Glomerulonephritis

Acute glomerulonephritis(AGN)

Teacher ： Yanli Zhang Department ： the Third hospital affiliated to ZhengZhou University

OUTLINE Introduction Etiology and

Laboratory

evaluation epidemiology Diagnosis Pathogenesis Treatment Pathology  Prognosis Clinical Prevention manifestations

1 Introduction The disease is the classic example of the acute nephritic syndrome: the sudden onset of gross hematuria , edema, hypertension, and renal insufficiency

It was the most common cause of

gross hematueria in children; now is IgA nephropathy

Introduction The course of AGN is less than 1 year Most AGN belong to acute

poststreptococcal glomerulonephritis (APSGN) AGN is 53.7% of urine system diseases during same time AGN is common during 5~14 years old Male: female is equal to 2:1

2 Etiology and epidemiology APSGN follows infection of throat or skin During cold weather, APSGN follows streptococcal pharyngitis ,whereas during warm weather ,APSGN follows streptococcal skin infections or pyoderma The disease is most commonly sporadic

3.Pathogenesis Although morphologic studies and a depression in the serum complement (C3) level strongly suggest that APSGN is mediated by immune complexes, the precise mechanisms by which nephritogenic streptococci induce complex formation remain to be determined.

pathogenesis Formation of immune complexes including antibodies and streptococcal antigens Localization (deposition) on subepithelial portion of glomerular basement membrane This leads to localized mesangial and endothelial cell proliferation

Streptococci infection complex formation C3↓

AGN

Mesangial cell proliferation Blood capillary close off

GFR↓

Oliguria or anuira

Salt and water retention

Edema hypertension

Mesangial matrix destroy Proteinuria hematuria

4. Pathology Most forms of AGN, the kidney appear symmetrically enlarged . On early phase , classic AGN appear endocapillary proliferative On light microscopy, AGN appear enlarged and relatively bloodless and diffuse mesangial cell proliferation with an increase in mesangial matrix

Pathology Polymorphonuclear leukocytes and neutrophil are common in glomeruli during the early stage of the disease. Crescents and interstitial inflammation may be seen in severe cases. On electron microscopy, electron-dense deposits, or “humps” are observed on the epithelial side of the glomerular basement membrances(GBMs)

In endocapillary proleferative GN, “hump” appear outside of basement

In endocapillary proliferative GN, appear enlarged and bloodless ,mesangial proliferation and

5.Clinical manifestations General manifestations Antecedent infection Typical manifestations Severe manifestations  Atypical manifestations

5.1 General manifestations Many people with glomerulonephritis have no symptoms  When symptoms occur, they are often flu-like, such as general fatigue, nausea, vomiting, loss of appetite, fever, and abdominal and joint pain. These types of general symptoms can continue for up to one month before symptoms of kidney failure appear.

5.2 Antecedent infection 90% patients have an antecedent streptococcal infection Respiratory and skin infections are chief Typical manifestation is 6~12 days after pharyngitis or 14~28 days after skin infection

5.3 Typical manifestations ①Edema : 70% show edema; unsunken; face and eyelid upper are generally involved ②Hemuturia: 50%~70% show gross hematosis ,after 1~2wk, change into microscopic hematosis

Typical manifestations ③Proteinuria: in general, <3g/d ④Hypertension:30%~80% show hypertension, during preschool age >120/80mmHg, school age >130/90mmHg Urine volume: decrease Resolution should occur within 2 weeks , if not , consider other causes

5.4 Severe manifestations Severe cycle bloodshot Hypertensive encephalopathy Acute renal failure

①Severe cycle bloodshot Cause: salt and water retention cause blood volume increase Alerting when AGN children show tachypnea or moist crackles Severe show dyspnea, gallop rhythm, edema worsen, even die

②Hypertensive encephalopathy Cause: vessel plasma Hypertension suddenly ascend >150~160/100~110mmHg Symptoms: headache, vomiting, diplopia, even convulsion, coma After hypertension controlled, these symptoms disappear

③Acute renal failure Causes: mesangial cell proliferation, blood capillary close off, GFR↓ Symptoms: Oliguria or anuira, electrolyte disturbances, metabolic acidosis

5.5 Atypical manifestations AGN has no symptoms: only microscopic hematouria, no other clinical manifestations AGN has symptoms out of kidney: has streptococcal history, serum C3 level is reduced, edema, hypertension is notable, but urine routine is normal AGN show nephritic syndrome: edema, proteinuria is notable, but pathology change is typical

6. Laboratory evaluation 1. Urine routine ： proteinuria 1+~3+ ， including RBC and cast 2. ASO↑ 3. C3↓ 4. ESR ↑ (erythrocyte sedimentation rate )

Laboratory evaluation 5. A 24 hour urine collection allows measurement of the excretion of proteins and creatinine. 6. Creatinine clearance from the bloodstream by the kidneys is considered an index of the glomerular filtration rate

kidney biopsy Kidney biopsy is essential to establish a diagnosis of atypical or prolonged AGN, determine the cause, and create an effective treatment plan and know its prognosis

7. Diagnosis ①For about 1~3wk before AGN has streptococcal infection ②Clinical manifestations: edema, hypertension, hematuria, proteinuria ③Urinalysis finding protein, RBC, cast ④Serum C3 level reduce and/or ASO↑

8. Treatment Goals of treatment Principles of treatment

Goals of treatment Stop the ongoing inflammation and lessen the degree of scarring that ensues. Decrease the damage to the glomeruli Decrease the metabolic demands on the kidneys Improve kidney function.

Principle of Management • [No special therapy] • 1. Bed Rest Reduce activities according to the progress of disease 2.Diet Restrict fluid and daily salt intake azotemia—restrict protein intake

Principle of Management • 3.Antibiotic therapy—Penicillin7~10d • 4.Symptomatic therapy Edema---Diuretics (furosemide, spironolactone) Hypertention---Antihypertensive drugs (nifepine) Hypertensive Encephalopathy---sodium nitroprusside

Principle of Management Kidney failure--- dialysis Once kidney failure has occurred, waste products must be removed from the bloodstream for the kidneys through a process called dialysis. A kidney transplant may also be an option.

9. Prognosis Recovery is >90%  with <1% mortality in past  chronic disease in 5-10%

10. Prevention Avoiding upper respiratory infections, as well as other acute and chronic infections, especially those of a streptococcal origin.

Cultures of the infection site, usually the throat, should be obtained and antibiotic sensibility of the offending organism determined.

Prevention Prompt medical assessment for necessary antibiotic therapy should be sought when infection is suspected.  The use of prophylactic immunizations is recommended as appropriate.