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ACUTE POST STREPTOCOCCAL

GLOMERULONEPHRITIS

Dr. GAP Nilawati SpA(K)


Nephrology Division of Pediatric Department
Faculty of Medicine Udayana University
Sanglah Hospital Denpasar
Hematuria
Def :
Presence of red blood cells (RBCs) in the urine

Confirm hematuria:
1. Dipstick
2. Microscopic
Hematuria:
1. Macroscopic Hematuria (gross hematuria)
2. Microscopic hematuria (> 3-5 RBCs/hpf)
Red urine, RBCs (-), dipstick (-)
Caused by:

1. Drugs: asetopenetidin, rifampicin


2. Toxin: benzene, carbontetrachloride
3. Deferoxamine administration
4. Heavy metal toxicity such as lead
5. Urates: common cause of orange-red
discoloration on diapers of infants
RBCs (-), dipstick test (+)
1. Hemoglobinuri
• Intravascular hemolytic (G6PD, PNH)
• intravascular Coagulation (Sepsis, HUS)
2. Myoglobinuri
• Myositis, crush injury, asphyxia

Causes of Hematuria:
1. Glomerular
• Erythrocyte cast
• Deform urinary RBCs
2. Non Glomerular
• Cast (-)
• Normal urinary RBC morphology
Etiology of hematuria

1.Renal bleeding
1.1. Glomerular hematuria
Acute glomerulonephritis
Membranoproliferative glomerulonephritis
Hereditary nephritis ( Alport Syndrome)
IgA nephropathy (Maladie de Berger)
Familial hematuria
Benign or persistent hematuria
1.2. extra glomerular hematuria
acute or chronic pielonephritis
kidney TBC
kidney tumor
hemangioma
policystic kidney
hidronephrosis
papillary necrosis
malformation (trombosis vena renalis)
trauma
idiopatic hypercalciuria
2. Extra renal bleeding
Urinary Tract Infection: cystitis, urethritis,
Urolithiasis
Trauma
Urinary Tract congenital anomaly
phymosis
stenosis meatus
“jengkol” intoxication
3. Systemic Disease
Henoch Schonlein syndrome
Systemic Lupus erytematosus nephritis
polyarteritis nodosa
subacute bacterial endokarditis
4. Hemolytic Disease
Leukemia
hemolytic uremic syndrome
idiopatic thrombocytopenia purpura
haemofilia
sickle cell glomerulopathy
5. Exercise
Substance and medicine which
caused hematuria
A. Metal: Arsenic
Gold
Phosphate
B. Chemotherapy medicine:
• Amfoterisin
• Ampisilin
• Kolistiimetat
• Kanamisin
• Metisilin
• Penicillin
• Polimiksin
• Sulfonamide
C. Drugs:

Acetylsalicylate Indometasin

Klorotiazid Fenasetin
Chlorpromazine Fenilbutason
Klonosin
Probenesid
Corticosteroid
Trifluoperasin
Cyclophosphamid
D. Organic substance
Carbon tetrachloride
Phenol
Propilenglikol
Turpentine
E. Anticoagulant
Heparin
Warfarin
APSGN
- This disease is a classic example of acute
nephritic syndrome, characterized by :
- gross hematuria
- edema
- hypertension
- kidney insufficiency
- APSGN is one of the most common gross
hematuria in children

Aetiology
– Infection of the throat or skin by strains of
group A β-Hemolytic streptococci (serotype
12 for throat) & (serotype 49 for skin)
Pathogenesis & path physiology
 Immunologic Disease (complex
immune)
 Ag-Ab complex in GBM → Immune
complex activated (alternative
pathway)
 GFR  & reabsorbs Na → edema

 Plasma Vol  → plasma renin 


Clinical Manifestation
 Incidence : 5 – 12 year
uncommon < 3 yr
 Latent phase 1-3 week
 Non specific Symptom
 Malaise, lethargy
 Abdominal or flank pain
 Hematuria
 Asymptomatic
 Gross hematuria (tea color/coca cola)
 edema  Salt and water retention
 Oliguria
 Hypertension (60%) → Encephalopathy, heart failure
 Decrease Renal Function
Diagnosis
 Clinical Symptom
 Encephalopathy → seizure
 Chest x ray → pulmonary vascular congestive
 Urinalysis: proteinuria, hematuria →
erythrocyte cast, granular cast
 Anemia
 C3
 Throat culture +/-
 ASTO , DNase B , anti hyaluronidase,
streptokinase
 Consider of Renal biopsy :
- Presence of Acute Renal Failure
- With Nephrotic Syndrome
- No Evidence of Streptococcal Inf
- Normal complement levels
- hematuria/proteinuria/diminished renal
function and/or a low C3 level persist
more than 2 month after onset
Differential Diagnosis
 SLE
 Acute exacerbation of Chronic
Glomerulonephritis
 IgA nephropathy
 Acute glomerulonephritis by other cause
- streptococcus pneumonia
- gram + / - bacterial
- bacterial endocarditic
- fungal, rickettsial, virus infection
COMPLICATIONS
 Acute Renal Failure
- hyper K
- hypo Ca
- acidosis
- hyper P etc
 Heart failure
 Pulmonal edema
 Encephalopathy (10%)
TREATMENT
 Bed rest on acute phase
 Fluid balance
 Sodium Restriction
 Diuretic for hypertension, heart failure,
edema pulmo
 Antibiotic (controversy)
 Anti hypertensive (Ca antagonist,
angiotensin-converting enzyme inhibitor,
vasodilators)
 Management of Acute Renal Failure
PROGNOSIS

 Complete recovery: > 95 %


 Recurrences are extremely rare
 C3 normal in 8 week
 Clinical symptom disappear on 2-3 week
 Microscopic hematuria consist much longer (1-2
year)
 Proteinuria/hypertension normal 4 – 6 week

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