Acute Glomerulonephritis-Post Streptoccocal GN: MBCHB Vi

ACUTE GLOMERULONEPHRITIS-
POST STREPTOCCOCAL GN
MBChB VI
Dr. Bernard B. O. Awuonda
http://ecampus.maseno.ac.ke Slide 1 of 5
Outline:
 Introduction
 History and physical examination
 Aetiology
 Clinical manifestation
 Investigations
 Management
 Summary
Introduction
 Often called the “nephritic syndrome.”
 Comprises a specific set of renal diseases in
which an immunologic mechanism triggers
inflammation and proliferation of glomerular
tissue that can result in damage to the
basement membrane, mesangium or capillary
endothelium.

Introduction ..2
 Characterized by sudden onset of hematuria,
proteinuria, and RBC casts.
 This clinical feature is accompanied by hypertension,
edema, azotemia (decreased GFR) and renal salt and
water retention.
History/presentation
Patients may complain of cola- or tea-colored
urine and decreased urine volume.
Edema occurs in many patients, typically face
and lower extremities
Shortness of breath may occur with significant
fluid overload.
Generalized malaise
History/presentation..2
Patients may also present with complaints more
specific to the associated disease:
◦ Joint pain or rash in lupus nephritis
◦ Hemoptysis in anti-GBM disease
◦ Sinusitis and pulmonary infiltrates in ANCA-
associated GN
◦ Abdominal pain and purpura in IgA-Henoch
Schönlein purpura
◦ Purpura and skin vasculitis in cryoglobulinemia-
associated GN
History/presentation..3
Macroscopic hematuria (coke-colored urine)
Sore throat
Impetigo
A prior URI of at least 1 week or skin lesions in the
proceeding 3 to 4 weeks suggests APSGN.
An upper respiratory infection URI in the proceeding
few days suggests IgA nephropathy.
Reduced urine output
Dyspnea, fatigue, lethargy
Headache
Seizures (hypertensive encephalopathy)
Symptoms of a systemic disease such as fever,
rash (especially on the buttocks and legs posteriorly),
arthralgia, and weight loss
Physical Exam
 A complete physical exam may discover clues to systemic
disease as a potential cause
◦ Sinus disease: ANCA-associated GN
◦ Pharyngitis or impetigo: Postinfectious GN
◦ Pulmonary abnormality: anti-GBM disease or lupus
nephritis
◦ Hepatomegaly or liver tenderness could point to
cryoglobulinemia-associated GN or IgA nephropathy.
◦ Purpura may point to ANCA-associated GN or Henoch
Schönlein purpura GN.
Physical Exam
 Hypertension
 Pallor
 Signs of volume overload (edema, jugular venous distention,
hepatomegaly, basal pulmonary crepitation, and a triple cardiac
rhythm)
 Impetigo or ecthyma (pyoderma)
 Signs of vasculitis such as rash, loss of fingertip pulp space
tissue, Raynaud, and vascular thrombosis
 Signs of a systemic disorder (see vasculitis above)
 Signs of chronic renal insufficiency such as short stature, pallor,
sallowness, edema, excoriations, pericardial friction rub,
pulmonary rales and effusion, uriniferous breath, asterixis,
myoclonus, and neuropathy
 Natural hx of disease is that of persistent
edema, recurrent infections and
progressive renal failure with death by age
of 5yrs.
 Treatment:
 Bilateral nephrectomy
 Chronic dialysis(indications for dialysis-
aeiou)
 Aggressive nutritional support
 Kidney transplant
Acute post streptococcal (APSGN)
 This is the prototype and most common cause
in childhood.
 Nephritis develops 1–3 weeks after
pharyngeal or cutaneous infection with
“nephritogenic” strains of group A β-
hemolytic streptococci.
 The incidence of GN is approx. 5-10% in
persons with pharyngitis and 25% in those
with skin infections.
Etiology:
The most common infectious cause of

acute GN is infection by
Streptococcus species i.e. group A
beta hemolytic esp. serotype 12
(URTI during winter) and 49 (skin
infection during summer and fall).
Pathophysiology:
 Previously M-protein of the organism was
thought to be responsible for PSGN but studies
on which this belief was based have been
discounted.
 Recently, nephritis-associated streptococcal
cationic protease and its zymogen precursor
(NAPR) has been identified as a glyceraldehyde-
3-phosphate dehydrogenase that functions as a
plasmin(ogen) receptor.
Pathophysiology..2
 Antibody levels to NAPR are elevated in
streptococcal infections (of group A, C, and G)
associated with glomerulonephritis, but are not
elevated in streptococcal infections without
glomerulonephritis, where as anti-streptolysin-
O titers are elevated in both circumstances.
 These antibodies to NAPR persist for years and
perhaps are protective against further episodes
of PSGN.
Clinical presentation
 Fever
 Headache
 Malaise
 Anorexia
 Nausea and vomiting
 High blood pressure
 Pallor due to edema and/or anemia
 Confusion
 Lethargy
 Loss of muscle tissue
 Enlargement of the liver
Signs and symptoms
a. Hematuria: dark brown or smoky urine
b. Oliguria: urine output is < 400 ml/day
(adults); <0.5-1 mls/kg/hour
c. Edema: starts in the eye lids and face then
the lower and upper limbs then becomes
generalized; may be migratory
d. Hypertension: usually mild to moderate
Clinical syndromes
 urinary (haematuria, proteinuria),
 nephritic (edemas, hypertension, gross
haematuria, proteinuria),
 nephrotic (edemas, proteinuria,
hypoproteinemia, hypercholesterolemia),
 mixed.
Clinical features
 Abrupt onset of:
 glomerular haematuria (RBC casts or
dysmorphic RBC).
 non-nephrotic range proteinuria (<2 g in 24 hrs).
 oedema (periorbital, sacral).
 hypertension.
 transient renal impairment (oliguria, uraemia).
INVESTIGATIONS
 Urinalysis with examination of sediment:
◦ Dysmorphic red blood cells (RBCs) or RBC casts on
urine microscopy indicate glomerular hematuria and
suggest the diagnosis of an acute glomerulonephritis.
 Electrolytes,
 Blood urea nitrogen (BUN),
 Creatinine,
 Complete blood count (CBC)
 Antistreptolysin O titer (ASOT)
 Streptozyme
INVESTIGATIONS..2
Complement levels (C3 and C4):
◦ C3 complement levels are abnormal in
postinfectious GN; C3 and C4 are abnormal in
lupus nephritis and MPGN; C4 can be low in
cryoglobulinemia.
Proteinuria:
24-hour collection or random urine
protein/creatinine ratio
INVESTIGATIONS..3
Antinuclear antibody (ANA) to rule out lupus
nephritis
ANCA antibody screen:
◦ MPO and PR3 antibodies
Anti-GBM antibody
Hepatitis B antigen
Hepatitis C antibody
INVESTIGATIONS..4
 Throat culture for b²-hemolytic streptococcus (positive in 15%
to 20% with APSGN)
 Serum chemistries will reflect the degree of renal failure
(raised serum urea and creatinine). The serum potassium and
phosphate will be elevated and the calcium decreased.
 ASOT (antistreptolysin O) titer. Positive in 60% of patients with
APSGN.
 Streptozyme test: A mixed antigen test for Î²-hemolytic
streptococcus. Together, the ASOT plus streptozyme tests
have greater than 85% sensitivity.
 ECG to assess ventricular size and for hyperkalemia.
INVESTIGATIONS
CXR to look for pulmonary edema and cardiac

size.
Renal ultrasound if presentation or course not
typical of APSGN. The ultrasound is to assess
the size and parenchymal texture.
DIAGNOSIS
 Dx depends on:-
 Positive pharyngeal or skin culture (if
available).
 Positive titers for antistreptococcal antigens
(ASO, anti-DNAse, or antihyaluronidase).
 Hypocomplementemia.
 Renal biopsy reveals diffuse proliferative GN.
 Treatment consists of correction of fluid and
electrolyte imbalance.
DDX- hematuria
 Non-glomerular  Glomerular
 Infection (bacterial, viral,  Acute glomerulonephritis
TB, schistosomiasis) (usually with proteinuria)
 Trauma to genitalia, urinary  Chronic glomerulonephritis
tract or kidneys (usually with proteinuria)
 Stones  IgA nephropathy
 Tumours  Familial nephritis
 Sickle cell disease  Thin basement membrane
 Bleeding disorders disease
 Renal vein thrombosis
 Hypercalciuria
Management
 Antimicrobial therapy
◦ Antibiotics (eg, penicillin) are used to control local

symptoms and to prevent spread of infection to close
contacts.
◦ Antimicrobial therapy does not appear to prevent the
development of GN, except if given within the first 36 hours.
 Loop diuretic therapy

◦ Loop diuretics may be required in patients who are
edematous and hypertensive in order to remove excess
fluid and to correct hypertension.
◦ Relieves edema and controls volume, thereby helping to
control volume-related elevation in BP.
Management
 Restricted fluid, sodium, potassium, and phosphate are initially
required
 Serum potassium-lowering agents (Kayexalate, furosemide,
bicarbonate, insulin/glucose, salbutamol). Intravenous calcium is
used to stabilize the myocardium in severe hyperkalemia.
 Phosphate binders
 Immunosuppressive agents such as prednisone,
cyclophosphamide, and sometimes azathioprine are used in the
treatment of vasculitis-associated GN, membranoproliferative
GN, and RPGN.
 Plasmapheresis may be used to treat RPGN. Penicillin is used in
APSGN but does not affect the course of the disease.
Complications
 Acute renal failure
 Hyperkalemia
 Hypertension
 Volume overload (congestive cardiac failure,
pulmonary edema, hypertension)
 Chronic renal failure
 Hypertensive encephalopathy
 Acute renal necrosis due to injury of capillary
or capillary thrombosis
Prevention
proper hygiene
prompt medical assessment for necessary
antibiotic therapy should be sought when
infection is suspected
prophylactic immunizations
Prognosis
 - Has a GOOD prognosis if treatment is
initiated early.
 - Supportive measures until spontaneous
recovery.
 - Control Hypertension.
 - Fluid balance.
 - Oliguric with fluid overload.
 - GN complicating SLE or systemic vasculitides:
immunosuppression with prednisolone,
cyclophosphamide or
azathioprine/Mycophenolate mofetil.

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ACUTE GLOMERULONEPHRITIS-

The most common infectious cause of

CXR to look for pulmonary edema and cardiac

◦ Antibiotics (eg, penicillin) are used to control local

 Loop diuretic therapy

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