This document discusses glomerulonephritis (GN), a group of kidney diseases caused by inflammation of the glomeruli. It begins by defining GN and distinguishing it from other causes of kidney disease. It then describes the glomerulus and classification of GN based on histopathology. Etiologies of GN including infections, autoimmune diseases, and idiopathic causes are reviewed. The clinical presentations of GN ranging from asymptomatic to nephrotic syndrome to rapidly progressive GN are covered. Diagnosis and treatment options focusing on controlling risk factors and underlying diseases are summarized.

1. GLOMERULO
NEPHRITIS
Dr. Muhammad Hussain Baloch
Assistant Professor/ Head of Nephrology
Department RMC & Allied Hospitals
Rawalpindi

2. GLOMERULO NEPHRITIS
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Implies an immune pathogenesis
All glomerular diseases not caused by GN 
D.D
DN, Amyloidosis, HTN & Hereditary
nephropathies (Alport’s synd.)
1O  clinical manifestations restricted to
kidney
 Part of multi system disease (SLE or
vasculitis)

3. GLOMERULUS

4. GLOMERULUS
Tuft of capillaries attached to
mesangum enclosed in
Bowmann’s capsule
Filtration Barrier
 Barrier is negatively charge
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5. CLASSIFICATION
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Based on Histopathology
Not IDEAL – One etiology may produce a variety of histologic patterns
OR
Various etiologies may produce similar pattern
 L.M focal or diffuse - segmental or global
 I.F or immunoperoxidase microscopy
 E.M  morphology of basement membrane
MCD
FSGS
Membranous Nephropathy
MPGN
Masangial proliferative GN
Post infectious GN
Crescentic G.N

6. ETIOLOGY
 Idiopathic
 Hereditary
 INFECTIONS: Staph, Strept, E.Coli Leptospirosis, T.Pallidum, Coxiella, bmcella,
listeria monocytogenes
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Schistosoma, Trichinella, Spiralis
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Hepatitis A,B,C, HIV, CMV, MUMPS, Influnsa, EBV and Echo
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Histoplasma, candida
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Plasmodum, Toxaplasma, trypanosoma
 Multisystem disease
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D.M
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HTN
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Amyloidosis
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Vasculitis - ANCA Vasculitis
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SLE
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Malignancies

7. CLINICAL PRESENTATION
1. ASYMPTOMATIC PROTEINURIA
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Proteinuria 150mg – 3 gram / day
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Hematuria > 2 RBCs/HPF
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FSGS Mesangial proliferative GN (IgA)

8. 2. NEPHROTIC SYND
 Proteinuria > 3.5g/day or > 40mg/hour/m2
 Hypoalbuminemia <3.5 g/dL
 Edema
 Hyperclolesterolemia
 Lipiduria

9. 
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 MCD Membranous GN
MEMBRANOUS GN
FSGS, Mesangioproliferative GN
MPGN – I, MPGN II
Diabetic glomerulosclerosis
Amyloidosis
LCDD

10. 3.Asymptomatic Microscopic Hematuria
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T.B.M Nephropathy
1gA Nephropathy
Alport’s Synd.

11. 4.RECURRENT GROSS HEMATURIA
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TBM Nephropathy
IgA Nephropathy
Alport’s synd.

12. 5.ACUTE NEPHRITIC SYND
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Oliguria
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Hematuria
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RBC casts
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Proteinuria usually <3g/day
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Edema  HTN
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 Acute diffuse Proliferative GN (Post staph and
post strept)
6.FOCAL OR DIFFUSE PROLIFERRATIVE GN
1GA AND LUPUS NEPHRITIS

13. 7. RPGN
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Renal Failure over day /weeks
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Proteinuria usually < 3g/day
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Hematuria RBC casts
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BP often normal

14. CRESCENTIC GN
 Anti GBM disease and syndrome
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MPA
W.G
Goodpasture’s disease
S.L.E
 CSS HSP HUS BEHCEST’S DIS.
 Essential Mixed cryoglobaulinemia  Rheumatoid vasculitis
 Penicillamine therapy
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Immue complex GN
ANCA GN

15. 8.CHRONIC GN
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Hypertension
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Renal Insufficiency
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Proteinuria > 3gram
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Small shrunken Kidneys

16. DIAGNOSIS
HISTORY
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Symptoms – few & Late
Urine
DM. HTN, Amyloid, SLE, Vasculitis
Family History – ALPORT’s HUS
NSAID use Heroin
Infections
Malignancies  G.I – Membranous Hodgkin this
–MCD Non Hodgkin MPGN

17. PHYSICAL EXAM Edema
LAB
 Urine
 Serological tests
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Anti dS DNA antibodies
Cryogloblins
RA Factor
Anti GBM antibodies
ANCA
A.S.O titres
Urine electrophoresis
Serum complements level

18. 
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IMAGING
USG
RENAL BIOPSY

19. TREATMENT
 B.P Control  Na+ restriction
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Target 125/75 mm of Hg
ACEIS & ARBs
 Proteinuria
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NSAIDS ?
Protein restriction 0.8 – 1 g/day,
Nephrectomy
 Hyperlipidemia
 Avoid nephrotoxic agents:
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NSAIDS
Radiocontrast
Aminoglycosides

20.  Treat edema
 Hypercoagulability heparin 5000 units s/c x
BD
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Management of infection
S.B.P
SPECIFIC THERAPIES