07 Post-streptococcal Glumerulonephritis - Gh

7/27/2019 07 Post-streptococcal Glumerulonephritis - Gh

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Post-streptococcal GlomerulonephritisBlock VII: Bloody urine and Puffy eyelidsTutor: Dr. A. QuilalaPrepared by: Goldie Hernandez

DEFINITION AGN follows infection of the throat or skin by certain

nephritogenic strains of group A -hemolyticstreptococci

This is a classic example of the acute nephriticsyndrome characterized by the sudden onset of gross hematuria, edema, hypertension, and renalinsufficiency.

one of the most common glomerular causes of grosshematuria in children, surpassed only by IgAnephropathy.

EPIDEMIOLOGY The incidence of poststreptococcal

glomerulonephritis has dramatically decreased indeveloped countries and in these locations is

typically sporadic; epidemics are less common. In underdeveloped countries usually affects childrenbetween the ages of 2 and 14 years, but indeveloped countries is more typical in the elderly,especially in association with debilitating conditions

It is more common in males, and the familial orcohabitant incidence is as high as 40%.

ETIOLOGY

Poststreptococcal glomerulonephritis followsinfection of the throat or skin by certain

nephritogenic strains of group A -hemolyticstreptococci.

Poststreptococcal glomerulonephritis commonlyfollows streptococcal pharyngitis during cold

weather months and streptococcal skin infections or

pyoderma during warm weather months. Skin and throat infections with particular M types of

streptococci (nephritogenic strains) antedate

glomerular disease M types 47, 49, 55, 2, 60, and 57 are seen

following impetigo

M types 1, 2, 4, 3, 25, 49, and 12 withpharyngitis.

Poststreptococcal glomerulonephritis due toimpetigo develops 2 6 weeks after skin infection

and 1 3 weeks after streptococcal pharyngitis.

PATHOPHYSIOLOGY

Post-streptococcus Glomerulonephritis is believed tobe an immune-mediated disease, in which an

immune complex containing a streptococcal antigen

is deposited in the affected glomeruli. Two nephritogenic streptococci antigens are

1. cationic cysteine protease streptococcalpyrogenic exotoxin B

2. nephritis-associated streptococcal plasminreceptor, which is a plasmin-binding protein

with glyceraldehyde phosphate dehydrogenase

(also known as presorbing antigen or PA-Ag)

CLINICAL PRESENTATION

1. EDEMA ( periorbital edema) The onset of puffiness of the face or eyelids

is sudden. It is usually prominent uponawakening and, if the patient is active,

tends to subside at the end of the day. In some cases, generalized edema and

other features of circulatory congestion,

such as dyspnea, may be present. Edema is a result of a defect in renal

excretion of salt and water

2. Gross hematuria Smoky, tea-colored, cola-colored, or fresh

bloody urine

This is often the first clinical symptom. Dark urine is caused by hemolysis of red

blood cells that have penetrated the

glomerular basement membrane and have

passed into the tubular system.

3. Proteinuria usually normalize after 4 weeks4. Oliguria5. Hypertension mild to moderate, typically subsides

promptly after diuresis

6. Systemic symptoms of headache, malaise, anorexia,and flank pain (due to swelling of the renal capsule)

are reported in as many as 50% of cases The acute phase generally resolves within 6 8 wk.

Although urinary protein excretion and hypertensionusually normalize by 4 6 wk after onset, persistentmicroscopic hematuria may persist for 1 2 yr after

the initial presentation.

LABORATORY INVESTIGATIONS

Urinalysis Results are always abnormal.


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Hematuria and proteinuria are present in allcases.

Urine sediment has red blood cells, redblood cell casts, white blood cells, granular

casts, and, rarely, white blood cell casts. Dysmorphic red blood cells indicative of

glomerular hematuria can usually be

detected by performing phase-contrast

microscopy. Red blood cell casts are best detected in

first, early-morning urine specimens

examined by the physician immediately

after the patient voids. Proteinuria may be mild or so severe that it

causes nephrotic syndrome. Evidence of preceding streptococcal infection

A positive throat culture report maysupport the diagnosis or may simply

represent the carrier state.

a rising antibody titer to streptococcalantigen(s) confirms a recent streptococcal

infection. antistreptolysin O titer is commonly

elevated after a pharyngeal infection but

rarely increases after streptococcal skin

infections. The best single antibody titer to

document cutaneous streptococcal

infection is the anti-deoxyribonuclease

(DNase) B level. The Streptozyme test is a useful and simple

diagnostic test that detects antibodies to

streptolysin O, DNase B, hyaluronidase,

streptokinase, and nicotinamide-adenine

dinucleotidase using a slide agglutination

test. Renal function test

This reflects the decrease in the glomerularfiltration rate that occurs in the acute

phase. The BUN concentration is elevated in 75%

of patients, and serum creatinine level is

increased in one half of the patients, but

profound decrease in GFR is uncommon in

children. Hyperkalemia, hypocalcemia, hyponatremia

and metabolic acidosis are seen only in

severe patients. Complete blood count

A mild normochromic anemia may bepresent from hemodilution and low-grade

hemolysis

Leukocytosis maybe present Serologic findings

Low serum complement levels indicative of an antigen-antibody interaction are a

universal finding in the acute phase of

PSGN. Most patients have marked depression of

serum hemolytic component CH50 and

serum concentrations of C3 Positive rheumatoid factor (30 40%),

cryoglobulins and circulating immune

complexes (60 70%), Kidney ultrasound not necessary if patient has

clear cut acute nephritic syndrome Renal biopsy

Light microscopy- glomeruli appear enlarged- demonstrates hypercellularity of

mesangial and endothelial cells,

glomerular infiltrates of

polymorphonuclear Electron Microscopy

- Subepithelial electron-dense depositsor humps are present which are

observed on the epithelial side of the

glomerular basement membrane Immunofluorescence microscopy

- Lumpy-bumpy deposits of immunoglobulin G and complement C3

along the capillary loops and within the

mesangium

COMPLICATIONS

Hypertension Acute renal failure Congestive heart failure

TREATMENT

Treatment of PSGN is largely that of supportive care Patients undergo a spontaneous diuresis within 7-10

days after the onset of their illness Diuretics Diet Fluid restriction, sodium restriction

(necessary) Antibiotics 10 day course of systematic antibiotic

therapy with penicillin V is recommended to limit

the spread of the nephritogenic organisms During the acute phase of the disease, restrict salt

and water.


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If significant edema or hypertension develops,administer diuretics.

- Loop diuretics increase urinary outputand consequently improve

cardiovascular congestion and

hypertension. For hypertension not controlled by diuretics, usually

calcium channel blockers or angiotensin-converting

enzyme inhibitors are useful. For malignanthypertension, intravenous nitroprusside or other

parenteral agents are used. Indications for dialysis include life-threatening

hyperkalemia and clinical manifestations of uremia. Restricting physical activity is appropriate in the first

few days of the illness but is unnecessary once the

patient feels well

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07 Post-streptococcal Glumerulonephritis - Gh