Acute post-streptococcal glomerulonephritis is characterized by sudden onset symptoms such as hematuria, edema, and hypertension, predominantly following infections from beta-hemolytic streptococci. It is an immune-mediated disorder leading to acute kidney injury, with a significant incidence in resource-poor countries and primarily affecting children aged 6-10 years. The prognosis is generally excellent, with most patients recovering renal function within weeks and a low incidence of chronic kidney disease thereafter.

1. Acute post streptococcal
glomerulonephritis
Dr Sajid Noor

2. Definition
 It is characterized by sudden onset of gross hematuria,
edema, hypertension and deranged RFTs.
 Most common Immune-mediated, glomerular inflammatory
disorder leading to acute kidney injury (AKI).
 85 % of cases follow an infection by beta-hemolytic
streptococci.

3.  It is classical self-limiting illness resulting from prior
pharyngeal or cutaneous infection with group beta-
hemolytic streptococci.
 Alternative etiologies
S.pneumoniae (rare), S.aureus and other non-
streptococcal bacteria. Viral infections (e.g.EBV, parvovirus
B19)

4. Epidemiology
 The disease burden is highest in resource-poor countries.
 Incidence 9.5–28.5 new cases per 100,000 person-years.
 Glomerulonephritis risk 5 % with pharyngitis and 25 % after
skin infection of nephritogenic S. pyogenes infections.

5. Pathogenesis
 Exact mechanism of glomerular injury is debated
 It though that to be an immune-complex mediated
disease.
 Pattern of hypocomplementemia in AGN reflects
activation of the alternative complement pathway (AP):
 plasma C3, C5, and properdin levels are transiently
decreased in the presence of preserved concentrations of
C4.

6.  Current hypotheses:
1. Antibodies bind to streptococcal antigen(s) planted in the
glomerular basement membrane leading to alternative
complement pathway activation.
2. Two streptococcal proteins, have been identified in the
GBM of APSGN patients and proposed as pathogenic
antigens.
3. Antigen-antibody complexes are formed in the circulation
and deposited in the glomeruli and may incite glomerular
damage through activation of the complement system.

7.  APIGN due to streptococcal pharyngitis peaks during
winter and early spring
 Due to Skin Infection (pyoderma) peaks in late summer
and early fall and the latter is more common in tropical
and subtropical regions.
 It occurs at any age but peaks in children ages 6–10 (2–12)
years.
 Male to female ratio 2:1.1.
 Siblings are also at risk of developing subclinical nephritis.

8. Clinical Features
 The clinical manifestations ranges from asymptomatic
microhematuria to severe disease Complications due to
hypertension, renal failure, and cardiac insufficiency.
 Hypertension
 Edema
 Hematuria
 Protienuria
 Oliguria.
 Acute kidney injury.


9.  Hypertension (60%)
Headache, vomiting, seizures,
somnolence/altered mental status, Risk of posterior
reversible encephalopathy syndrome (PRES) with visual
changes and focal neurological signs

10.  Edema.
Facial/periorbital, dependent, or generalized
edema (more frequently in young children) Ascites, pleural
effusion, Cardiac insufficiency (orthopnea, dyspnea,
cough, pulmonary crackles/edema, and gallop rhythm)

11.  Hematuria.
Dark-brown urine (cola- or tea-colored) in one-
third of patients; remainder microscopic hematuria.

12.  Proteinuria.
Mild to moderate, rarely nephrotic range
(>1g/m2/day)
 Oliguria.
Transient oliguria in 50 %, complete anuria rare

13.  Acute kidney injury.
Nausea, vomiting fatigue, weakness, pallor
 Others.
Back pain and abdominal discomfort, fever, weight
gain (edema)

14. Investigations
 Urine.
 Dipstick analysis
Hematuria, proteinuria
 Urine microscopy
Red blood cell (RBC) and mixed cellular casts
Dysmorphic RBCs
Leukocytes (sterile pyuria)
 Proteinuria
<2 g/l in 85 % of cases (U protein/creatinine <2 g/g)
Nephrotic presentation may herald poor renal outcome

15. Complement
Reduced plasma C3 and CH50 in >90 % of cases
Normalize within 6–12 weeks after presentation.
Plasma C4 generally normal.

16. Bacterial
Pharyngeal swab
Index patient and siblings (opportunity of
preventing spread of nephritogenic strain)
Culture of beta-hemolytic streptococci
Rapid streptococcal antigen test
Skin swab
Suspected pyoderma

17. Serology.
Antistreptolysin O titer (ASOT);
Elevated in 70–80 % 1–5 weeks after infection, decrease
to preinfection levels after several months.
Unreliable for streptococcal pyoderma or infection by
other organisms
Streptozyme test;
Detecting antibodies against several streptococcal
antigens (streptolysin O, DNaseB, hyaluronidase, streptokinase,
anti-nicotinamide adenine dinucleotidase (NADase)
Anti-Dnase B;
Elevated in 80–90 % of cases of pyoderma-associated
APSGN

18. Kidney biopsy Indications (rare):
Alternative diagnosis (e.g., MPGN, IgA).
Normal serum C3/CH50.
Persistently low serum C3 or CH50 (>12 weeks after
onset).
Persistent GN/deteriorating renal function.

19. Natural resolution.
 The acute phase usually lasts 4-10 days when urine output
gradually increases; edema subsides and RFTs return to
normal.
 Gross hematuria seldom persists beyond the weeks but
microscopic hematuria may persist for 1-2 years.
 Low grade proteinuria may be found up to months after
onset of AGN.
 Long-term prognosis is excellent.
 The incidence of CKD remains 1% after APSGN

21.  General/Supportive treatment
1. Bed rest:
Patient should be preferably hospitalized for close
monitoring of BP and any derangement of RFTs and treatment of any
complications as they arise.
1. Antibiotics:
2. Dietary restrictions:

22. Treatment;
 Hypertension and fluid overload;
Restriction of sodium and fluid intake
Loop diuretics (furosemide)
Antihypertensive drugs
If blood pressure is not controlled with
diuretics Preferably calcium channel blocker or angiotensin-
converting enzyme inhibitor (ACEi)

23.  Pulmonary edema (rare);
 Hypertensive urgency or emergency (with or
without CSN symptoms);
Loop diuretics, Oxygen therapy
Oral agents (nifedipine, hydralazine, minoxidil)
Intravenous agents (nitroprusside, nicardipine,
labetalol)

24.  Hyperkalemia;
Loop diuretic
K restriction,
sodium polystyrene sulfonate
Inhaled bronchodilator,
IV calcium or bicarbonate, or insulin drip
If refractory, dialysis

25. Dialysis or continuous veno-venous hemofiltration
Life-threatening hyperkalemia
Severe fluid overload unresponsive to diuretics
Rapidly progressive GN with persistent oligoanuria

26. Antibiotics;
Obtain throat cultures from patient, family members, and
close contacts
Treat those infected to minimize spread of nephrito-
genic strain
Oral penicillin V for 10 days (<25 kg = 250 mg twice
daily, >25 kg 500 mg twice daily)
Erythromycin (40 mg/kg for 10 days) or derivative for
patients allergic to penicillin

27. Prognosis and Outcome;
Short- and long-term prognosis of APSGN in children is excellent.
95 % of the patients recover renal function within 3–4 weeks.
Chronic or progressive kidney disease <1 % of children (higher percentage in
adults).
Recurrence of APSGN extremely rare due to streptococcal type-specific, long-
lasting immunity and limited number of nephritogenic GAS strains.

28. Thank You