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