1. GLOMERULONEPHRITIS

2. Dr S Chakradhar

3. Relatively uniform, involve most or all glomeruli Focal lesions:
Diffuse lesions:
Relatively uniform, involve most or all glomeruli
Focal lesions:
Involve only some glomeruli; others normal
Segmental:
Involve only one part of the glomerulus
Mesangial:
Deposits of immunoglobulins in mesangial matrix
Membranous:
Thickening of BM
Proliferative lesions:
Increased number of glomerular cells
Sclerotic lesions:
Glomerular scarring from previous glomerular injury
Crescent lesions:
Accumulation of proliferating cells in Bowman's space
Dr S Chakradhar

4. Glomerulonephritis / Glomerulopathy / Glomerular Diseases
Group of disease in which the disease affects the Glomerulus and is often inflammatory in nature.
The disease is Immunologically mediated and involves both kidneys symmetrically.
Classification A.
Primary - When major problem starts in the Glomerulus
Secondary - when involvement is part of systemic disease. B.
Inherited
Acquired
Proliferative
Non proliferative
Dr S Chakradhar

5. Non Proliferative
Characterized by numbers of cells (lack of hypercellularity) in the Glomerulus
They usually cause nephrotic syndrome.
Proliferative
Characterized by increased number of cells in the Glomerulus (hypercellular).
Usually present as a nephritic syndrome and usually progress to end- stage renal failure (ESRF) over weeks to years

6. Inherited Glomerular Disease Alport’s Syndrome
Classification:
Inherited Glomerular Disease
Alport’s Syndrome
Thin Basement Membrane Disease
Acquired Glomerular Disease
Non Proliferative
Minimal change GN
Focal Segmental Glomerulosclerosis (FSGS)
Membranous glomerulonephritis
Proliferative
IgA nephropathy (Berger's disease)
Henoch-Schönlein purpura
Post-infectious
Membranoproliferative/mesangiocapillary GN
Rapidly progressive glomerulonephritis
Dr S Chakradhar

7. Pathogenesis of glomerular injury
Circulating Immune Complex Deposition
Injury resulting from deposition of antigen-antibody complex in the glomerulus
Endogenous antigens (e.g. DNA in SLE, tumor antigens)
Exogenous antigens (e.g. infectious products - streptococci)
There is type III hypersensitivity reaction
Dr S Chakradhar

8. 2. In Situ Immune Complex Deposition
Injury by antibodies reacting in situ within the glomerulus either with
Insoluble fixed (intrinsic) glomerular antigens
Glomerular basement membrane/anti-GBM nephritis - Goodpasture syndrome
Heymann antigen - Membranous glomerulopathy
Mesangial antigens
Others – unknown antigen
Planted antigen within the glomerulus
Exogenous – drugs, infectious agents
Endogenous – DNA, IG A
Dr S Chakradhar

9. Secondary mechanisms / Mediators of Glomerular injury Cells
Chemical mediators
Dr S Chakradhar

10. Clinical presentations (Glomerulo syndromes) Nephrotic syndrome
Acute nephritic syndrome
Renal failure – Acute or Chronic renal failure
Asymptomatic hematuria or proteinuria, or a combination of these two, Is usually a manifestation of subtle or mild glomerular abnormalities.
Hypertension It may be the first findings in some pt with certain glomerular disease
Dr S Chakradhar

11. Alport syndrome
Arise from a mutation or deletion of the COL4A5 gene on the X chromosome
Defect in the synthesis of collagen (important structural component of basement membranes in the kidney, inner ear, and eye)
Accumulation of abnormal collagen results in a progressive degeneration of the GBM
Dr S Chakradhar

12. Thin Basement Membrane Disease (benign familial hematuria)
Is an autosomal dominant inherited disease characterized by thin glomerular basement membranes on electron microscopy.
It is a benign condition that causes persistent
Microscopic haematuria,
Without associated HTN, Proteinuria or reduced GFR.
Dr S Chakradhar

13. ACUTE Nephritic Syndrome
It is a clinical manifestation in which several different renal diseases giving rise to a group of specific symptoms
It is an immune mediated inflammatory bilateral disease of the kidney which affects almost all the Glomeruli, characterized by:
Haematuria – RBC casts or dysmorphic RBC
Proteinuria – usually less than 1gm
HTN
Edema
Renal impairment – Oliguria, uremia, raised urea & creatinine
Dr S Chakradhar

14. Post-infectious / Acute glomerulonephritis (Acute diffuse proliferative glomerulonephritis)
Occur essentially after any infection, but classically occurs after infection with Streptococcus pyogenes
Post Streptococcal
Non-Post Streptococcal
Normal
Dr S Chakradhar

15. Pathogenesis Ag – Ab Immune Complex  Immune Injuries
GBM fracture Haematuria, Proteinuria
Cells proliferation  capillary lumen narrowed Glomerular blood flow↓  ↓ GFR Oliguria, AzotemiaARF
Retention of water & sodium ↑ Blood Volume
a. Oedema
b. hypertension
c. Hypertensive Encephalopathy 
Circulatory Congestion  Cardiac Failure
Dr S Chakradhar

16. Pathology
Dr S Chakradhar

17. Patient is usually a child of 5-10 years age
Clinical features
Symptoms:
Patient is usually a child of 5-10 years age
History of streptococcal infection (e.g. pharyngitis) 1-3 weeks before may present
Puffy face & swelling of the whole body gradually.
Scanty & smoky colored urine.
Dull aching pain at renal angle.
Low grade fever.
Systemic symptoms: Anorexia, nausea, vomiting, constipation & sore throat may be
Dr S Chakradhar

18. Signs: 1. Puffiness of face. 2. Temperature is raised. 3
Signs: 1. Puffiness of face. 2. Temperature is raised. 3. Periorbital & ankle oedema present. 4. Tenderness over renal angle. 5. BP is normal or raised in 50% cases.
Dr S Chakradhar

19. 4. Acute or chronic renal failure 5. Nephrotic syndrome Encephalopathy
Complication:
1. Hypertension
2. Pulmonary oedema
3. Heart failure
4. Acute or chronic renal failure
5. Nephrotic syndrome
Encephalopathy
Causes of death in AGN:
1. Acute circulatory congestion with pulmonary Oedema (LVF).
2. Hypertensive encephalopathy.
3. Acute renal failure.
Dr S Chakradhar

20. Total output: decreased. Colour: Smoky. Specific Gravity: Raised
Investigation
1.Urine:
Total output: decreased.
Colour: Smoky.
Specific Gravity: Raised
Proteinuria: Mild (usually <2 gm/dl).
Microscopic: RBC & RBC cast, WBC 
2. Blood:
TC and DC: leucocytosis with increased Polymorphs
ESR: often High
Blood urea and Creatinine : High.
Serum electrolyte: K & Na.
Dr S Chakradhar

21. Cardiomegally & pulmonary oedema (if complication).
3. X-ray of chest:
Cardiomegally & pulmonary oedema (if complication).
4. Throat swab C/S.
5. ASO titer (anti DNAase) - elevated
6. Serum C3 level is low (returns to normal 6 12 weeks)
6. Renal biopsy: confirmatory
Dr S Chakradhar

22. Protein restriction in renal failure Low sodium in presence of oedema
Treatment
Bed rest : Is indicated as long as there are clinical manifestations of active disease, such as Oedema, Hypertension, or Gross Haematuria.
Diet
Protein restriction in renal failure
Low sodium in presence of oedema
Fluid
Restriction of fluid
Diuretics
Frusemide 40 – 80 mg/day
Dr S Chakradhar

23. Dose adjusted according to BP Pulmonary Oedema Propped up position
Hypertension
Drug of choice:
Nifedipine
Methydopa
Prazosin
Dose adjusted according to BP
Pulmonary Oedema
Propped up position
O2 inhalation
Diuretics – Frusemide
Morphine 2.5 mg + Phenargan 25 mg IV or IM
Specific treatment :
Inj. Benzyl Penicillin 10 lakhs units IM 6 hourly for 10 days
Dr S Chakradhar