Other anomalies of stigmata
Enlarged kidneys or bladder
INFANCY (1 TO 24 MONTHS)
Poor feeding
Vomiting
27
Failure to gain weight
Excessive thirst
Frequent urination
Staining or screaming on urination
Foul- smelling urine
Pallor
Fever
Persistent diaper rash
Seizures (With or without fever)
Dehydration
Enlarged kidneys or bladder
CHILDHOOD (2 TO 14 YEARS)
Poor appetite
Vomiting
Growth Failure
Excessive thirst
Enuresis, Incontinence, frequent urination
Painful urination
Swelling on face
Seizures
Pallor
Fatigue
Blood in urine
Abdominal or back pain
Edema
Hypertension
Tetany
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Laboratory Test
• Urine and blood tests- detection of renal problems
• Urinalysis- most important test
Glomerular Filtration Rate- is a measure of amount of plasma from which a given substance is totally cleared in 1
minute.
*clearance of creatinine- is the most useful clinical estimation of glomerular filtration rate
Nursing Care Management
• Observation of the child for any manifestations that may indicate dysfunction
• Accurate measurement and recording of weight, intake and output, and blood pressure
• Preparing infants, children, and parents for tests and collection of urine and blood specimens
• Assist with more complex diagnostic test (e.g., radiography, cystoscopy)
Genitourinary Tract Disorders

Urinary tract Infection
Urinary tract infection is a clinical condition that may involve the urethra and bladder and the ureters, renal pelvis,
calyces, and renal parenchyma. Because it is often impossible to localize the infection, the broad designation UTI is
applied to the presence of significant numbers of microorganisms anywhere within the urinary tract. Infection of
urinary tract may be present with or without clinical symptoms.
Etiology
Escherichia coli and other gram- negative enteric organisms are most commonly implicated; all are common to anal,
perineal and perianal region. Other organism associated with UTI includes Proteus, Pseudomonas, Klebsiella,
Staphylococcus aureus, Haemophilus, and coagulase- negative staphylococci. A number of factors contribute to the
development of UTI, including anatomic, physical, and chemical conditions or properties of the host’s urinary tract.
Anatomic and Physical Factors: The structure of the lower urinary tract is believed to account for the increased
incidence of bacteriuria in Females The short urethra, which measures approximately 2cm in young girls and 4cm in
mature women, provides a ready pathway for invasion of organisms,
The single most important host factor influencing the occurrence of UTI is urinary stasis. Ordinarily urine is sterile,
but 37* C it provides an excellent culture medium Under normal conditions the act of completely and repeatedly
emptying the bladder flushes away any organisms before they have an opportunity to multiply and invade
surrounding tissue.
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Incomplete bladder emptying may result from reflux, anatomic abnormalities, or extrinsic ureteral or bladder
compression. Urinary stasis may also occur because of dysfunctional voiding describes a constellation of symptoms
that are closely associated with the development of UTIO and secondary vesicoureteral reflux.
Treating constipation and administering antibiotic therapy for UTI reduces the recurrence of infection; failure to
relieve the fecal retention in spite of adequate treatment of the UTI may result in recurrence.
Other Extrinsic factors that can contribute to UTI include Catheters, especially short- term indwelling catheters, and
administration of antimicrobial agents. Sexual intercourse may produce transient bacteriuria in females and is
associated with an increased risk of UTI.
Altered Urine and Bladder Chemistry: Several mechanical and chemical characteristics of urinary tract promote
urine sterility. Adequate fluid intake promotes urinary transport and lowers the concentration of pathogens in the
urine. Diuresis also enhances the antibacterial properties of the renal medulla, probably as a result of increased
blood flow, which hastens leukocytosis, and diuresis promotes the mechanical removal of pathogens.
Much has been reported about the use of cranberry juice for the prevention of UTI. This mechanism was thought to
result from increased urine acidity and adherence of bacteria to the bladder lining.
Pathophysiology
Invasion of the bacteria first line of defense in the lower urinary tract is complete evacuation by voiding
inflammation in the bladder and urethral walls in apparent within 30 minutes of invasion by bacterial pathogen
polymorphonuclear leukocytes rapidly migrate to the bladder wall completely injected within 2 hours
Clinical Manifestation
Children < 2 yrs. Old:
• Failure to thrive
• Feeding problems
• Vomiting
• Diarrhea
• Abdominal distention
• Jaundice
Newborn:
• Fever
• Hypothermia
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• Sepsis
• Frequent or infrequent voiding
• Constant squirming
• Irritability
• Strong- smelling urine
• Abnormal stream
• Persitent diaper rash
Children > 2 yrs. Old:
• Enuresis or daytime incontinence in the child who has been toilet trained
• Fever
• Strong foul- smelling urine
• Increased frequency of urination
• Dysuria
• Urgency
• Abdominal pain or costovertebralangle tenderness (flank pain)
• Hematuria
• Preschoolers may vomit
• There is a high frequency of obstructive uropathy in young infants infants and boys which is characterize by:
o Dribbling of urine
o Straining with urination
o Decrease in force and siize of the urinary stream
o High fever
o Chills
o Flank pain
o Severe abdominal pain
o Leukocytosis
31
Diagnostic Evaluation
Urine with possible infection- appears cloudy, hazy or thick with noticeable strands of mucus and pus; it is also fishy
and unpleasant, even when fresh
A presumptive UTI diagnosis can be made on the basis of microscopic examination of the urine , which opften
reveals pyuria and the presence of at least one bacterium in a gram stain. However, a normal urinalysis may also
be present in asymtomatic bacteriuria.
The diagnosis of UTI is confirmed by the detection of bacteria in a urine culture, but urine collection is often difficult,
espacially in infants and very small children.
The most accurate tests of bacterial content are suprapubic aspiration and pro[erly performed bladder
chatetherization.
Tests to detect bacteriuria are being used with increased frequency in UTI s creening. The plastic dipstick and agar-
coated slide tests are quick and inexpensive methods for detecting infection before opbtaining finsl culture results.
Localization of the infection site may involve more specific tests including urethral cathetrization, bladder washout
procedures, and radioisotope renography. Other gtests, suchj as ultrasonography, VCUG, intravenous pyelography,
and dimercaptosuccinic acid can may be performed after the infection subsides to identify anatomic abnormalities
cotributing to the develoment of infection and existing kidney changes from a recurrent infection.
Theraputic Management
Objectives of treatment of children with UTI are:
(1) Eliminate the current infection
(2) Identify contributing factors to reduce the risk of recurrence
(3) Prevent urosepsis
(4) Preserve renal funtion
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• Antibiotic therapy is guided by laboratory culture and sensitivity test
• Antiinnfective agents (penicillins, sulfonamide, cephalosporins, nitrofurantoin, and tetracyclines
• Children suspected with pyelonephritis and ffever are admitted to the hospital and given appropriate
antobiotics intravenously for a minimum of 48 nhours. Blood and urine culture are obtained on
admission and after therapy
Nursing Care Management
• Identification of of children with UTI
• Education of parents regarding prevention and treatment of infection
• Annual health examination should include in routine
• Instruct parents to observe regularly for clues that suggest UTI
• Collecting an appropriate specimen is essential when infection is suspected
• For children unr 3 to 4 years of age, the procedure can be explained using a doll
• For those who are older, a simple drawing of the bladder, urethra, ureters, and kidneys makes the explanation
more understandable
• If surgery is subsequently indicated, the child will be able to encounter the impending operation with these
facts and undestanding of these procedures, which helps to decrease fear and anxiety regarding more
extensive medical- surgical intervention
• Adequare fluid intake for prevention
• Caffeinated or carbonated beverages are avoided
Prevention:
• Sexually active adeoloscent girls are advised to urinate as soon as possible after intercourse to flush out
bacteria introduced during sex play
• Children who experience recurrent infections complicated by VUR may be given a suppressive or
prophylactic for a period of months or several years
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Vesicouretral Reflux
-refers to the flow of bladder into the ureters. Reflux increases the chance for and perpetuates febrile
urinary infection, because with each void urine is swept up the ureters and then allowed to empty after voiding.
Primary refux refults from a congenital anomaly that affects the uterovesical junction. Ectopic or orthotopic
implantation of the ureter, abnormal tunneling of the intramural ureteral segment, and defects in the confiiguration of
the ureter orifice are associated with primary reflux.
Secondary refux occurs as a result of an acquired condition such as UTI or obstruction. UTI can produce transient
reflux. Neuropathic bladder dysfunction, particularly when poor bladder compliance coexist with bladder outlet
obstruction, may produce secondary refluxas urine seeks to escape the high pressures of the lower urinary tract.
Reflux with infection is the most common cause of pyelonephritis in children. Refluxed urine ascending into
collecting tubules of the nephrons allows the microorganisms to gain access to the renal parenchyma, initiating renal
scarring.
Therapeutic Management
• Non operative therapy is effective in controlling infection
• Therapy consists of continuous low- dose antibactrial therapy with frequent urine cultures, which can usually
be performed at home by dip slide or dipstick methods
• Renal utrasonography is performed 1 month postoperatively to check for ueretral obstruction
• A follow up VCUG is done 3 months after injection to assess for correction of reflux
Nursing Management
• Medical regimen should be emphasized to parents and older children
• Nurses should encourage parents to have theis other children screened using renal utrasonography and
cystography
• Importance of hygiene and frequent voiding schedule are also discussed
Glomerular Disease
Acute Glomerulonephritis
34
- As a classifiacation includes a number of distinct entities. It may be a primary event or manifestation
of a systemicdisorder, and the disease can range from minimum to severe.
- The common features include oliguris, edema, hypertension and cisculatory congestion, hematuria
and proteinuria.
- Acute poststreptococcal glomerulonephritisis the most common of the noninfectious renal disease in
childhood and the one for which a cause can be established in the majority of the cases
Etiology:
- It is now generallyaccepted that APSGN is an immune- complex disease. Most streptococcal

infections do not cause APSGN
- A latent period of 10 to 14 days occurs between the streptococcal infection of the throat or skin and
the onset of clinical manifestations
- The peak incidence of disease corresponds to incidebce of streptococcal inbfections. Disease

secondary to streptococcal pharyngitis is more common in the winter or spring.
Pathophysiology:
Streptococal infection release of a membranelike material from the specific organism into the circulation
antibodies are formed immune- compex reaction occurs after appropriate period immune compelxes become
trapped in the glomerular capillary loop
Clinical Manifestation:
• Mild cold
• Initial sign of nephrotic reaction include
o Puffiness of the face (especially around the eyes)
o Anorexia
o Passage of dark- colored urine
o Edema (more prominent on extremities and abdomen)
o Urine is cloudy, smoky brown or describe as tea or cola
• Pale
• Irritable
• Lethargic
• Headache
35
• Abdominal discomfort
• Dysuria
Diagnostic Evaluation:
Urinalysis during the aute phase characteristically shows hematuria, proteinuria, and increased specific gravity. The
specific gravity is moderately elevatedand seldom exceeds a.020. Proteinuria generally parallels the hematuria but is
not the massive proteinuria seen in nephrotic syndrome. Gross discoloration of urine reflects its red blood cell and
hemoglobin content.
Cultures of the pharynx are positive for streptococci in only a few cases, and the numbers are not significantly greater
than the normal carrier incidence in many communities.
Serologic tests are necessary for diagnosis. Antibody response to the extracellular products of the streptococci
provide indirect evidence of previous streptococcal infection. These include streptolysin O (ASO), antistreptokinase
(ASKase), antihyaluronidase (AHase), antideoxyribonuclease B (ADNase-B), and anticotyladenine dinucleotidase
(ANADase).
Therapeutic Management:
• Recognition and treatment of complications
• Those with substantial edema, hypertention, gross hematuria, or significant oliguria should be hospitalized
• Bed rest is no longer recommended during the acute phase because ambulation does not seem to have an
adverse effect on the course of the disease once the hematuria, edema, hypertention, and azotemia have
abated
• Regular measurement of vital signs, body weight, and intake and output is essential to monitor the disease’s
progress and detect complications that may appear at any time during the course of the disease
• Any hypertension must be anticipated and identified early
• Blood preassure measurement are taken every 4 to 6 hours
• Dietary restrictions depend on the stage and seveity of disease, especially the extent of edema
• Moderate sodium restriction is usually instituted for children with hypertension or edema
• Antibiotic therapy is indicated only for those children with evidence of persistent streptococcal infections
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Nursing Care Management:
• Careful assessment of disease status
• Regular monitoring of vital signs, fluid balance and behavior
• Assessmant of the child’s appearance for signs of cerebral complication is the important nursing function
• For most children a regular dietis allowed but should contain no added salt
• Foods high in sodium and salted treats are eliminated
• Children with mild edema and no hypertension, as well as convalescent children being treated at home, need
follow- up care
• Parents are instructed regarding general measures, including activity, diet, and prevention of infection
Chronic or Progressive Glomerulonephritis

- The majority of cases of renal glomerulonephritis associated with systemic disease. These pose
relatively few problems of diagnosis, and their natural course is fairly predictable
- Chronic glomerulonephritis describes a variety of different disease processes that may be

distinguished from each other by renal biopsy
- Rapidly progressive glomerulonephritis is the term used to describe an acute illness with severe,
acute onset that causes rapidly progressive detorioration of renal function in weeks to months
Pathophysiology:
In most cases of CGN, immunologic mechanisms can be implicated either through direct attack on the kidney or
secondary to the accumulation of immune complexes in the glomerular filter or fibrin deposition from previously
damaged glomeruli. Either can contribute to further glomerular damage and can initiate chronic changes in the
glomerular structure
• Hypertension
• Edema
• Proteinhuria
• Cardiac failure
37
• Dyspnea
• Osteodystrophy
• Anemia
Laboratory findings may include proteinuria, with casts and red and white blood cells. Failing renal function is
evidenced byelevated blood urea nitrogen, creatinine, and uric and acid levels. Electrolyte alterations include
metabolic acidosis, elevated phosphorus, and decreased calcium levels.
• Some forms of CGN are treated with corticosteroids or cytotoxic agents
• Marked hypertension is controlled with antihypertensive agents
• Anemia may require recombinant erythropoietin and iron supplements
• Dialysis and transplantation may be needed to restore relatively good health
Nephrotic Syndrome
- Is the most common presentation of glomerular injuryin children. It is defined as massive proteinuria,
hypoalbiminemia, hyperlipidemia, and edema, but disorder clinical manifestation of a large number
of distinct glomerular disorders in which increased glomerular permeability to plasma protein results
in massive urinary protein loss.
Types of Nephrotic Syndrome
1. Primary- when the syndrome is restricted to glomerular injury
2. Secondary- when it develops a part of synthetic illness
• Minimal Change Nephrotic Syndrome- the disease is rare is in children younger than 6 months of
age, uncommon in infants younger than 1 year of age, and unusual after the age of 8 years.
38
• Secondary Nephrotic Syndrome- nephrotic syndrome may occur or inassociation with glomerular
damage of known or presumed cause.
• Congenital Nephrotic Syndrome- the hereditary form of nephrotic syndrome is caused by recessive
geneon an autosome.
Pathophysiology:
Glomerular membrane becomes permeableto proteins, especially albumin which leak through the membrane and
are lost in the urine the serum albumin level is reduced COP in the capillaries decreases hydrostatic
pressure exceeds the pull of the COP fluids accumulates in the interstitial spaces and body cavities tubular
reabsorption of sodium and water is increased in attempt to increase intravascular volume
• puffiness of the face (especially around the eyes)
• present of periorbital edema
• abdominal swelling
• labial or scrotal sweling
• edema ofintestinal mucosa may cause:
o diarrhea
o loss of appetite
o poor intestinal absorption
• volume of urine decreased
• skin pallor
• irritability
• weight loss
Massive proteinuria is reflected in urinary excretion of protein that often reaches levels in excess of 2 g/m2 of body
surface/ day which relatively greater clearance of low- molecular- weight proteins. Total serum protein
concentrations are reduced and plasma lipids elevated. Serum cholesterol may be as high as 450 to 1500 mg/dl.
39
• bed rest during edema phase
• salt is restricted during periods of massive edema
• diet generous in protein
• corticosteroid therapy
• immunosuppressant therapy
• diuretics
• daily monitoring of intake and output
• daily weight
• assessment of edema
• diuresis with medications and salt and water restriction
• patient must be protected from contact with infected roommates
• parents are taught to detect signs of relapse and to bring child for treatment at the earliest indications
• the child should receive close medical or nursing observation to detect unusual but more serious side effects
Renal Tubular Disorders

- Disorders of renal tubular function include a variety of conditions involving one or more abnormalities
in specific mechanisms of tubular transport or reabsorption, although initially glomerular function is
normal or comparatively less impaired.
- Manifestations of tubular disorders are primarily metabolic disturbances or deficiencies, such as

failure to thrive, metabolic bone disease, or persistent acidosis.
Tubular Function
- The function of tubules is the reabsorption of substances from the glomerular filtrate, including
sodium, potassium, chloride, bicarbonate, glucose, phosphate, and amino acids
40
- The primary functions of distal renal tubules are acidification of urine; potassium secretions; and
selective differential reabsorption of sodium, chloride and water, which determines the final urinary
concentration.
Renal Tubular Acidosis
- Is a syndrome of sustained metabolic acidosis kin which there is impaired reabsorption of

bicarbonate or excretion of net hydrogen ion but in which glomerular function is normal or
comparatively less impaired .
Proximal Tubular Acidosis
- Proximal tubular acidosis is caused by impaired bicarbonate reabsorption in proximal tubule. It may
occur as an isolated defect (primary); however, more often it appears in association with other
proximal tubular disorders (secondary).
- Complications are rare. The disorder to be transient and resolves spontaneously in time
Distal Tubular Acidosis (Type I)
- Is caused by the kidney’s inability to establish a normal pH gradient between tubular cells and
tubular contents. Its most characteristic feature is the inability to produce a urinary pH below 6.0
despite the presence of severe metabolic acidosis.
- May occur as primary, isolated defect in association with other diseases or disorders. Most
secondary causes are rare.
• Administration of sufficient bicarbonate or citrate
• correct associated electrolyte disorders, especially hypokalemia
• Citrate solutions
• Mixture of sodium and potassium
• Sohl solution is effective but has disadvantage of requiring preparation by pharmacist
• Recognizing the possibility of renal tubular acidosis in children who fail to thrive
• Helping parents understand the importance of adhering to medication plan
41
• Children are taught the importance of taking the medications as soon as they are old enough
Nephrogenic Diabetes Insipidus

- is the major disorder associated with a defect in the ability to concentrate urine
- the disease is more variable in female carriers of the defective gene, who may exhibit only a mild
defect in urine- concentrating ability
Clinical Manifestations:
• vomiting
• unexplained fever
• failure to thrive
• severe recurrent dehydration
• hypernatremia
• copious amount of dilute urine
• growth retardation
• provision of adequate volumes of water to compensate urinary loss
• drinking and voiding
• low- sodium, low-solute diet
• use of chlorothiazide or ethacrynic acid diuretics to increase the reabsorption of sodium and water
• anti-inflammatory drugs are administered in conjunction with chlorothiazide
• supplemental potassium may be required to prevent hypokalemia
• families need to be taught o administer medications and help with diet planning
42
• families need to adapt to away- from- home fluid needs and avoid activities that contribute hydration when
fluids may not be available
• genetic counselling is recommended
Miscellaneous renal Disorders
Haemolytic Uremic Syndrome
- is an acute renal disease characterized by a triad of manifestations: ARF, hemolytic anemia, and
thrombocytopenia
Etiology:
• majority of HUS no causative agent
• genetic factors
• prostacyclin deficiency
• neuraminidase
• agglutination
• associated with rickettsia organisms
• viruses such as coxsackievirus, echovirus, adenovirus; E. coli; pneumococci, shigella, salmonella organisms
Pathophysiology:
Injury appears to be endothelial lining of the small glomerular arterioles endothelium becomes swollen and
occluded with deposition of platelets and fibrin clots RBC varec damaged fragmented RBC are removed by the
spleen acute hemolytic anemia fibrin- split products to appear in serum and urine
• diarrhea and vomiting
• upper respiratory tract infection, or occasionally, varicella, measles, or UTI
• anorectic
• irritable
43
• lethargic
• Pallor
• Bruising, purpua, rectal bleeding
• Hypertensive
Triad of anemia, thrombocytopenia, and renal failure is sufficient for diagnosis. Renal involvements evidenced by
proteinuria, hematuria and urinary casts; blood urea nitrogen and serum creatinine levels are elevated.
• Fluid replacement
• Treatment of hypertension
• Correction of acidosis and electrolyte disorders
• Blood transfusion are administered for severe anemia
• Parents are often ill prepared for the impact of hospitalization and treatment
• Support and understanding are especially important aspects of care
Familial Nephritis (Alport Syndrome)
- The syndrome of chronic hereditary glomerulopathy consists of hematuria, high frequency

sensorineural deafness, ocular disorders and CRF.
- The disease appears to be inherited as an autosomal dominant trait.
Unexplained Proteinuria
Can be categorized as:
(1) Transient
44
(2) Persistent
(3) Orthostatic, or postural
Renal Trauma
- Serious injuries of the genitourinary tract are not uncommon in pediatric age- group, with peak incidence
between ages 10 and 20m years
- Renal injury can be suspected in children who complain of flank pain, and often these are abrasions or
contusions on the overlying skin
• Surgical exploration is indicated if there are multiple injuries
• Bed rest for children with less severe injuries
• Care of both child and family is primarily supportive
• Post surgical care if indicated
Renal Failure
- is the inability of the kidneys to excrete waste material, concentrate urine, and conserve electrolytes.
- Two terms are often used in relation to renal failure need some clarification: azotemia is the accumulation of
nitrogenous waste within the blood, whereas uremia as a more advanced condition in which retention of
nitrogenous products produces toxic symptoms.
Acute Renal Failure
- Is said to exist when the kidneys suddenly are unable to appropriately regulate the volume and composition of
urine in response to food and fluid intake and the needs of the organism
Etiology:
- Can develop as a result of a large number of related or unrelated clinical conditions: poor renal perfusion;
acute renal injury; or the final expressions of chronic, irreversible renal disease.
45
Pathophysiology:
Severe reduction in the glomerular filtration rate elevated blood urea nitrogen level decreased tubular
reabsorption of sodium increased concentration of sodium stimulation of the rennin mechanism significant
reduction in renal blood flow
• Oliguria
• Urinary output less than 1mg/hr. (anuria)
• Edema
• Drowsiness
• Circulatory congestion
• Cardiac arrhythmia
• Hyperkalemia
Careful history is obtained to reveal symptoms that may be related to glomerulonephritis; obstructive uropathy; or
exposure to nephrotoxic chemicals, such as ingestion of heavy metals or inhalation of carbon tetrachloride or other
organic solvents or drugs
• Effective management is prevention
• Fluid therapy
• Nephrotoxic drugs
• Foley catheter is inserted to rule out urine retention
• Mannitol or furosimide may be administered rapidly when there is persistent oliguria
• Hyperkalemia may be minimized by reducing catabolism and correcting acidosis

46
• Calcium gluconate (IV), sodium bicarbonate (IV), glucose and insulin(IV)
• Administration of cation to bind potassium and remove it from the body
• Dialysis or continuous hemofiltration
• Monitoring fluid balance, laboratory data and physical manifestations
• Monitoring or assessing fluid electrolyte balance
• Daily intake of small amount fluid served in containers
• IV fluid management
• Presence of supportive, empathetic nurse can provide comfort and stability in threatening and unnatural
environment
• Providing support and reassurance of parents is among major responsibilities
Chronic Renal Failure
- Kidneys are able to maintain the chemical composition of fluid within normal limits until more than 50% of
functional renal capacity is destroyed by disease or injury
- Insufficiency begins when the diseased kidneys can no longer maintain the normal conditions
Etiology:
Common causes:
• Congenital renal and urinary tract malformations
• Vesicourethral reflux
• Glomerular and hereditary renal disease
• Hereditary nephritis
• Congenital nephritic syndrome
• Renal vascular disorders
Pathophysiology:
47
Increasing number of nephrons are totally destroyed few normal nephrons are able to make sufficient adjustments
to stresses to maintain reasonable degrees of fluid and electrolyte balance restricted tolerance to excess or
restrictions severe reduction in the number of the functioning nephrons kidneys are no longer able to maintain
fluid and electrolyte balance
Clinical Manifestations:
• Loss of normal energy
• Blood pressure is sometimes elevated
• Showa less interest in normal activities
• Pallor
• Anemia
• May have headache
• Muscle cramps
• Nausea
• Bleeding tendencies are apparent in bruises, bloody diarrheal stools, stomatitis, bleeding from lips and mouth
• Unpleasant uremic odor to breath
- Usually suspected on the basis of any number of clinical manifestations, a history of prior renal disease, or
biochemical findings
- The onset is usually gradual, and the initial signs and symptoms are vague and nonspecific
• Children are allowed unrestricted activity and to set their own limits regarding rest and exrent of exertion
• Dietary protein intake is limited to the recommended child’s age
• Potassium is not restricted as long as creatinine clearance remains at acceptable limits
• An active vitamin D is prescribed and water- soluble vitamins supplementation
• Reduction of dietary phosphorus
• Decreasing dietary intake of protein for acidosis
48
• Sufficient sources of folic acid and iron should be provide for anemia
• Low- sodium diet and fluid restriction or diuretics for hypertension
• Team effort is more important than ever involves coordination of personnel from medicine etc.
• Diet therapy can become progressively more restrictive and more intense
• Parents may need help in learning to select appropriate foods, read labels carefully for dodium and potassium
content
• The child is required to take variety of medications
Renal Replacement Therapy
- Technologic advances in the care of children with ARF and CRF provide several renal replacement therapies
for maintaining excretory function in acute disease and for prolonging life in those with ESRD
- Dialysis is the process of separating colloids and crystalline substances in solution by the difference in their
rate of diffusion through s semipermeable membrane
- Methods of dialysis currently available for clinical management of renal failure are:
• Hemodialysis, in which blood is circulated outside the body through artificial passage of water and
solutes
• PD, wherein the abdominal cavity acts as a semipermeable membrane through which water and
solutes of small molecular size move by osmosis and diffusion
• Hemofiltration, in which blood filtrate is circulated outside the body by hydrostatic pressure
Hemodialysis
- Is the preferred dialytic method for children with acute conditions such as life- threatening hyperkalemia, or
poisoning with dialyzable compounds
- Is technically difficult children less than 20 kg because their delicately balanced cardiovascular dynamics may
be upset by rapid changes in blood volume and systemic blood pressure
Procedure:
49
- Requires a special dialysis equipment- the hemodialyzer (artificial kidney). Hemodialyzers are available in 2
forms: parallel flow(plate) and hollow fiber
- Hemodialysis requires one of three blood access: grafts, fistulas, or external access device
- The preferred site in the radial artery and a forearm vein
- The creation of a subcutaneous arteriovenous fistula by anastomosing segment of radial artery and
brachiocephalic vein produces dilation and thickening of superficial vessels of the forearm to provide easy
access for repeated venipuncture
- If vessels are inadequate for an autogenous fistula, a synthetic graft may be placed in the arm or thigh with
either a loop or straight configuration
- For a long- term external vascular access, cuffed, dual lumen catheters can be surgically placed similarly to
other central venous access devices
- dietary limitations are necessary in chronic dialysis to avoid biochemical complications
- seizures during or after hemodialysis are now uncommon
Home Dialysis
- with proper cannulization and proper training and education of both the child and the parents, hemodialysis can
be performed at home
- time spent in transportation is eliminated, the environment is more pleasant and secure, the child is able to
assume more active role in the treatment program
- the patient is equipped with a dialysis unit that is used with the vascular access established for outpatient
dialysis
• patient need assurance about the nature of the preparations for dialysis and the conduct of the treatment
• dietary restrictions are particularly burdensome for both children and parents
• allowing children, especially adolescents, maximum participation in and responsibility for their own treatment
program is helpful
• after weeks, months, or years of hemodialysis, the parents and the child feel anxiety associated with the
prognosis and continued pressures of the treatment
Peritoneal Dialysis
- for acute conditions, PD is quick, relatively easy to learn, and safe to perform and requires minimum equipment
and especially trained nurses
50
- PD is a slow, gentle process, which decreases the stress on body organs that can occur with the rapid
chemical and volume changes of hemodialysis. The procedure is indicated for neonates, children with severe
cardiovascular disease, or those who are poor risks for vascular access
- Chronic Pd is preferred form of dialysis for children and parents who are independent, families who live a long
distance from medical center, infants, school- age, children, and adolescents who prefer fewer dietary
restrictions and gender form of dialysis
Procedure:
- In an acute situations PD catheter insertion may be accomplished at the bedside; catheters for long- term use
are placed surgically in the operating room with the patient under anesthesia
- At the time of dialysis a commercially prepared dialysis solution is allowed to flow by gravity through the
catheter and into the peritoneal cavity, where it remains while equilibrium between plasma and dialysis fluid
takes place
- In PD each pass or cycle is characterized by inflow time, dwell time, and drain time
- An acute PD catheter may remain in place for several weeks provided that aseptic techniques adhered to by all
who enter the system
Home Dialysis
- The development of satisfactory methods for CAPD and its alternative, CCPD, has provided additional means
for managing ESRD at home
- Dialysis solution is instilled into the peritoneal cavity through the surgically implanted indwelling catheter. The
warmed solution is allowed to enter the peritoneal cavity by gravity and remains a variable length of time
according to the procedure used
• The nurse is responsible for teaching the family
• Family must learn how to take the vital signs before and after dialysis
• Family need to know how to vary the composition of dialysis solution to compensate for variations of vital signs
• Parents of the young child using CAPD are taught how to exchange bags and manage the procedure at home
• The nurse discuss the diet, medication, and activity and explores feelings about the entire therapeutic program
with the child and the family
• Family is instructed to contact the appropriate persons at the earliest evidence of peritonitis
51
Continuous Venovenous Hemofiltration
- Third type of dialysis or renal replacement therapy used primarily in acute settings in continuous Venovenous
hemofiltration
- This type of therapy uses specialized equipment to ultrafiltrate blood continuously at a very slow rate, with this
procedure, fluid balance may be achieved within 24 to 48 hours after initiation
- Continuous Venovenous hemodialysis air used to remove excess fluid from patients with severe oliguric fluid
overload
- CVVHD is an ideal from of renal replacement therapy for children with fluid overload from surgical procedures
who do not have severe biochemical abnormalities
Transplantation
- Is the preferred means of renal replacement therapy in the pediatric age- group
- Offers the opportunity for a relatively normal lifestyle
- Kidneys for transplant are available from two sources: (1) a living related donor, usually a donor , usually
parent, grandparent, or sibling, or (2) a cadaver donor, wherein the family of a dead or brain- dead patient
consents to donation of a healthy kidney
Procedure:
- The kidney graft is placed in the extraperitoneal space, usually the anterior iliac fossa; the renal artery is
anastomosed to the internal iliac hypogastric artery; the renal vein is anastomosed to the hypogastric vein
and the ureter is implanted into the bladder or anastomosed to the recipient’s ureter
- The primary goal of transplantation is the long- term survival of the grafted tissue
Selection of Donor Tissue
- The source of donor kidney is either a live person or a cadaver soon after death
- The closer the genetic relationship between the donor and recipient, the better the possibility of a long- term
survival
- Unrelated donors are least likely to be compatible
Suppression of the Immune Response
- The immunosuppressant therapy of choice in kidney transplantation is corticosteroids in conjunction with

cyclosporine and azathioprine
52
- Other therapies include antilmphocyte globulin or monoclonal antibodies, administered intravenously for
14 days either for induction or rescue from rejection
Rejection
- Is the most cause of transplant failure
- Can be one of the three types: hyperacute, acute or chronic
- Acute rejection usually occurs between the first few days and months after transplantation but may occur years
later, especially if the patient becomes poorly complaint with immunosuppressant medications
• It is important to remember that transplantation is a treatment that makes a much less negative impact on the
normal life activities of the child
• Corticosteroid therapy
• Working with children and their families during the various stages of renal failure
• Nurses must become familiar with the family
• Family and child need help bin accepting what is happening to them
Critical Thinking Exercises:
Urinary Tract Infection and Constipation
During your assessment of Ginger, a 4 year old admitted to the hospital for a severe urinary tract infection (UTI), her
mother tells you that Ginger has bowel movements every third or fourth day. They are usually large, hard- formed
stools, and Ginger sometimes has trouble evacuating the stool.
Questions:
1. Evidence- Is there a sufficient evidence to draw conclusion about Ginger’s UTI and constipation?
53
2. Assumptions- Describe an underlying assumption about each of the following:
a. UTIs and females
b. Normal bowel patterns for a 4 year old children
c.Association between UTIs and constipation
3. What priorities for nursing care should be established for Ginger?
4. Does the evidence support your nursing intervention?
5. What alternative perspectives might you have?
Answers:
1. Yes. Ginger’s mother reports a history of constipation with large, hard formed stools occurring only every 3 or
4 days. Ginger was diagnosed with a UTI severe enough to be admitted to the hospital
2. a.) The structure of the lower urinary tract is believed to account for the increased incidence of bacteriuria
in females.
b.) A history of hard, large stools occurring every 3 to 4 days is not normal elimination pattern for 4 year old
children.
c.) The presence of a large stool mass within the colon is likely to cause pressure on the bladder and urethra
and not allow the bladder to empty completely. Stasis on the urine can lead to infection
3. The first priority at this time is to begin to treatment for the UTI. Ginger’s diet and fluid intake should be
evaluated and plan developed to prevent constipation in the failure.
4. Yes. Ginger’s history reflects chronic problems with constipation that must be addressed.
5. Ginger might have the risk factors associated with UTIs in children, and these should be explored further. The
single most important host factor influencing the occurrence of UTI is urinary stasis. Other possible of urinary
stasis may need to be considered
Nephrotic Syndrome
Reese is an 8- year old boy with relapsing nephrotic syndrome who has become steroid dependent. During your
initial assessment in the outpatient clinic you identify the following: (1) weight has increased 2 kg (4.4 lbs.) in the
past few weeks; (2) blood pressure is 100/70 mmHg, (3) mother reports that Reese air not urinating very much, and
she does not know how he has been drinking; (4) while you are measuring Reese’s abdominal girth, he guards his
abdomen and complains of stomach ache; and (5) his temperature 38 C (100.4 F) orally. You should first do which
of the following correct actions?
54
1. Examine Reese’s abdomen while eliciting a thorough history of illness symptoms for the past 24 hours from
his mother.
2. Elicit a 24 hour recall of food and fluid intake from Reese and his mother together.
3. Obtain a clean- catch urine specimen. Divide the specimen so that you can perform a dipstick analysis
immediately and retain the other specimen for possible urinalysis and culture after consultation with primary
health practitioner.
4. Explore the mother’s understanding of Reese’s illness and it’s relationship to his current condition to begin
outlining your teaching plan for this family.
Questions:
1. Evidence- Are there sufficient data to support your answer?
2. Assumptions- Describe some underlying assumptions about the following:
a. Peritonitis in children with nephrotic syndrome
b. Infection in a child on corticosteroid therapy
3. What are the priorities for discharge planning at this time?
4. Does the evidence support your conclusion?
5. Are there alternative perspectives to your conclusions? What are they?
Answers:
1. Yes. The best response is 1. One of the complications of severe nephrotic syndrome is peritonitis. A careful
abdominal examination and thorough history can provide important information.
2. a. Peritonitis can occur secondary to migration of intestinal bacteria across the bowel wall and into the protein-
rich acidic fluid.
b. Infection is a constant source of danger to edematous children and those receiving corticosteroid therapies.
3. The fever and abdominal pain are the first priority. Actions 3 and 4 must be addressed, along with evaluation of
the current stress level in the home, after the fever and pain have been addressed. Although his weight gain and
reduced urinary output are major concerns, they are secondary to peritonitis. Obtaining a urine specimen for
dipstick analysis is part of the initial assessment for Reese.
4. Yes. Children who are on steroid therapy are highly susceptible to complications of steroids that Reese is
currently exhibiting warrants a complete evaluation for peritonitis.
5. There are no better alternatives to evaluate the symptoms Reese is experiencing. Waiting and observing the
symptoms is not recommended for a child on immunosuppressive therapy.
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NCM-104 PEDIATRIC NURSING

21. Anatomy and A. Renal Physiology

Physiology of the 1. Glomerular filtration

Renal system 2. Tubular function

3. Renal development and

function in early infant

B. Renal Pelvis and Ureters:

Structure and function

C. Urethrovesical unit: structure

A. Signs and Symptoms of

Urinary tract Disorders in

Diagnostic 1. neonatal period

E. Radiologic and other test of

the urinary system function

F. Blood test of the renal function

23.Congenital E. Epispadias / Extrophy complex

Abnormality/ F. Renal Dysplasia/Hypoplasia

Autoimmune G. Polycystic Kidney Disease

Disorders H. Systemic Lupus Erythematosus

A. Urinary Tract Infection

24. Infectious Diseases A. Acute Renal Failure

B. Chronic Renal Failure

25. Renal Tumor

26. Renal Failure

• urine culture sensitivity.

• Observation of any manifestation

URINARY TRACT INFECTION:

-10% will have a febrile UTI. During first 2 year of life.

-impossible to localize the infection.

-UTI is applied to the presence micro organism of the urinary tract

-females have higher risk for developing UTI.

• Bacteriuria-presence of bacteria in urine.

Escherichia coli organism can be responsible for UTI.

-found in the anal and perineal region.

Other organisms are PROTEUS,PSEUDOMONAS,

ANATOMIC and PHYSICAL FACTORS:

ALTERED URINE AND BLADDER CHEMISTRY

- Manifestation of UTI depends on the age of the child.

SIGNS AND SYMPTOMS:

Neonatal period (birth to 1 month.)

• To eliminate current infection

Abnormal retro grade flow of the urine into the

serve as reservoir for the bacteria.

• more likely to be associated with recurring kidney infection

• Daily dose of anti-biotic

• Urine culture (2to3 months)

• Progressive renal injury is greatest when infection

• Early diagnosis of children at risk is important

• instruct patient to observe symptoms of UTI

• Infants, young children not able to express their

• Unexplained irritability may assist suspected UTI

• collect appropriate specimen.

• Acceptable clean-voided specimen

• suprapubic aspiration of urine

• 3 to 4 yrs explain w/ doll

• older may use simple diagram

-females wipe from front to back after voiding/defecating

-void as soon as possible after intercourse

-reccurent UTI frequently maintain low-dose of antibiotics

Normal urine flow

-congenital or aquired, unilateral or bilateral

-can occur at any level of the upper or lower urinary tract