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Fifth stage
Pediatric
Lec-2
د.ندى العلي
19/10/2015
ACUTE GLOMERULONEPHRITIS
Acute glomerulonephritis is characterized by hematuria(65%), hypertension(75%), and
edema(50%). The hematuria is usually grossly evident as tea-colored or cola-colored urine. In
some children, however, the hematuria may be microscopic only .
This clinical syndrome can be considered to present in many ways:
acute nephritis with no or mild renal failure
acute nephritis with rapidly progressive renal failure
nephritis-nephrotic
subclinical form.
DISEASES THAT USUALLY PRESENT AS ACUTE GLOMERULONEPHRITIS
Acute poststreptococcal glomerulonephritis
Henoch-Schönlein purpura with nephritis
Postinfectious (nonstreptococcal) glomerulonephritis
Interstitial glomerulonephritis
Radiation nephritis
Acute poststreptococcal glomerulonephritis
Acute poststreptococcal glomerulonephritis (APSGN) is a common form of
glomerulonephritis in childhood
Although poststreptococcal nephritis may happen at any age, the peak incidence occurs at
age 7 years, with a slight predominance among boys. It is uncommon before age 3 years and
in adults
ETIOLOGY
Poststreptococcal nephritis is the consequence of the host's immune response to a
nonrenal infection with group A beta-hemolytic streptococci (GABHS
Not all GABHS strains are nephritogenic. Types 12 and 49 are the strains most
commonly associated with nephritis
Infection with a nephritogenic strain does not guarantee an episode of nephritis,
because a variety of incompletely understood factors determines the host response
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CLINICAL PRESENTATION
Mild and subclinical cases are common. Renal involvement characteristically manifests
8 to 14 days after a pharyngeal infection or 14 to 21 days after a skin infection caused
by the nephritogenic streptococci
Most patients who have acute poststreptococcal nephritis present as an acute
glomerulonephritis, with macroscopic hematuria present in about 65% of the cases.
Patients will usually have oliguria and, in rare cases, anuria.
Fluid retention leads to edema that usually is periorbital and rarely, severe
Intravascular overload caused by salt and water retention can lead to signs of
congestive heart failure.
Approximately 75%of the patients have hypertension also related to salt and water
retention.
Patients who have severe hypertension may have symptoms of headache, drowsiness,
vomiting, personality and visual changes, and convulsions.
Although arteriolar spasm is commonly found on funduscopic examination,
papilledema and hemorrhages are rare, even with severe hypertension
Anorexia and pain in the abdomen or flank are common, although palpation of the
abdomen usually reveals no significant findings.
Although a history of preceding skin or pharyngeal infection supports the diagnosis,
such a history cannot be elicited in many cases
In rare cases, in which convulsions or symptoms of cardiovascular dysfunction are the
primary complaint, unrecognized poststreptococcal nephritis is the underlying etiology
LABORATORY FINDINGS
The urine usually is tea colored and opaque.
The specific gravity generally is increased,
and hemoglobin can be detected by chemical testing.
Any proteinuria that is present usually parallels the degree of hematuria and rarely
reaches the nephrotic syndrome range.
Microscopic examination usually reveals erythrocyturia, pyuria and granular or cellular
casts
Measurement of serum complement shows a reduction of C3 in most of the patients
and, early in the course, a reduction of C4 in 50%.
The erythrocyte sedimentation rate (ESR) usually is elevated
With severe oliguria, azotemia and acidosis may been seen.
The plasma volume usually is expanded, causing a decline in hemoglobin, and
hematocrit levels by dilution. Hemolysis, a shortened erythrocyte half-life, and reduced
erythrocyte production may contribute to these hematological changes.
Salt retention with a decreased fractional excretion of sodium .
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Evaluation of a Child with Hematuria
1. Complete history and physical examination (particularly blood pressure, optic discs,
skin, abdomen, genitalia)
2. Confirmation of true hematuria by urine microscopic examination
3. Urine culture
4. Urine calcium, protein, creatinine
5. Complete blood count including platelets, serum electrolytes, BUN/serum creatinine
(calculate creatinine clearance), calcium, total protein and albumin
6. Streptozyme, C3, C4, ANA
7. Renal ultrasonography
8. Renal biopsy in selected cases
Evidence of a preceding streptococcal infection is important to support the diagnosis.
The antistreptolysin O (ASO) titer is elevated in 80% of patients, although increases in
titer are less common in patients who have skin infection and in those who receive
early treatment with antibiotics.
If other streptococcal antibodies (antihyaluronidase, antideoxyribonuclease B) are
measured, 95% of patients will have serological evidence of preceding streptococcal
infection.
Cultures often are negative for GABHS by the time nephritis develops and are
particularly affected by pretreatment with antibiotics
The chest roentgenogram in patients who have hypertension usually reveals a large
heart with prominent pulmonary vasculature& pulmonary edema
Ultrasound examination usually reveals bilaterally enlarged kidneys
TREATMENT
Acute poststreptococcal glomerulonephritis most often resolves spontaneously. Even
so, the practitioner must be aggressive in treating hypertension, oliguria, and the
resulting vascular overload, pulmonary edema, and encephalopathy that occur in the
acute phase of the illness, because these can be fatal.
Although mild hypertension may resolve spontaneously, more severe degrees of
hypertension should be controlled with antihypertensive agents that act quickly.
Because increased intravascular volume is theorized to be the main determinant of
hypertension in acute glomerulonephritis
, diuretics are a mainstay of therapy
Control of severe hypertension often will require the use of intravenous
,labetalol
Oral
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in a dose of 0.1 to 0.2 mg/kg may be effective
.Slower-acting, less potent antihypertensive drugs are not good initial choices but can
be substituted once blood pressure has been acutely stabilized .
The signs of congestive heart failure usually resolve with control of the hypertension.
Occasionally a patient develops acute renal failure severe enough to require dialysis
A 10-day course of antibiotics usually is given to eradicate any remaining GABHS and,
thus, prevent the spread of the organism to others.
There is no evidence that such treatment affects the course of nephritis in the patient.
Close contacts should be screened for streptococcal infection and treated if present
Hospitalization for patients who have this disease needs to be determined individually
Although many children who have mild episodes do well as outpatients,
the sudden development of hypertension and oliguria may produce life-threatening
symptoms quite rapidly, necessitating hospitalization.
After the acute phase, the child may be allowed to resume normal activities gradually.
Every child should be followed up regularly until the serum complement values return
to normal.
To be certain of the diagnosis, a renal biopsy may be indicated for a child whose clinical
or laboratory findings are atypical. Any child whose C3 value does not return to normal
within 8 weeks should have a kidney biopsy .
COURSE
Diuresis usually ensues by one week from onset, heralding resolution of the acute
illness. Creatinine should normalize by 3 to 4 weeks.
Gross hematuria resolves within 1 or 2 weeks, although microscopic hematuria may
persist for more than 1 year.
Proteinuria should resolve by 3 months, and complement levels should normalize by 6
to 8 weeks
PROGNOSIS
Studies have shown that more than 95% of children who have acute poststreptococcal
glomerulonephritis recover from their illness.
For most children, the critical period(5_10) early in the illness when potentially fatal
hypertension or fluid overload presents a
danger.
Treating the streptococcal infection does not prevent PSGN; however, if the patient
still has active streptococcal infection, antibiotic treatment is warranted
Recurrences of APSGN are rare.
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The presence of nephrotic-range proteinuria or extensive crescents by biopsy indicate
a poor prognosis.
The failure of complement levels to normalize by 8 weeks suggests the presence of a
form of nephritis other than ASPGN, such as membranoproliferative
glomerulonephritis, the nephritis of chronic infection, or lupus nephritis .
The prognosis for renal recovery in other forms of chronic GN and in RPGN is variable
and related to the disorder and disease severity at diagnosis.