CARE OF CHILD SUMMARY OF FINAL TOPICS: Infectious Diseases I.

Nephrotic Syndrome
WITH
GENITOURINARY 1. GENITOURINARY A. Urinary Tract Infection
DYSFUNCTION 2. CNS
3. MUSCULOSKELETAL B. Acute Glomerulonephritis
4. ENDOCRINE
5. INTEGUMENTARY
C. Interstitial Nephritis

Anatomy and A. Renal Physiology

Glomerular filtration Renal Tumor

Physiology of the

Renal system Tubular function

A. Wilms Tumor
Renal development and
function in early infant

B. Renal Pelvis and Ureters: Renal Failure

Structure and function GUS -ADPIE

A. Acute Renal Failure
C. Urethrovesical unit:
B. Chronic Renal Failure
Structure and function
C. Dialysis

D. Renal Transplant
A. Signs and Symptoms of Urinary tract
Assessment and Disorders in

Diagnostic evaluation Different Ages:

Neonatal period
Assessment:
Infancy
 Physical examination
Childhood  History taking
 Radiology
B. Physical test
Clinical Manifestation:
C. Chemical test
 The incidence and type of kidney or urinary tract
D. Microscopic test
dysfunction changes w/ the age and maturation of the
E. Radiologic and other test of the child.
urinary system function
Eg. Enuresis has greater significance at age 8 than at
F. Blood test of the renal function age 4.

 In newborn, urinary tract disorders are associated with

Congenital number of obvious malformation of other body system.
A. Phimosis

Abnormality/ B. Hydrocele Laboratory test:

Autoimmune C. Crytorchydism  Urine culture sensitivity.

Disorders D. Hypospadias
E. Epispadias / Extrophy complex
F. Renal Dysplasia/Hypoplasia
Nursing considerations:
G. Polycystic Kidney Disease
H. Systemic Lupus Erythematosus
 Determine presence of pathogen.
 Renal/bladder ultrasound (allows vision of renal
parenchyma)
• Testicular (scrotal) ultrasound (allows vision
visualization of scrotal content including testis.)
 Observation of any manifestation.
 Maintain intake and output measurement.
 Check blood pressure.
 Clinical estimation of creatinine.
  Urine collection (12 or 24 hours). Most pathogens favor on alkaline medium.
URINARY TRACT INFECTION Urine pH of about 5 hampers bacterial multiplication.
Diagnostic Evaluation:
10% will have a febrile UTI. During first 2 year of
life. Manifestation of UTI depends on the age of the child.
Impossible to localize the infection. Diagnosis of UTI is confirmed by detection of bacteriuria.
UTI is applied to the presence micro organism of Infants and very small children are often difficult for urine
the urinary tract. collection.
Peak incidence of UTI not caused by structural Perineal flora in bag specimen is most frequent cause
anomalies occurs bet. 2 and 6 years of age. of false positive result.
Females have higher risk for developing UTI.  should be first thing in the morning
Suprapubic aspiration (most accurate in 2years of age).
Classifications Dipstick test (quick and in expensive).
Percutaneous kidney taps.
Bacteriuria- Presence of bacteria in Ultrasonography.
urine. Voiding cystourethrogram (VCUG).
Asymptomatic bacteriuria- Significant bacteriuria with no evidence of
clinical
infection. Signs and Symptoms:
Symptomatic bacteriuria- Bacteriuria accompanied by physical sign of
urinary infection. Neonatal period (birth to 1 month)
Recurrent UTI- Repeated episode of bacteriuria.
Persistent UTI- Persistent bacteriuria
 Poor feeding
despite antibiotic treatment.
 Vomiting
Febrile UTI- Bacteriuria accompanied
 Failure to gain weight
by fever.
 Rapid respiration
Cystitis – Inflammation of the bladder.
 Respiratory distress
Urethritis – Inflammation of the urethra.
 Screaming on urination
Pyelonephritis – Inflammation of the
urinary tract and kidney.
Urosepsis- Febrile urinary tract infection
INFANCY (1 TO 24 MONTH)
coexisting with systemic signs of
bacterial illness.
Etiology  Excessive thirst
 Frequent urination
 Foul smelling urine
Escherichia coli - Organism can be responsible for UTI.
 Pallor
 Fever
80% cases
CHILDHOOD (2 TO 14 YRS)
Found in the anal and perineal region.
 Poor appetite
Other organisms PROTEUS,PSEUDOMONAS,  Vomiting
 Growth failure
KLEBSIELLA,STAPHYLOCOCCUS AUREUS,  Swelling of face
 Blood in urine
HAEMOPHILUS. Therapeutic management:

Anatomic and Physical Factors: To eliminate current infection.

Identify contributing factors
Lower urinary tract is believed to account for the increased Prevent systemic spread of infection.
incidence of bacteriuria in females. Preserve renal function.
Short urethra which measures about 2 cm. (0.75inch.) in young o defects such as primary reflux or bladder neck
girls. obstruction.
4 cm in mature women provides a ready pathway for invasion of Surgical correction is necessary
organism.
Closure of urethra at the end of micturation may return VESICOURETERAL REFLUX
contaminated bacteria to the bladder.
Longer male urethra 20cm (8 inch) in an adult. Antibacterial  Abnormal retro grade flow of the urine into the ureters.
properties of prostatic secretions inhibit entry and growth of  Urine is swept up into the ureters then flows back into
pathogens. the empty bladder, where its serve as reservoir for the
Fewer UTI among male infants. bacteria.
 More likely to be associated with recurring kidney
Altered Urine and Bladder Chemistry: infection.
 Bacteria from urine has access to bladder going to
Mechanical and chemical characteristics of the urine and bladder kidney results to kidney infection.
mucosa help urinary sterility.  Associated with UTI most common cause of renal
Increased fluid intake promotes flushing and lower the scarring to children.
concentration of organisms.
Diuresis enhance the antibacterial properties of the renal medulla.Management:
  Prevention of bacteria
 Daily dose of anti-biotic
 Urine culture (2to3 months)
 Voiding cystourethrogram
Prognosis:
 Progressive renal injury is greatest when infection occurs (2 yrs).
 Early diagnosis of children at risk is important.
Nursing Considerations:
 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 with 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.
 Recurrent UTI frequently maintain low-dose of antibiotics.
OBSTRUCTIVE UROPATHY
 Functional abnormalities of urinary system that obstruct.
 Normal urine flow.
 Congenital or acquired, 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 Considerations:
 Identify case
 assisting diagnostic
 parents & children needs counseling
 maintain adequate urine flow
NEPHROTIC SYNDROME
 Includes massive proteinuria, hypoalbuminemia, hyperlipemia and Diagnostic Evaluation:
edema.
o Idiopathic nephrosis (primary)
o Glomerular damage
o Congenital form
 Glomerular membrane normally permeable to albumin.
 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 Management:
 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.
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 become 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.
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 Manifestation:
Edema:
 Especially periorbital
 Facial edema more prominent in the morning
 Spreads during the day to involve extremities and
abdomen
Anorexia
Urine:
 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.
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 . Serotypes have been traced to undercooked meat,
especially ground beef.
Pathopysiology:
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.
Diagnostic Evaluation:
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.
Therapeutic Management:
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.
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.
Diagnostic Evaluation:
 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.
Therapeutic Management:
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.
Clinical Manifestation:
Abdominal swelling or mass
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 filtration rate, an elevated blood urea nitrogen
level, and a significant reduction in renal blood flow.
Diagnostic Evaluation:
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.
Therapeutic Management:
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.
Clinical Manifestation:
Specific:
 Oliguria
 Anuria uncommon
Nonspecific (may develop):
 Nausea
 Vomiting
 Drowsiness
 Edema
 Hypertension
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.
Diagnostic Evaluation:
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.
Therapeutic Management:  History of phryngitis or tonsiltis 2 to 3 weeks before
symptoms
In irreversible renal failure the goals of medical management
are to: Types:

 Promote maximum renal function.  Acute: Occurs 2 to 3 weeks after a streptococcal

 Maintain body fluid and electrolyte balance within safe infection.
biochemical limits.  Chronic: Can occur after the acute phase or slowly
 Treat systemic complications.
over time.
 Promote as active and normal a life as possible for the
child for as long as possible.
Complications:
Clinical Manifestation:
 Renal failure
Child may complain of:  Hypertensive encephalopathy
 Pulmonary edema
 Headache  Heart failure
 Muscle cramps
 Nausea Assessment:

Other signs and symptoms:  Periorbital and facial edema that is more prominent in
the morning
 Weight loss  Anorexia
 Facial edema  Decreased urinary output
 Malaise  Cloudy, smoky, brown-colored urine
 Bone or joint pain  Pallor, irritability, lethargy
 Growth retardation  In the older child, headaches, abdominal or flank pain,
 Dryness or itching in the skin dysuria
 Bruised skin  Hypertension
 Sensory or motor loss  Proteinuria that produces a persistent and excessive
 Amenorrhea foam in the urine
 Uremic syndrome (untreated)  Azotemia
 Gastrointestinal symptoms  Increased blood urea nitrogen and creatinine levels
 Anorexia  Increased antistreptolysin O titer (used to diagnose
 Nausea and vomiting disorders caused by streptococcal infections)
 Bleeding tendencies
1. Bruises Interventions:
2. Bloody diarrheal stools
 Monitor vital signs, weight, intake and output, and the
3. Stomatitis
characteristics of urine.
4. Bleeding from lips and mouth
 Limit activity, provide safety measures.
SUPPLEMENT  Nutrition
o Restrictions depend on the stage and severity of the
Glomerulonephritis (Acute Poststreptococcal disease, especially the extent of the edema.
Glomerulonephritis) o In uncomplicated cases, a regular diet is permitted but
sodium is restricted to a no added salt to foods diet.
 Glomerulonephritis is a term that includes a variety of o Moderate sodium restriction is prescribed for the child
disorders, most of which are caused by an with hypertension or edema.
immunological reaction. o Foods high in potassium are restricted during periods
 The disorder results in proliferative and inflammatory of oliguria.
changes within the glomerular structure. o Protein is restricted if the child has severe azotemia
 Destruction, inflammation, and sclerosis of the
resulting from prolonged oliguria.
glomeruli of both kidneys occur.
 Monitor for complications (renal failure, hypertensive
 Inflammation of the glomeruli results from an antigen-
encephalopathy, pulmonary edema, and heart failure).
antibody reaction produced by an infection elsewhere
 Administer diuretics (if significant edema and fluid
in the body.
overload are present), antihypertensives (for
 Loss of kidney function develops.
hypertension), and antibiotics (to the child with evidence
of persistent streptococcal infections) as prescribed.
Causes:
 Initiate seizure precautions and administer anti-
 Immunological diseases convulsants as prescribed for seizures associated with
 Autoimmune diseases hypertensive encephalopathy.
 Streptoccocal infection, group A, B-hemolytic
  Instruct the parents to report signs of bloody urine,
headache, or edema.
 instruct the parents that the child needs to obtain
treatment for infections, specially sore throats and upper
respiratory infections.
Nephrotic Syndrome
Nephrotic syndrome is a kidney disorder charactererized by:
 massive proteinuria
 hypoalbuminemia
 edema
The primary objective of therapeutic management is:
 to reduce the excretion of urinary protein
 maintain protein free urine.
Assessment Findings:
 Child gains weight.
 Periorbital and facial edema is most prominent in the
morning.
 Leg, ankle, labial or scrotal edema occurs.
 Urine output decreases; urine is dark and frothy.
 Abdominal swelling occurs.
 Blood pressure is normal or slightly decreased.
Interventions:
 Monitor vital signs, intake and output, and daily
weights.
 Monitor urine for specific gravity and albumin.
 Monitor for edema.
 Nutrition: A regular diet without added salt is
prescribed if the child is in remission; sodium is
restricted during periods of massive edema.
 Corticosteriod therapy is prescribed as soon as the
diagnosis has been determined (monitor child closely
for signs of infection).
 Immunosuppressant therapy may be prescribed to
reduce the relapse rate and induce long term
remission; therapy may be administered along with
the corticosteroid.
 Diuretics may be prescribed to reduced edema.
 Plasma expanders such as salt-poor human albumin
may be prescribed for the severely edematous child.
 Instruct the parents about testing the urine for
albumin, medication administration, side effects of
medications, and general care of the child.
 Instruct the parents regarding the signs of infection
and the need to avoid contract with other children
who may be infectious.
Nephroblastoma (Wilms’ tumor)
Wilm’s tumor is a tumor of the kidney that may
present unilaterally and localized or bilaterally,
sometimes with metastasis to other organs.
Is the most common intra-abdominal tumor in
children, and the most curable.
The peak incidence is at 3 years of age.
The occurrence is associated with a genetic
inheritance and with a several congenital anomalies.
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.
Etiology:
Unknown
Siblings of children with Wilms’ tumor have a higher
risk of developing the disorder.
Pathophysiology:
The tumor originates from immature renoblast cells
located in the renal parenchyma.
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.
It is classified into five stages:
Stage I tumor is confined to one kidney.
Stage II tumor extends beyond kidney but can be resected.
Stage III tumor has residual nonhematogenous tumor cells
confined to the abdomen.
Stage IV tumor is characterized by distant metastases
involving lung, liver, bone, or brain.
Stage V tumor involves both kidneys.
Assessement Findings:
Swelling or mass within the abdomen (mass is
characteristically firm, nontender, confined to one
side,and deep within the flank.
Abdominal pain
Urinary retention and/or hematuria
Anemia (caused by hemorrhage within the tumor)
Pallor,anorexia, lethargy (resulting from anemia)
Hypertension (caused by secretion of excess
amounts of rennin by the tumor)
Weight loss and fever
Symptoms of lung involvement such as dyspnea,
shortness of breath, and pain in the chest, if
metastasis has occurred.
Interventions Preoperatively:
Monitor vital signs, particularly blood pressure.
Place a sign at the bedside: “Do not palpate
abdomen.”
Palpation of the abdomen may rupture encapsulated
tumor which may spread to distant sites.
Measure abdominal girth.
Interventions Postoeratively:

Monitor temperature and blood pressure closely.

Monitor for signs of hemorrhage and infection.
Monitor intake and output and urine output closely.
Monitor for abdominal distention; monitor bowel
sounds and for other signs of gastrointestinal activity
because of the risk for intestinal obstruction.
 PHIMOSIS - The foreskin remains so tight that it
interferes with voiding.
 HYDROCELE - The fluid can be revealed by prenatal
sonography.
 CRYPTORCHIDISM - Is failure of one or both testes
to descend from the abdominal cavity to the scrotum.
They may descend anytime up to 6weeks after birth;
they rarely descend after that time.
 HYPOSPADIAS - Is a urethral defect in which the
urethral opening is not at the end of the penis but on
the ventral (lower) aspect of the penis.
 EPISPADIAS - Is a similar defect in which the
opening is on the dorsal surface of the penis.
 RENAL HYPOPLASIA - Hypoplasia means reduce
growth. Hypoplastic kidneys contains fewer lobes
than normal kidneys and are small and under develop
.
 POLYCYSTIC KIDNEY DISEASE - Means that large
fluid filled cysts have formed in place of normal kidney
tissue. The most frequent type of polycystic kidney
seen in children is inherited as autosomal necessive
trait.
 SLE - SLE is an autoimmune disease in which
autoantibodies and antigens cause deposits of
complement on the kidney glomerulus.