Urinary Tract Disorders

 When renal disease is suspected, the history

should include –
 Family hx of renal disease
 Preceding acute or chronic illnesses (e.g,

UTI, pharyngitis, impetigo, or endocarditis)

 Rashes or joint pains
 Growth delay or failure to thrive (FTT)
 Polyuria, polydipsia, enuresis, urinary

frequency, or dysuria
 Documentation of hematuria, proteinuria,
or discolored urine
 Pain (abdominal, costovertebral angle, or
flank) or trauma
 Sudden weight gain or edema
 Drug or toxin exposure
 Physical Examination -
 Height, weight, skin lesions, pallor, edema,

or skeletal deformities.
 Anomalies of the ears, eyes, or external

genitalia may be asso with renal disease

 Abdomen palpation with attention to the

kidneys, abdominal masses, musculature,

and the presence of ascites
 Lab evaluation of renal function
 Urinary Tract Infection (UTI)

 UTI - infection of one or more structures of

the urinary tract.
 Classification –

 Lower urinary tract (e.g., cystitis, urethritis).

 Upper urinary tract (e.g., pyelonephritis).
 Bladder (cystitis) is the most common site.

 Identification of the site of infection

important in determining the treatment.

 UTI is the most common disorder of the
genitourinary tract.
 Incidence of UTI in infants is about 40 per

1,000 with the rates being equal among sexes

until 3 months of age.
 Risk for UTI is 4 times greater in the female.

 Uncircumcised boys more likely to have UTI.

 Escherichia coli - the most common bacteria

organism that infects the urinary tract.

 Less commonly seen (chronic conditions)
colonization occurs from Klebsiella
pneumonia, Enterobacter, Proteus species,
and Pseudomonas.
 Virus and fungi, particularly Candida species,

may also cause UTI.

 Pathophysiology of UTI

 During infancy, bacteria frequently enter the

urinary tract thro’ the blood.
 After infancy, bacteria enter the urinary tract

by ascending thro’ the urethra.

 Females at increased risk for infection due to

their short urethra.

 Males are less susceptible due to longer

urethra and secretions from the prostate

(antibacterial properties).
 If UTIs are found in males, it is important to
investigate for urinary tract anomalies.
 Structural anomalies and abnormal function

of the urinary tract play a role in the

pathogenesis of UTI.
 Anomalies - vesicoureteral reflux, neurogenic

bladder - common with spina bifida.

 Other factors include urinary stasis,
congenital anomalies of the urinary tract, an
obstruction in the urinary tract, and urinary
catheters.
 Normally, emptying the bladder frequently

completely washes out any organisms.

 Stasis may be caused by reflux, dysfunction of

the voiding mechanism, and infrequent

voiding.
 Clinical Manifestations

 The presenting signs and symptoms of UTI

often vague, esp in young children.
 Symptoms in the older child generally include:

 Malodorous urine, dysuria

 Urinary frequency, fever
 Vomiting, diarrhea
 Irritability and poor feeding
 Diagnosis

 Urinalysis and urine culture with sensitivity

are performed to diagnose UTI.
 The method of urine sample collection has

great impact on the interpretation of results.

 The presence of bacteria and WBCs in the

urine confirm the diagnosis of a UTI.

 If pyelonephritis is suspected, a serum sample

may be required.
 The child with pyelonephritis usually presents
with –
 Elevated WBC
 Elevated ESR
 Increased C-reactive protein (CRP)
 Treatment

 Treatment for UTI includes:

 Eradicating the infection
 Preventing re-infection by identifying

contributing factors.
 Correcting underlying causes of infection.
 Preserving renal function.

 Treatment depends upon the child’s age,

other existing medical conditions, and ability
to maintain hydration.
 Oral antibiotic therapy to treat UTI –
 Septrin
 Amoxicillin
 Cephalosporin
 Nitrofurantoin
 All antibiotics are given for 7 - 10 days.

 Follow-up urine culture should be performed

48 to 72 hrs after initiating treatment.

 For infants or young children 2 months to 2
years of age who appear toxic, dehydrated, or
unable to retain oral fluids, initial antibiotic
therapy should be given IV and hospitalization
should be considered.
 Acute Glomerulonephritis (AG)

 Lecture Outline –
 Definition
 Pathophysiology
 Clinical manifestations
 Diagnostic evaluation
 Medical management
 Complications
 Nursing management
 Definition of AGN

 Acute glomerulonephritis –
 Refers to a group of kidney diseases in
which there is an inflammatory reaction in
the glomeruli.
 It is not an infection of the kidney, but
rather the result of the immune
mechanisms of the body.
 Pathophysiology

 Occurs after an infection elsewhere in the

body.
 May develop secondary to systemic disorders.

 An antigen-antibody rxn produces immune

complexes that lodge in the glomeruli,

producing thickening of glomerular basement
membrane; the renal vasculature,
interstitium, and tubular epithelium may also
be affected.
 Immune complexes activate a variety of
secondary mediators - complement pathways,
neutrophils, macrophages, prostaglandins,
and leukotrienes.
 These affect vascular tone and permeability,

resulting in tissue injury.

 Eventual scarring and loss of filtering surface

may lead to renal failure.

 Clinical Manifestations

 Mild disease frequently discovered thro’ a

routine urinalysis.
 Hx of infection: pharyngitis or impetigo from

GABHS, viral infections EBV, HBV.

 Tea-colored urine, oliguria

 Puffiness of face, edema of extremities.

 Fatigue and anorexia, possible headache

 Hypertension and headaches.

 Anemia from loss of RBCs into the urine.
 The clinical course of AGN proceeds as follows

from onset of symptoms to recovery - more

than 90% of pts regain normal renal function
within 60 days:
 Diuresis usually starts 1 to 2 weeks after
onset of symptoms.
 Renal clearances and blood urea
concentration return to normal.
 Edema decreases, and hypertension
lessens.
 Microscopic proteinuria or hematuria may
persist for many months.
 Diagnostic Evaluation

 Urinalysis for hematuria, proteinuria, cellular

elements, and various casts.
 24-hr urine for protein - increased

 Creatinine clearance – reduced

 Elevated BUN and serum creatinine

 Low albumin level

 Increased antistreptolysin titer - rxn to

streptococcal organism
 Decreased serum complement
 Needle biopsy of the kidney reveals

obstruction of glomerular capillaries from

proliferation of endothelial cells.
 Management

 Management is symptomatic.
 Drugs –

 Antihypertensives
 Diuretics
 Drugs for management of hyperkalemia

(due to renal insufficiency)

 H2 blockers - prevent stress ulcers
 Phosphate-binding agents - reduce

phosphate and elevate calcium.

 Antibiotic therapy initiated to eliminate
infection if still present.
 Fluid intake is restricted.

 Dietary protein is restricted moderately if

there is oliguria and the BUN is elevated;

restricted more drastically if acute renal
failure develops.
 Carbohydrates are increased liberally to
provide energy and reduce catabolism of
protein.
 Potassium and sodium intake is restricted in

presence of hyperkalemia, edema, or signs of

heart failure.
 AGN - Complications

 Hypertension, heart failure, endocarditis

 Fluid and electrolyte imbalances in the acute

phase, hyperkalemia, hyperphosphatemia,

hypervolemia
 Malnutrition

 Hypertensive encephalopathy, seizures

 ESRD
 Nursing Assessment

 Obtain medical hx; focus on recent infections

or symptoms of chronic immunologic
disorders (e.g., SLE, scleroderma).
 Assess urine specimen for blood, protein,

color, and amount.

 Perform PE; look for signs of edema, HTN, and

hypervolemia (engorged neck veins, ↑JVP,

adventitious lung sounds, cardiac
arrhythmias).
 Evaluate cardiac status and serum lab values
for electrolyte imbalance.
 Nursing Diagnoses –

 Ineffective (renal) tissue perfusion related

to damage to glomerular function
 Excess fluid volume related to
compromised renal function
 Nursing Interventions

 Promoting Renal Function

 Monitor vital signs, I&O, and maintain
dietary restrictions during acute phase.
 Encourage rest during the acute phase until
the urine clears and BUN, creatinine, and BP
normalize.
 Rest facilitates diuresis.
 Administer medications
 Evaluate pt's response to medications –

 Antihypertensives
 Diuretics
 H2 blockers
 Phosphate-binding agents
 Antibiotics (if indicated)
 Improving Fluid Balance

 Monitor fluid bal; replace fluids according to

pt's fluid losses and daily body wgt.
 Monitor pulmonary artery pressure and CVP

during acute hospitalizations.

 Monitor for signs and symptoms of heart

failure – e.g., distended neck veins,

tachycardia and enlarged and tender liver.
 Observe for hypertensive encephalopathy and

any evidence of seizure activity.

 Patient/Family Education

 Explain that pt must have follow-up

evaluations of BP, urinary protein, and BUN
concs to determine if there is exacerbation of
disease activity.
 Encourage pt to treat any infection promptly.

 Tell pt/family to report any signs of

decreasing renal function and to obtain

treatment immediately.
 Evaluation

 Urine output adequate; vital signs stable

 No edema, shortness of breath, or

adventitious heart or lung sounds

 Nephrotic Syndrome (NS)

 Clinical entity characterized by massive

proteinuria and hypoalbuminemia leading to
edema and hyperlipidemia.
 NS can be classified as primary or secondary:

 Primary/idiopathic NS results from

glomerular disease of the kidney.
 Secondary NS results in renal malfunction -
systemic disease, drugs/toxins that
ultimately put a stress on the renal system.
 Primary NS –
 The most common type of NS in children.
 Slightly more common in male children.
 Usually affects children between 2 - 6 yrs.
 Etiology believed to be an immune

response.
 The immune response is to a glomerular

disease or a systemic infection that alters

the structure of the glomerulus.
 Pathophysiology

 NS results when there is a threat to the

immune system and an inflammatory
response is evoked.
 The glomeruli become increasingly permeable

to plasma protein resulting to proteinuria.

 Massive proteinuria resulting in hypoalbu-

minemia.
 Fluids shift from the intravascular to the

interstitial spaces.
 Tissue edema, ascites and hypovolemia
develop.
 Once the volume diminishes in the vascular

spaces, renal blood flow declines and urine

output diminishes.
 Renin production is stimulated to maintain

volume and systemic pressure.

 The result is secretion of aldosterone which

causes tubular reabsorption of sodium.

 Water follows the sodium leading to more
congestion and edema.
 Serum cholesterol and triglyceride levels rise

from the stimulation of lipoprotein

production in the liver in the face of
hypovolemia and falling serum protein levels.
 As blood volume falls, hemoconcentration

causes an increase in RBCs and platelets.

 The net result is a slowing of the blood flow
and ultimately the clumping or clotting of
RBCs and platelets.
 That coupled with protein losses puts the

child at risk for coagulation or clotting

problems.
 Clinical Manifestations

 Edema - usually the first clinical feature.

 Kidney inflamm causes anorexia, abdominal

pain/tenderness
 Abdominal swelling, fatigue, history of recent

respiratory infection.
 Increased weight/rapid weight gain and ↑ BP.

 Hyperlipidemia - most likely due to ↑hepatic

lipid metabolism in response to hypo-

proteinemia.
 Diagnosis

 Serum albumin levels diminished

 Lab evaluation –

 Urinalysis for protein, RBC casts,

 Serum albumin, cholesterol, triglycerides,

hemoglobin, hematocrit, platelet count,

electrolytes, BUN, and creatinine.
 Complement levels and antistreptolysin O

titer (ASOT) done to rule out other glomerular

diseases.
 The presence of proteinuria and RBC indicates
kidney inflammation.
 The rise in serum cholesterol, triglycerides,

hematocrit, and platelet count indicates some

problem with hypoproteinemia in the serum.
 The serum electrolytes will be altered as renin

and aldosterone levels change and sodium is

reabsorbed.
 BUN, creatinine rise if kidney function fails.
 Treatment

 Treatment focuses on –
 Reducing proteinuria
 Controlling edema
 Preventing infection

 The mainstay of treatment is corticosteroid

therapy with prednisone.

 A typical protocol is to start with a high dose

of either drug (2 mg/kg/day; max 80 mg/day).

 Treatment is continued until the child
becomes free of proteinuria.
 The medication is gradually tapered over a

period of several wks and then stopped as

long as the child remains asymptomatic.
 The rate of relapse is high - 60% to 70% (often

triggered by viral URTIs).

 Relapse is treated with a short course of high-

dose daily steroids.

 Diuretics can sometimes be used when
edema is severe and causes resp compromise.
 Where there is failure to respond to steroid

therapy or when side effects bring trouble,

other immunosuppressant meds given, e.g,:
 Cyclophosphamide
 Chlorambucil
 Cyclosporin
 If an infection develops as a result of long-
term steroidal use, an antibiotic is given.
 Albumin may be given if the edema is marked

and causes the child to have decreased

mobility, poor oral intake, or decreased urine
output.
 The albumin is followed by furosemide to

reduce potential for fluid volume overload

and to enhance diuresis.
 Salt intake is usually limited to control edema
and reduce the risk for hypertension esp
when daily glucocorticoids are given.
 Nursing Management

 Focuses on –
 Maintaining fluid and electrolyte balance
 Administering meds
 Preventing infection and skin breakdown
 Pt education

 Child’s vital signs monitored every four hrs

 Signs of hypovolemia noted.

 I&O documented every shift.

 Monitor fluid with special attention to sodium
restrictions .
 Any urine output less than 1 to 2 mL/kg/hr is

to be reported .
 Serum and urine electrolyte tests need to be

evaluated.
 Assess for signs of edema.
 Daily weights should be measured at the
same time of day and on the same scale in the
same clothing.
 Assessment of breath sounds for rales or

wheezes may indicate pulmonary edema.

 Meds (diuretics, steroids, or immunosupp

agents) administered.
 Note the signs of infection, including ↑ temp,
changing CBC with differential, cough, sore
throat.
 The child should be protected from visitors,

personnel, or other clients who may have

infections.
 Ensure good hand-washing while caring for

the child.
 Give antibiotics to prevent or treat infection.
 The child’s skin needs to be protected from

breakdown esp if edema is present.

 The child should be repositioned every 2 hrs.

 Place the edematous extremity on a pillow or

other support making sure that the circulation

is not impeded.