Acute Glomerulonephritis

MOHD ZAMIR GHOUSE

060100848

FAKULTAS KEDOKTERAN
UNIVERSITAS SUMATERA UTARA
2010
Introduction
• The glomerular filtration barrier (blood-urine) has 3 special
layers:
1. Endothelial cells
2. Glomerular basement membrane
3. Podocytes
• Diseases that injure the glomeruli are called glomerular
diseases.
• Lab analysis often shows persons with glomerular disease to
have:
1. Proteinuria
2. Hematuria
Definition
• AGN is a disease characterized by sudden appearance of:
1. Edema
2. Hematuria
3. Proteinuria Nephritic syndrome
4. Hypertension
5. Oliguria

• This is due to the immunologic response which triggers

inflammation and proliferation of glomerular tissue that
results in damage to the glomerular layers.
Incidence
• Most cases occur in patients aged 2-12 years

• Only 10% of cases occur in patients older than 40 years

• Less than 5% of cases occur in patients younger than 2 years
old.
• Male to female ratio 2:1
• In children, most common is post infectious AGN, the majority
of which is post streptococcal AGN.
Etiology
• Include post infectious, renal and systemic etiologies.

Post infectious Renal Systemic

• Bacterial • MPGN • Vasculitis
• Virus • IgA nephropathy • Collagen vascular
• Fungal • Idiopathic rapidly disease (eg. SLE)
• Parasitic progressive GN • Polyarthritis
nodosa
• Henoch-Schonlein
Purpura
• Goodpasture
syndrome
• Drug induced (eg.
Gold,
penicillamine)
Pathophysiology
• A streptococcal “nephritogenic” neuraminidase may alter
hosts’ IgG.
• These causes IgG/anti-IgG immune complexes to be formed
and deposits in the glomeruli which causes damage to the
glomeruli tissue.
• In patients with moderate-severe AGN, reduction in GFR
causes expansion of the ECF which is responsible for edema,
hypertension, anemia, circulatory congestion and
encephalopathy.
Clinical manifestation
• Edema (appx. 85% of cases)

• Gross hematuria (30% of cases) cardinal signs

• Hypertension

• Oliguria
• Shortness of breath or dyspnea on exertion 2 ͦ pulmonary
edema.
• Pallor
Laboratory studies
• APSGN remains a clinical FBC UFEME LFT
diagnosis and diagnosis
of exclusion.
• Several lab studies may C3,C4
BUSE Urine C&S
suggest either post levels
infectious, renal or
systemic causes of GN
• Results of the following Throat/skin ASOT/
tests may suggest other swab anti-DNase B
possible DDx.

PT/APTT USG
Differential diagnosis
• Other post infectious AGN

• IgA Nephropathy (Berger disease)

• Membranoproliferative glomerulonephritis (MPGN)

• Chronic Glomerulonephritis
• Vasculitis
Management
• Management is aimed to: • Antibiotics
1. Eradicate source of  Penicillin 25-50mg/kg/d PO tds for
infection by a course of 10 days
antibiotics  Erythromycin 30-50mg/kg/d PO
tds for 10 days
2. Control hypertension
with anti hypertensive • Anti hypertensive
drugs (if severe)  Labetalol 0.5-2mg/kg/hr. IV
3. Control fluid intake or  Nitroprusside 0.5-2mcg/kg/hr. IV
the usage of diuretics to
minimize edema and • Diuretics
fluid overload  Furosemide 1-3mg/kg/d PO bd

4. Restriction of high salt

and protein diet in acute
phase.
Prognosis
• Ultimate prognosis of PSGN largely depends on the severity of
the initial insult
• Complete recovery occurs in >95% of patients within 5 years.

• Prognosis is worst if there is:

1. Heavy proteinuria
2. Severe hypertension
3. Significant elevations of creatinine levels

• About 1-3% of patients progress to chronic renal failure.

Case report

MOHD ZAMIR GHOUSE

060100848
Personal identification
DOA : 24th November 2010

• Name : Loh Win Son

• DOB : 4th August 2004
• Age : 6 years old
• Sex : Male
• Race : Chinese
• Address: Kuala Perlis
• Source of referral : Pediatric clinic

• Chief complaint : dark colored urine one day prior to

admission
History of presenting illness
• Patient was apparently well
until one day before
admission at night when he
noticed his urine dark in color.
• His mother also said she saw
the urine and describes it as
being tea colored. She said
that it was the first time she
noticed it.
• Patient went to KK the next
morning and urinalysis was
done and noted to have +3
proteinuria and hematuria
with granular casts. Was then
referred to HTF.
However there was no:
• Body swelling
• Loin pain
• Pain upon urination
• Abdominal pain
• Headache
• Dark/pale colored stool
• Sore throat
• History of recent skin infection
or trauma
Mother said that patient looks pale and
with decreased urine output.
Associated symptoms
• 3 days before onset of dark colored urine patient had fever
with cough and runny nose.
Fever : - low grade continuous throughout day, temperature
wasn’t documented. Fever subsided after given syrup
paracetamol obtained from clinic.

Cough : - productive whitish sputum worsens at night and in

cold weathers, also exaggerated when patient drinks
cold water. Was given cough syrup.
+ difficulty in breathing without any chest tightness occasionally.
Currently not eating well because he vomits each time taking
food since his illness.
No other significant findings in system review.
 Past Medical History
Illness Past admissions Allergies Surgical history

• Patient has • First admission • Patient will • No past surgical

recurrent cough and have history
episodes of runny nose when
cough whenever exposed to cold
exposed to cold weather.
weather or cold • No other known
beverages food or drug
• Had an episode allergies
of difficulty in
breathing last
year, was given
neb salbutamol
at casualty. No
admission and
no similar attack
since.
Birth history

Antenata Age of conception was at 26 years old

●

●
Was compliant to doctors advices and
follows routine follow up during pregnancy
l history ●
No significant illness during pregnancy

Birth Born term at 38th week gestation

●

●
Spontaneous vaginal delivery
●
Birth weight of 2.9kg

history
●
No complications during birth
●
Baby was also perfectly well
Immunization and feeding history
• Immunization is currently complete and up to date, however
no confirmation could be done as she did not bring the
immunization card.

• He is currently on normal adult diet. Not eating well since

illness.
Developmental history
• No history of developmental delay.

• Currently in kindergarten and always will be among the top 3

students in class.
• Socially active and communicates well with his surroundings
Family history
Social history
• Patient is 6 year old with 2 younger brothers
• He is active, cheerful and friendly. Often plays with his
Gameboy or with his brothers.
• They all live with their parents in a house located in Kuala
Perlis
• Father of patient owns a plaster ceiling shop while mother is a
housewife.
• They are both financially stable
• Mother is taking full care of her kids at home
• No recent travel to endemically diseased areas
General examination
• He was generally alert and conscious, playing with his toys and
brothers.
• He looks nutritionally well with no signs of distress or gross
deformity.
• His hydration status was good with moist mucous membrane
and intact skin turgor.
• There was mild pitting edema noted on both lower limbs up to
one third of tibia
• No jaundice, cyanosis or pallor
Vital signs
• Level of consciousness : Alert
• Pulse rate : 144x/min with good volume
and regular
• Respiratory rate : 30x/min
• Blood Pressure : 112/70mmHg
• Temperature : 36.4 Celsius
• Weight : 28.3kg plotted at 75th centile
• Height : 115cm plotted at 50th centile
Physical examination
• Throat was injected
• Nasal discharge
Head • No other abnormal findings

• No abnormal findings
Neck

• On auscultation breath sound was vesicular with

fine crepitation on both lungs
Respiratory • No other abnormal findings
 • No abnormal findings
Cardiovascular

• Slightly distended with no visible veins or protruding umbilicus

• On palpation was soft and non tender
Abdomen • No abnormal findings

• No scrotal swelling
• No other abnormal findings
Genitalia
Summary
• My patient Loh Win Son, a 6 year old Chinese boy from Kuala
Perlis who came with his mother to the paediatric clinic HTF
on 24th November 2010 with the chief complaint of dark
coloured urine for one day prior to admission. Upon urine
examination there was + haematuria and + proteinuria. On
examination there was no raised BP, throat was injected, mild
pitting oedema noted up to 1/3 of tibia, lungs with fine
crepitation. There was no other abnormal findings.
• Symptoms are correlated with recent history of respiratory
tract infection and not associated with history of trauma.
Diagnosis

Provisional Differential
diagnosis diagnosis
• Acute glomerulonephritis • Nephrotic syndrome
TRO other causes of • IgA nephropathy
hematuria • Membranoproliferative
• Underlying bronchial asthma glomerulonephritis
exb. URTI
Investigations
• 24th November 2010

Full Blood Count Urine FEME

• WBC 11.0 x10^9/L • Urine glucose NORMAL
• RBC 6.0 x10^6/L (high) • Bilirubin NEGATIVE
• Hb 14.0 g/dL • Ketone +3
• Ht 41.0 % • Specific gravity 1.038
• MCV 70.4 fl (low) • Blood +3
• MCH 23.5 pg (low) • Urine pH 6.5
• MCHC 33.4 g/dL • Protein +3
• PLT 395 x10^3/uL • Urobilinogen 3.2
• Neutrophils 6.83 x10^3/uL • Nitrite NEGATIVE
• Lymphocytes 2.53 x10^3/uL • Leucocytes NEGATIVE
• Monocytes 1.32 x10^3/uL (high) • Color Red
• Eosinophils 0.22 x10^3/uL • Turbidity Slightly cloudy
• Basophils 0.00 x10^3/uL • Microscopic >2250 Rbc with
granular casts
 BUSE/creatinine/LFT PT/APTT
• Sodium 137 mmol/L • Prothrombin time 11.6 sec
• Potassium 4.7 mmol/L • INR 0.96
• Chloride 96 mmol/L • APTT 22.2 sec
• Urea 8.5 mmol/L (high) • APTT Ratio 0.8
• Creatinine 0.05 mmol/L
• Total bilirubin 5.4 ummol/L
• AST 39 U/f
• ALT 31 U/f
• Total protein 76 g/f
• Albumin 46 g/f
• Globulin 31 g/f
• ALP 177 U/f (high)
• A/G Ratio 1.5
Plan
• Syrup Erythromycin ethynilsuccinate (EES) 425mg bid
• T. Paracetamol 500mg PRN
• Neb Salbutamol 1:3
• Monitor vital signs 4 hourly
• Strict input output chart
• To take daily protein
• C3 and C4 levels
• Urine culture and sensitivity
• Anti Streptolysin-O titre (ASOT)
• Throat swab
• USG kidney, ureter and bladder
 Follow up
• 25th November 2010 (day one)

Subjective Objective Analysis Plan

• Comfortable and • Alert and • AGN tro other • For 24hr protein
active conscious cause of analysis
• Tolerating orally • HR : 120x/min haematuria with • Monitor vital signs
well • RR : 43x/min URTI 4 hourly
• Hydration status • SpO2 : 96% under • To review urine
good room air culture and
• No signs of • Temperature : 37 ultrasound results
oedema Celsius • To review ASOT
• Currently no fever • BP : 110/84mmHg results
• Cough has reduced • Weight : 27.3kg • Continue syrup EES
since yesterday • Lungs with 435 bid (day 2)
• No runny nose • Give neb
occasional rhonchi
• No vomiting and and crepitation Salbutamol 4
diarrhoea • Heart : Dual hourly
• No pain and rhythm no murmur
headache • Abdomen : Soft &
non tender
• 26th November 2010 (day two)

Subjective Objective Analysis Plan

• Comfortable and • Alert and conscious • AGN tro other cause • To discharge today
active • HR : 118x/min of haematuria, URTI • Review C3, C4, ANA,
• Started to eat • RR : 28x/min has resolved RF and throat swab
normally • SpO2 : 96% under results on TCA (one
• Tolerating orally well room air week)
• Hydration status • • To inform mother
Temperature : 37
good Celsius collect urine from
• No more fever, cough • Sunday and send to
BP : 114/70mmHg lab on Monday
and runny nose • Weight : 28kg
• No vomiting and (24hrs protein)
• Lungs clear • Continue syrup EES
diarrhoea •
• No pain and Heart : Dual rhythm (D3) for 5 days
no murmur • Syrup Salbutamol
headache •
• No signs of oedema Abdomen : soft and 3mg tds
non tender
• No longer pallor
according to mother

Urine FEME was done again noted to have :

Ketone +2
Blood +3
Protein +3
Rbc 900
I/O Monitoring
 Input output monitoring on first day of admission
• Input : 500ml
• Output : 295ml
• Balance : +205ml

Urine output ≈ 0.43cc/kg/hr.

 Input output monitoring on second day of admission

• Input : 950mls
• Output : 580mls
• Balance : +370

Urine output ≈ 0.86cc/kg/hr.

Review of results
• ASOT levels are not raised
• There was no growth noted on urine culture
• USG results were normal
• C3, C4 and throat swab results are still pending and will be
reviewed when patient come as outpatient in one week

• Patient was discharged on Friday (26th November 2010) at

noon with :
1. Syrup EES 425mg bid for 5 days (day 3 now)
2. Syrup Salbutamol 3mg tds
3. To come again at paediatric clinic in one week to review
pending results
Discussion
• Patient was generally asymptomatic throughout his stay in the
hospital apart from having dark colored urine.
• We should review the 24hr protein loss to determine the amount
of protein loss per day.
• Diagnostic studies of PSGN like ASOT is not conclusive, probably
because was done too early in the course of the disease.
• Serum C3 and C4 levels shall be reviewed to exclude any other
possible cause of hematuria other than AGN.
• Patient was discharged on the note that there was no
hypertension and diuresis has begun. Monitoring course of the
disease as outpatient is sufficient.
• Patient might have the possibility of having bronchial asthma
considering there’s positive history in the family. He also has
occasional episodes of cough. Such diagnosis shouldn’t be
discarded and should be treated
 References
1. Behrman RE, Kliegman RM, Jenson HB. Nelson Textbook of Paediatrics: 19th Edition: Chapter
503.1, Post-streptococcal Acute Glomerulonephritis.
2. Brouhard BH, Travis LB. Acute postinfectionus glomerulonephritis. In: Edelman CM, ed.
Pediatric Kidney Disease. 1992:1169-221.
3. Tom lissauer, Graham Clayden. Illustrated Textbook of Paediatrics: 3rd Edition: Chapter 18,
Kidney and urinary tract disorders. 2007:307-320.
4. Travis LB, Dodge WF, Beathard GA, et al. Acute glomerulonephritis in children. A review of the
natural history with emphasis on prognosis. Clin Nephrol. 1973;1(3):169-81
5. Oda T, Yamakami K, Omasu F, et al. Glomerular plasmin-like activity in relation to nephritis-
associated plasmin receptor in acute poststreptococcal glomerulonephritis. J Am Soc
Nephrol.2005;16(1):247-54
6. Herman A, Kappler JW, Marrack P, Pullen AM. Superantigens: mechanism of T-cell stimulation
and role in immune responses. Annu Rev Immunol. 1991;9:745-72
7. Haycock GB. The treatment of glomerulonephritis in children. Pediatr Nephrol. 1988;2(2):247-
55
8. Vander, Sherman, Luciano. Human physiology, the mechanism of body function. McGraw Hill.
Chapter 16: Basic principles of renal physiology.1994:515-517.
9. Sharon Taylor, Andrew Raffles. Diagnosis in color paediatrics. Mosby-Wolfe. Chapter 6: Kidney
and Urinary tract.1997: 173-185.