Investigations and management of acute glomerulonephritis in children

1. Weekly case discussion
 presented by
Dr Fareed Alam
PGR pediatrics dept
PHQ hospital Gilgit

2. Patient’s Profile
Name Hashim
Age 8 year
Gender Male
Resident of Kargah
Date of admission 20-09-23
Admitted via Emergency

3. Presenting complaints
 cough 4 days
 Breathing difficulty 4 days
 Body swelling 3 days
&
 Cola colored urine 2 day

4. History of presenting illness
According to mother , patient was apparently alright 4 days
back when he developed cough, which was gradually
started , initially mild in intensity and then progressively
aggravated over time, non-productive ,aggravated by lying
flat and relieved by sitting upright, associated with
breathing difficulty, which was gradually started, of
moderate to severe intensity ,continuous, aggravated by
exertion and lying flat and relieved by sitting erect with
difficulty in sleeping at night.
Patient has also history generalized body swelling which
was gradually started as puffiness around eyes face and
progressively involved bilateral feet ,lower limbs and hands
which was more in the morning then comparatively
decreased as the day progressed

5. Body swelling was followed by cola colored urine from 2
days which was sudden in onset, present throughout the
urinary stream, with no history of pain during micturition,
urinary hesitancy, urgency and history of decreased
frequency of urine (normally patient used to void 3-4
times/day) now 1-2 times /day of small volume with no
aggravating and relieving factor noted by patient.
Patient had history of pustular skin lesions 2 weeks back
which were gradually started from face hands and then
involved whole body associated with itching and high
grade fever ;resolved by taking treatment from doctor
(record not available).

6. There is no previous history of any of the above symptoms
in the past.
No history of headache ,altered sensorium,blurring of vision
and seizure.
No history of chest pain,palpitations,cyanosis and wheeze in
the chest.
No history of acute upper respiratoy symptoms in past.
No history of hearing loss and vision disturbance.
No history of loose motions,vomiting and fever.
No history of joint pain and body rash.

7. No history of petechia/bruises on body,gingival bleed,
epistaxis,hemoptesis,hematemesis and malena.
No history of
alopecia,photophobia/photosensitivity,oral ulcers,rash
on face ,joint pain and body pain.
No history of polyphagia,polydipsia and polyurea.
No history of any drug intake and inscet bite.

8. Past history:
Past medical and surgical history is not significant.
Vaccination history:
Unvaccinated
Family history:
Family composed of total 8 family members; including both
parents and 6 siblings out of non consanguineous marriage. All are
healthy and alive with no family history of chronic illness and
congenital issues in family.
Birth history:
Birth history is uneventful, SVD at home.
Developmental history
No history of developmental delay,having normal speech ,hearing
and intellect.

9.  Socioeconomical history:
living in his own kacha house with one room and a
washroom, father is a labourer and belong to lower
socio-economic status.

10. On examination:
clinically extremely sick looking child sitting on bed ,concious and alert
with obvious respiratory distress,having facial puffiness and bilateral pitting
pedal with vitals of
Pulse rate: 130/mint
R/Rate: 60/mint
TEMP: 100F
BP: 140/120.
PO2: 52% at room air.
Weight 28kg
Systemic examination:
Chest: shape of chest was normal with no obvious scar marks,visible
veins,equal chest movement on both side with chest expansion of 2-3cm.
On auscultation there was bilateral NVB, decreased air entery at the base of
both with wide spread crackles on both side.

11. Abdomen was distended with slit like umbilicus , wide spread scar marks,
tense on palpation ,tenderness on right hypochondrium on deep palpation
with hepatomegaly i.e. palpable 5cm BRHC.
CVS : S1 and s2+no added sound .
CNS : GCS 15/15; pupils :R/R/R
Power 5/5, tone normal in all limbs.
Reflexes were intact.

12. SUMMARY
8 year old male previously all well presented to us with
complaints of cough for 4 days, breathing difficultyand
generalized body swelling for 3 days and cola colored urine for
1 day. Patient had history pustular skin lesions 2 weeks back
which were resolved by taking treatment from doctor. On
examination extremely sick ,tachypneic having facial puffiness
and pedal edema, decrease air entry in chest with bilateral
crackles and distended abdomen with slit like umbilicus and
hepatomegaly.

13. Differential diagnosis:
 Acute glomerulonephritis (post streptococcal).
 Nephrotic syndrome .
 Acute kidney injury.
 Good pasture syndrome.
 IgA nephropathy .

14. Management:
Initial general management include:
Admitted. in ward
Maintained iv line.
O2 inhalation with bubble CPAPwas started immediately.
Passed NG tube.
Foleys catheter .
Input output monitoring started ..
Vitals monitoring: blood pressure,spo2,temp and heart rate.
Laboratory investigations were advised.

15. Treatment:
IV antibiotics ( inj calamoux and inj Ceftriaxone).
IV fluids ( restricted fluid)
Inj lasix 20 mg bd.
After nephrologist and cardiologist consultation further medications
were included in treatment plan :
fluids were stopped.
tablet lisinopril 2.5mg x OD
inj Lasix 40mg x OD
tablet disprin 300mg x OD
Tab digoxin 0.25mg half tab x OD (started after echo report).

17. Investigations:
CBC
Tlc 16.9 neutrophils 86% and lymphocytes 29 %
Hb 12.2 g/dl
Mcv 79fl
Plt 593/ul
Renal function test
Serum urea 39mg/dl
Serum creatinine 1mg/dl

18. Serum electrolyte
Sodium: 143mmol/dl
Potassium: 4.7mmol/dl
Chloride: 112mmol/dl
Bicarbonate: 20.7mmol/dl
PH: 7.6
Urine RE:
Albumin: trace.
Wbcs: 2-3/hpf
RBCS: numerous.

19. RBS: 93mg/dl.
Serum cholesterol: 122mg/dl.
Serum triglyceride: 114mg/dl.
Uric acid: 5mg/dl
Serum albumin: 2.3g/dl.
ASO TITRE: 534.7iu/ml

21. X ray reporting:
Non homogenous opacification of right midlower lung zone
representing acute consolidative changes.
b/l hilar congestion.
b/L cp angle are intact.

23. ECHO REPORT:
LVEF: 45-50%
SWMA shows mild global hypokinesia (post myocarditis sequel)

25. Course of hospital stay

27. Acute Glomerulonephritis:
An acute inflammation of renal glomerular parenchyma due to deposition of
immune complexes characterized by sudden onset of oliguria hematuria,
hypertension, and edema.
:Etiology:
Streptococcal infection.(beta hemolytic group A)
Non streptococcal.
Bacterial: infective endocarditis, shunt nephritis, syphilis, S pneumonia.

28. Viral causes: HBV, mumps, varicella, coxackie infective mononucleosis.
Autoimmune: good pasture syndrome , HSP,SLE, IgA nephropathy.
Pathology:
Gross:
Both kidneys enlarged.
Ischemic
Microscopy:
Glomeruli enlarged,infiltrated by polymarphs and epithelial crescents.

29. Immunofluorescence:
Lumpy bumpy deposition of igG antigen and c3.
Electron microscopy:
Mesangial proliferation and mesangial matric deposition.
Lump of immune deposition on the epithelial side of GBM.

30. Pathophysiology:
Oliguria:
Spasm of afferent arteriole (decrease blood flow).
Obliteration of lumen by mucosal edema and cellular infiltration.
Crescents causes obstruction.
Increased absorption of Na and water from renal tubules.
Hypertension:
Increase absorption of Na and water from renal tubules.
Inc sympathetic activity.
Inc arterial spasm.
Inc cardiac output.
Oedema:
Retention of Na and water from renal tubules.
Circulation of unknown antigen causing peripheral vasodilatation.

31. Post streptococcal glomerulonephritis:
Etiology:
Usually occurs 7-14 days after throat infection
and 2-6 weeks after skin infection by group A B-hemolytic streptococci.
Streptococcal antigens involved in immune reaction i.e zymogen precursor of
exotoxin.
Age group:
5-12 years
Male predominance.
Seasonal variation: during winter and rainy season serotype M1 M4 and M12
causes acute pharyngitis and during summer serotype M49 causes skin
infection.

32. Pathogenesis:
Cross reaction of streptococcal pyogenic exotoxin-b and other M proteins
with the various component of glomerular basement membrane.
Type 3 immunological reaction in which glomeruli are damaged due to
deposition of igG antibody antigen and complement c3.
Clinical features:
Fever.
Facial puffiness.
Edema feet
Oliguria
Cola colored urine, breathing difficulty, hypertension, abdominal pain.
Atypical presentation include hypertensive encephalopathy i.e confusion
convulsion etc.
Pulmonary edema due to CHF
Acute renal failure

33. DIAGNOSTIC CRITERIA:
At least two of the following criteria must be present.
1:positive throat or skin culture for streptococcus.>confirmatory or carrier
state.
2:Streptococcal product like anti streptokinase anti DNAse B ASO titre are
elevated.
3:Hypocomplementemia> serum c3 reduced by 90% but c4 is normal.

34. Ivestigations:
Urine analysis:
Proteinuria> non selective 1+ or 2+ e red cells.
hematuria:
RFTS:
Blood urea and creatinine increses due to dec GFR.
Low c3 complement.
ASO TITRE.
ESR (Increased)
c3 and c4 levels.
throat swab culture and anti DNAse B antibody.

35. Management:
Give complete bed rest.
Vital monitoring.
Fluid and salt restriction.
Input output monitoring.
Daily weight monitoring.
Propped up position and provide oxygen.
Mange hypertension: (anti hypertensive drugs e.g ca channel blocker ACE
inhibitors )
Diuretics if significant edema fluid overload are present.
Infection control by antibiotics e.g penicillin to eradicate streptococci in
throat or skin.
Management of complications, like CCF hypertensive encephlopathy,.

36. Complications:
Hypertensive encephalopathy.
Hypertensive heart failure.
Hypocalcaemia.
Hyperkalemia.
Acute renal failure.
hyperphosphatemia
Prognosis:
Complete recovery in 95% cases.
1-5% mortality.
1-5% develops chronic GN, chronic renal failure.

37. 
 Thank you: