Glomerulonephritis is inflammation of the glomeruli in the kidney. It can be caused by inherited factors, immune system attacks, metabolic issues, or abnormal protein deposition. There are several classifications based on histopathology and presentations. Nephrotic syndrome involves injury to the podocytes and features massive proteinuria. Minimal change disease is a common cause in children characterized by podocyte foot process effacement. Focal segmental glomerulosclerosis often presents in adults with nephrotic syndrome. Membranous nephropathy can be primary or secondary to other conditions. Nephritic syndrome typically involves hematuria and modest proteinuria with preserved kidney function. Immunoglobulin A nephropathy and

1. Glomerulonephritis
Dr. Debashis Priyadarshan Sahoo
PGT, First year
Department of General medicine
NEIGRIHMS

2. Glomerular diseases:
• There are many causes of glomerular damage.
1. Inherited causes
2. Immunological injury
3. Metabolic causes
4. Deposition of abnormal proteins
• Hallmark: Proteinuria

3. Glomerulonephritis:
• Inflammation of glomeruli.
• Classified on the basis of histopathological appearances
Nephrotic presentations Nephritic presentations Rapid progressive
glomerulonephritis
presentation
1. Minimal change disease
2. Focal segmental glomerular
sclerosis
3. Membranous nephropathy
1. IGA nephropathy
2. Mesangiocapillary
glomerulonephritis
1. Focal necrotizing GN (Small
vessel vasculitis)
2. Diffuse proliferative GN
(Post streptococcal)
3. Anti GBM disease

4. Nephrotic syndrome:
• Injury in Podocyte.
• Little evidence of inflammation and cell proliferation.
• Fulminant presentation: MCD, primary FSGS
• Indolent presentation: Membranous nephropathy, secondary FSGS

5. • Features:
1. Massive proteinuria: >3.5g/day
2. Hypoalbuminemia, S. albumin: <2.5g%
3. Oedema: decreased oncotic pressure
4. Hyperlipidemia
5. Lipiduria
• Common presentations:
1. Adults: FSGS
2. Child: MCD

6. Minimal change disease:
• Most common cause of nephrotic syndrome in children.
• Peak age: 2-8years
• Cause: reversible dysfunction of podocytes
• Presentation is usually severe.
• Features:
1. Puffy eyes, Vulval/scrotal edema, Pedal edema with diurnal variation
2. Weight gain
3. Decreased oncotic pressure/ Decreased albumin: Selective proteinuria,
Bilateral transudative pleural effusion and ascites.

8. • Work up:
1. BUN/Creatinine: normal
2. Urine RE: Oval fat bodies
3. Nephrotic range proteinuria
4. Decreased complement level (C3)
5. Kidney biopsy: (LM: Normal, EM: Effacement of podocyte foot processes)
• Treatment:
1. High dose steroids (Prednisolone 1mg/kg for 6 weeks) F/B tapering
2. If responds incompletely, Steroid resistant nephrotic syndrome, Immunosuppressive therapy
given: Cyclosporine/ Tacrolimus.

9. FSGS:
Nephrotic syndrome in adult is commonly FSGS.
Nephrons at corticomedullary junction are affected.
C/F:
1. Haematuria/ Cola coloured urine
2. Hypertension – Headache
3. Nephrotic range proteinuria
4. Renal insufficiency
Aetiology:
1. Idiopathic
2. Infections: HIV, HBV, Parvo virus
3. Reflux nephropathy, Hypertensive nephropathy, Heroin addiction, Pamidronate
4. Alport syndrome, sickle cell anaemia

11. Work-up:
1. KFT
2. Urine RE: >3RBC/hpf, (N) centrifuged specimen <3 RBC/ hpf
3. Kidney biopsy
a. LM: Eosinophilic deposits, hypercellular glomerulus
b. EM: Hyaline deposits (Effacement of podocyte, vacuolization, detachment)
Treatment:
• Primary: ACEI, Steroids for 4-16 week till complete remission
• Secondary: Treat the cause.

12. MGN:
• MC in geriatric population.
• Causes:
Primary: Antibody against PLA2 receptor
Secondary:
1. Connective tissue disorder (RA/SLE/Scleroderma/MCTD)
2. Autoimmune disorders (Hashimoto thyroiditis/Graves disease)
3. Infection (HBV/HCV/Leprosy/Malaria)
4. Solid organ tumors
5. Drugs (Penicillamine, Captopril, Mercury)
• C/F:
1. Puffy eyes, pedal edema, anasarca
2. Hypertension

14. • Work-up:
1. Urine: Oval fat bodies
2. BUN and Sr. Creatinine increased
3. ANA + , Anti PLA2 Ab +
4. HIV/HBV/HCV
5. Workup for malignancy
6. Kidney biopsy: Hypercellularity, PMN cells, C3/IgM/IgG, Subepithelial deposits +, Spikes
• Treatments:
1. Low protein diet
2. Furosemide
3. ACEI
4. Statins
• Complications: Renal vein thrombosis.

15. Nephritic syndrome:
• Typically present with non visible hematuria and modest proteinuria.
• Decreased GFR and increased renin leads to:
1. Hypertension
2. Hematuria
3. Sub nephrotic range proteinuria
• Subtypes:
1. IgA nephropathy
2. Mesangiocapillary glomerulonephritis

16. IgA nephropathy:
• Most common type of glomerulonephritis.
• It can present in many ways. Non visible hematuria and hypertension are
common and universal.
• Often detected during screening/ annual medical check-up.
• Increased IgA deposition in mesangium:
1. Capillaries (N)
2. GFR (N), BP (N/elevated)
3. Microscopic haematuria
• If patient develops URTI, IgA level rises and gross hematuria develops.

17. • O/E: BP (N/Elevated) , No
edema
• Work-up: >3RBC/hpf, Normal
C3
• Treatments: ACEI and high dose
steroids (In highly progressive
disease)

18. MPGN:
• Increased mesangial cellularity and thickening of glomerular capillary wall.
• Types:
Type 1:
 Deposition of immunoglobulin within glomeruli.
 Caused by chronic infections (HCV), autoimmune disease (SLE) and monoclonal
gammopathy (Cryoglobulinimia)
 Biopsy shows mesangial deposits between basement membrane and endothelial cells (tram
tracking)
Type 2:
 Deposition of complements in glomeruli, inherited or acquired defect in complement
pathway.
 Dense Deposit Disease

19. • Treatment:
1. Identification and
treatment of underlying
disease
2. Immunosuppression:
MMF, Cyclophosphamide
3. Anti C5 inhibitor:
Eculizumab

20. RPGN:
• Rapid loss of renal function over days to weeks, usually in association
with hypertension and edema.
• Features:
• Urine RE: Non visible hematuria, variable proteinuria, characteristic
red cell casts, dysmorphic RBC
• Renal biopsy: Crescentic lesions
• Occurs in: Small vessel vasculitis, PSGN, IgA nephropathy and other
nephropathies.

22. PSGN:
• Type III hypersensitivity reaction
• Immunological manifestation after nephritogenic streptococcus infection (Impetigo/
pharyngitis).
• Antigen: Streptococcal pyogenic exotoxin B (SPEP)
• Molecular mimicry mediated by Anti DNAase and Anti hyaluronidase
• Immune complex (+) – Complement mediated vasculitis.
• C/F:
1. Hematuria, cola colored urine/ smoky urine (freshly voided sample)
2. Hypertension: Sudden onset LVF/ Dyspnea/ pulmonary edema
3. Renal insufficiency with uremia

24. • Work-up:
1. Urine RE: >3RBC/hpf, RBC cast, Dysmorphic RBC
2. Decreased C3 and normal C4
3. Increased Anti DNAase and Anti Hyaluronidase
4. Kidney biopsy: hypercellularity/ PMN infiltration/ IgG, IgM, C3 deposition/ subepithelial deposits
5. Immunofluorescence: Starry sky appearance
• Treatment:
1. Acute pulmonary edema: Furosemide
2. Hypertensive crisis: IV labetalol and ACEI
3. Hemodialysis