ACUTE GLOMERULONEPHRITIS

by
Dr. Oyebode Ayodel.A.
On
1st June, 2018
 outline
• Introduction
• Epidemiology
• Aetiology
• Pathophysiology
• Pathology
• Clinical features
• Investigations
• Treatment
• Complication
• Prognosis
• Conclusion
• References
 introduction
• Acute glomerulonephritis is an inflammatory condition
affecting mainly the glomerulus with infiltration and
proliferation of acute inflammatory cells.Onset of symptoms is
usually acute including
oliguria,hypertension,haematuria,proteinuria and renal
impairment.
 Epidemiology
• AGN occurs worldwide but the prevalence is much higher in the
developing world and is more frequent in children and young adult.
• Geographic and seasonal variations in the prevalence of PSGN are more
marked for pharyngeally associated GN than for cutaneously associated
disease.
• Postinfectious GN has no predilection for any racial or ethnic group. A
higher incidence (related to poor hygiene) may be observed in some
socioeconomic groups.
• Acute GN predominantly affects males (ie, 2:1 male-to-female ratio).
• Latent period is about 2-3 or more weeks.
 Aetiology
• Infectious or non Infectious
infectious include
– Streptococcal: Poststreptococcal GN (commonest)
– Nonstreptococcal postinfectious glomerulonephritis
• Bacterial - typhoid, secondary syphilis,
meningococcemia, and infection with methicillin-
resistant Staphylococcus aureus (MRSA)
• Viral - Hepatitis B, infectious mononucleosis,
mumps, measles, varicella, vaccinia, echovirus,
parvovirus, and coxsackievirus
• Parasitic - Malaria, toxoplasmosis
 Non infectious
a) Immune disorders:good pasture`s syndrome,serum
sickness,SLE
b) Vasculitis:churd strauss dx,cryoglobulinaemia,wegeners
granulomatosis
c) Drugs:gold pamidronate,penicillamine,propylthiouracil
 pathophysiology
AGN is an immune complex disease
Formation of soluble immune complexes
Activation of complement cascades
Formation of C3a and C5a(complement split
product)
Clearance of subendothelial deposits-
endothelial injury
no access to subepithelial deposits
 pathology

• The kidneys appear symmetrically enlarged. All glomeruli appear

enlarged and relatively bloodless and show diffuse mesangial cell
proliferation with an increase in mesangial matrix
• Polymorphonuclear leukocytes are common in glomeruli during the
early stage of the disease.
• Crescents and interstitial inflammation may be seen in severe cases.
These changes are not specific for poststreptococcal glomerulone-
phritis.
• Immunofluorescence microscopy reveals lumpy-bumpy deposits of
immunoglobulin and complement on the glomerular basement
membrane (GBM) and in the mesangium.
• On electron microscopy, electron-dense deposits, or “humps,” are
observed on the epithelial side of the GBM
 Clinical features
• renal involvement varies from asymptomatic microscopic hematuria with
normal renal function to acute renal failure.
• edema, decreased volume and frequency of urination, systemic
hypertension, proteinuria, uremic symptoms, costovertebral tenderness
(ie, enlarged kidneys [rare]), and gross hematuria.
• consequences of the disease process which include loss of appetite,pallor,
generalized itching, tiredness, listlessness, nausea, easy bruising, facial
swelling, leg edema, and shortness of breath.
• Rashes in vasculitis and henoch schonlein purpura.
• Signs of fluid overload such as periorbital swelling,pulmonary
oedema,hypertension,ascitis ,raised JVP, pedal edema
• nephrotic syndrome may develop in 10–20% of cases.
 Investigations
• Urinalysis:proteinuria, haematuria
• Urine m/c/s:leucocyte and red cell casts in urine.
• Full blood count and diff
• Reduced serum C3 levels in 90% of cases, normalises 2-6wks
after onset
• U/E and Cr:
• Positive throat culture comfirms the diagnosis
• Rising antibody titre: antiSO, anti DNAse
• Elevated C-reactive protein and ESR.
• Renal biopsy reveals hypercellularity in all of the glomerulus
not infrequently associated with crescent formation.
 Indications for renal biopsy
• Persistently low C3 levels beyond 8 weeks
• Persistent heavy proteinuria after 6 month
• Atypical presentation-nephrotic
syndrome,acute renal failure with estimated
GFR <30ml/min/1.73m2.
 Treatment
• Specific treatment:eradication of streptococcal antigen
supportive
 careful attention to fluid balance
 Dietary salt restriction
 Use of loop diuretics
 Blood pressure control
 complications
• Acute renal failure
• Congestive cardiac failure
• Hyperensive encephalopathy
• Nephrotic syndrome
• Chronic renal insufficiency and ESRD
 Clinical course
• The clinical course of PSGN is usually
predictable
Oedema resolves within 5-10days
Blood pressure normalises within 2 weeks
Gross haematuria disappears within 2weeks
Persistent proteinuria-6month
Intermittent proteinuria-1year
Microhaematuria-2year.
• The prognosis for patients with PSGN is generally favourable with over
95% experiencing complete resolution and healing,only a few develop
complications
• Complete recovery is common
 Conclusion
• AGN is an inflammatory condition affecting
mainly the glomeruli secondary to an
immunological mechanism.the condition is
common in children,treatment is mainly
supportive and prognosis is good
 references
• Nelson textbook of paediatrics 18th edition
• Paediatrics and child health in the tropics –
Azubuike
• Starship children health clinical guideline on
glomerulonephritis
• Coovadia HM,Adhikari M, Mord-Maroger LO.
Clinicopathologic features of nephritic
syndrome.
• Thank you for your attention.