This document presents a case of an 8-year-old male patient presenting with facial swelling and dark urine. Investigations revealed hematuria, proteinuria, elevated creatinine and low C3 complement levels. A renal ultrasound showed enlarged kidneys. The differential diagnosis includes post-infectious glomerulonephritis given the recent sore throat and positive throat swab for Group A streptococcus. Nephritic syndrome is characterized by glomerular inflammation and injury leading to hematuria, proteinuria, hypertension and possible renal failure. Treatment involves managing complications, antibiotics if infection is present, dialysis for severe cases, and steroids if associated with nephrotic syndrome. Prognosis depends on severity and underlying cause

1. CASE PRESENTATION
• CC: 8 yr old male Pt with facial swelling and dark urine
• HPI: Started 3 days prior to admission with facial swelling
followed with dark (coca colored) urine & ↓ urine output
while he was drinking fluids well. But no urinary frequency,
no urgency, no dysuria.
• ROS: unspecified abdominal pain, negative for recent skin
infection, no skin rash, no cough, no rhinorrhea, no fever,
no arthralgia nor weight loss

2. CASE PRESENTATION cont……
• PMH: had sore throat and fever 2 weeks ago that
resolved w/o attending any hospital
• Family hx: he lives with his parents, he is the 4th child
in a family of 5 children.
• Social hx: he performs well at school, UBUDEHE cat
3.

3. CASE PRESENTATION cont……
• P/E:
 tired appearing but in no acute distress
 T⁰: 37, HR:100, RR:20, BP:145/90, SaO2: 99% in RA.
peri-orbital edema, otherwise well
CVS: CRT˂ 2s , heart sounds are normal no added
sound, warm peripheral extremities.
CNS, RS, GIT and GUS are unremarkable
• WHAT IS YOUR DIFFERENTIAL DIAGNOSIS???

4. CASE PRESENTATION
(INVESTIGATIONS)
• Dipstick: urine - His urine is tea colored, RBCs 4+, protein 2+
• Urinalysis: RBCs are too numerous to count, 5-10 WBCs per F,
RBC casts
• Na+ 132, K 5.0, Urea 19.0, creatinine 110umol/l,
• Complements C3: 0.5(0.8-1.8), C4:normal
• Renal U/S: enlarged kidneys with normal cortical region, No
stones detected
• ↑ASO titer & positive throat swab to GAS
Management?????

5. NEPHRITIC SYNDROME
DUKUNDANE Alexandre(MD)
University of Rwanda
Supervisor: Dr Claude Ntiyamira

6. Outline
• Introduction
• Epidemiology
• Etiology
• Pathophysiology
• Clinical manifestations
• Differential diagnosis
• Paraclinical investigations
• Management
• Complications
• Prognosis
• Take home message.

7. Introduction
• Neprotic syndrome is a syndrome caused by numerous
disorders that are all characterized by glomerular injury
accompanied by inflammation.
• It may progress to renal failure.

8. Nephritic syndrome consists of
combination of some of the
following signs:
• Hematuria with acanthocytes
• RBC casts and other cellular casts in urine
• Proteinuria including nephrotic range proteinuria
• Elevated blood pressure
• Mild to moderate ascites
• Sterile pyuria
• Oliguria
• azotemia

9. Epidemiology
• It comprise 10-15% of glomerular diseases and 25-
30% of all cases of ESRD.
• The most common cases occur in patients aged 5-15
years.
• PSGN remains the most common cause in Africa.
• PSGN outbreaks are common in in children aged 6-10
years.
• Males affected than female (2:1).

10. Etiology
GN may be isolated to kidney( primary GN) or be a
component of systemic disorder( secondary GN).

11. Etiology
A. Post-infection glomerulonephritis:
• In children, the most common cause is post
streptococcal glomerulonephritis( group A beta
hemolytic streptococcus).
• Usually it develops 1-3 weeks after acute infection with
group A beta hemolytic streptococci( skin or sore throat).
• Other bacterial infections include: endocarditis,
pneumonia, typhoid fever.
• Viral infections: EBV, parvovirus B19, Rubella,…….
• Parasitic infections: plasmodium falciparum, schistosoma
mansoni,…

12. Pathophysiology
• The pathogenesis is not fully understood.
• The current evidences suggest that most cases are
due to immunologic response to a variety of different
etiologic agents;
• Immunological response leads to activation of
biological processes which result in glomerular
inflammation and injury.
• Glomerular lesions are the results of glomerular
deposition or in situ formation of immune complexes.

14. Pathophysiology
• humoral immune response to a variety of etiologic
agents → immunoglobulin deposition and complement
activation, → leukocyte recruitment, → release of
growth factors/cytokines → glomerular inflammation
and injury → damaged podocytes → hematuria + RBC
casts ± proteinuria

17. CLINICAL MANIFESTATIONS
Typical Non specific symptoms
• hematuria
• Proteinuria < 50mg/kg
/day or 40mg/m2/h
• hypertension
• edema
• Elevated urea&creat
• oliguria
• malaise,
• lethargy,
• abdominal pain
• flank pain
• fever

18. Differential Diagnosis
• Nephrotic syndrome
• AKI/CKD
• Rapid progressive glomerulonephritis
• UTI
• Kidney malignancy.

20. Investigations
• Urine dipstick test
• Urinalysis ( RBC cast, proteinuria, WBC)
• Urea,cratinine and electrolyte.
• FBC
• ASOT( Anti-streptolysin O titer )
• ANA. Anti nuclear antibodies
• Throat swab (culture)

21. Investigations
• Viral hepatits screaning, TB screaning, HIV
• immunoglobulin, antibodies,
• Imaging ex: abdominal ultrasound
• Serum complement
• Kidney biopsies

22. Renal Biopsy Indications
• Age < 1year and > 10 years
• HTN
• Resistance to steroids
• Acute Renal Failure
• Persistent Hematuria
• Persistent Proteinuria
• Low C3 level persist > 2 months after onset
• Absence of evidence of streptococcal infection

23. Management
Treat life-threatening complications first:
- Hyperkalemia
- Hypertension
- Metabolic Acidosis
- Seizures
- Hypocalcemia

24. Pharmacological Management
Hypertension
• treat fluid overload with furosemide 1–2mg/kg bd ;
• ACEI :
Captopril 0.3-0.5mg/kg/dose
• Calcium channel blocker:
Amlodipine 0.2mg/kg/dose
Nifedipine o.2-1mg/kg/dose

25. Pharmacological Management
• If there is infection: 10 days course of antibiotics.
• If associated with nephrotic syndrome; steroids are
given.
• Dialysis to support kidney function in severe cases.
• Surgical management: Renal transplant.

26. Indications of dialysis
• Volume overload
• Persistent hyperkalemia
• Severe metabolic acidosis
• Blood urea nitrogen greater than 100–150
mg/dL

27. Management
Non pharmacological management
Bed rest
A diet modification
 reduction of salt, potassium and fluid in take
Dialysis

28. Complications
• Acute renal dysfunction
• Hypertension
• Heart failure
• Hyperkalemia
• Hyperphosphatemia
• Hypocalcemia
• Acidosis

29. Prognosis
• Recover from nephritic syndrome varies according to
its severity and the underlying cause.
• Post-infectious usually self-resolving (recovery > 95%
of renal function).
• Most patients begin to feel better fairly soon, especially
if treatment is prompt.
• Factors which cause the prognosis to be more serious
Malnutrition
HIV infection
Chronic illness

30. Take home message
• Glomerular injury and inflammation
• Hematuria, proteinuria, edema, HTN, uremia, and
oliguria are classical symptoms.
• Look and treat first life threatening complications.
• Steroids are not usually indicated unless it is
associated with nephrotic syndrome.

31. References
1. The Harriet Lane Handbook - A Manual for Pediatric
House Officers, 2015
2. https://emedicine.medscape.com/article/239278-
treatment
3. University of Tennessee Medical Centre acute
nephritic syndrome Accessed 23 February 2018
4. UpToDate
5. Medscape
6. AMBOSS

32. THANK YOU FOR YOUR
KIND ATTENTION