1. Glomerulonephritis is an
infamation of the
glomerular capilaries

5. Causes of nephritic syndrome
Primary glomerulonephritis
– Acute GN
• Post streptoccocal
• Non streptococal
Rappidly progressive GN
Membranoproliferative GN
Focal GN
IgA nephropathy GN

6. Systemic disease:
SLE
Polyarteritis nodosa
Wegener’s granulomatosis
Henoch schonlein purpura
cryoglobulinaemia

7. Classification of glomerular disease
Primary glomerulonephritis
– Acute GN
• Post streptoccocal
• Non streptococal
Rappidly progressive GN
Minimal change GN
Membranous GN
Membranoproliferative GN
Focal GN
IgA nephropathy GN
Chronic GN

8. SECONDARY SYSTEMIC GLOMERULAR
DISEASE
Lupus nephritis
Diabetic nephropathy
Amyloidosis
Polyarteritis nodosa
Wegener’s granulomatosis
Henoch schonlein purpura
Goodspasture’s syndrome
Systemic infectious diseases

9. Hereditary nephritis
Alport’s syndrome
Fabry’s disease
Nail patella syndrome

10. Nephritis Caused by Circulating
immune Complexes
With
circulating
immune
complexmediated disease,
the gromerulus is considered “innocent
bystander” because it does not incite the
reaction.
The antigen is not of glomerular origin.
 It may be endogenous, as in the GN
associated with SLE, or
 it may be exogenous, as is probable in the
GN that follows certain bacterial, viral,
parasitic and spirochetal infections.
Often the inciting antigen is unknown, as
in most cases of membranous nephropathy.

11. 
Whatever the antigen may be,
antigen-antibody complexes are formed
in situ or in the circulation and are then
trapped in the glomeruli,

where they produce injury, in large
part
through
the
activation
of
complement and the recruitment of
leukocytes.

Regardless of the mechanism, the
glomerular lesions usually consist of
leukocytic infiltration into glomeruli and
variable proliferation of endothelial,
mesangial, and parietal epithelial cells.

12. Electron microscopy reveals the immune
complexes as electron-dense deposits
or clumps that lie at one of three sites:
in the mesangium,
between the endothelial cells and the
GBM, or
between the outer surface of the GBM
and the podocytes.
Seen in most cases of poststreptococcal
or acute infection-related GN.

13. Nephritis Caused by in Situ Immune
Complexes
Anti-Glomerular Basement
Membrance (GBM) Antibody
Glomerulonephritis.
 In this type of injury, antibodies
are directed against fixed antigens
in the GBM.

14. Cell-Mediated Immune
Glomerulonephritis
 It has often been suggested that
sensitized T cells, formed during the
course of a cell-mediated immune
reaction, can cause glomerular injury.
 In some forms of experimental GN
in rodents, the disease can be
induced by transfer of sensitized T
cells.

15. T cell-mediated injury may account for
the instances of GN in which either
there are no deposits of antibodies or
immune complexes or the deposits do
not correlate with the severity of
damage.

16. Mediators of Immune Injury
 Glomerular damage, reflected
by loss of glomerular barrier
function,
is
manifested
by
proteinuria and, in some instances,
by reduction in GFR.
A major pathway of antibody –
initiated injury is complementleukocyte-mediated

17. 
Activation of complemnt leads to the
generation of chemo tactic agents and
the recruitment of neutrophils and
monocytes.

Neutrophils release proteases, which
cause GBM degradation; oxygen-derived
free radicals, which cause cell damage;
and arachidonic acid metabolites, which
contribute to reduction in GFR.

This mechanism applies only to some
types of GN.

18. 
Some models suggest complementdependent but not neutrophil-dependent
injury, due to an effect of the C5 lytic
component of complement,

which
causes
epithelial
cell
detachment and stimulates mesangial
and epithelial cells to secrete various
mediators of cell injury.

Thus giving rise to altered GBM
composition and thickening.

19. Other mediators of glomerular
damage include
(1)monocytes and macrophages,
which infiltrate the glomerulus in
antibodyand
cell-mediated
reactions and, when activated,
release
a
vast
number
of
biologically active molecules;
(2) platelets, which aggregate in the
glomerulus
during
immunemediated
injury
and
release
prostaglandins and growth factors;

20. (3) Resident glomerular cells, which
can be stimulated to secrete
mediators such as cytokines
arachidonic
acid
metabolites,
growth factors, nitric oxide, and
endothelin; and
(4) fibrin-related products, which
cause leukocyte infiltration and
glomerular cell proliferation as a
consequence of intraglomerular
thrombosis.

21. Other Mechanisms of Glomerular Injury
Two that deserve special mention are
podocyte injury and injury secondary to
nephron loss.
Podocyte Injury:
This can be induced by antibodies to
visceral epithelial cell antigens; by
toxins, certain cytokines; or by still
poorly characterized factors, as in some
cases of focal and segmental
glomerulosclerosis.

23. Such injury is reflected by
morphologic
changes
in
the
podocytes,
which
include
effacement of foot processes,
vascularization, and retraction and
detachment of cells from the GBM,
and functionally by proteinuria.
 In most forms of glomerular
injury,
loss
of
normal
slit
diaphrangms is key in the
development of proteinuria.

24. Nephron Loss.
 Once
any
renal
disease,
glomerular or otherwise, destroys
sufficient functioning nephrons to
reduce the GFR to 30% to 50% of
normal progression to end-stage
renal
failure
often
proceeds.
develop proteinuria, and their
kidneys
show
widespread
glomerulosclerosis.

25. These remaining glomeruli undergo
hypertrophy to maintain renal function.
 This is associated with hemodynamic
changes, including increases in single
nephron, GFR, blood flow, and
transcapillary pressure.
These adaptations in the intact
glomeruli are ultimately maladaptive
and lead to further endothelial and
epithelial cell injury, increased
glomerular permeability to proteins,
and accumulation of proteins and lipids
in the mesangial matrix.

26. TYPES OF GLOMERULONEPHRITIS:There are different types of GN
It may involve either the nephrotic
syndrome or nephritic syndrome
Diagnosis made by C/F or by renal
biopsy

27. Types of glomerulonephritis (ACUTE NON
STREPTOCOCAL)
Minimal change disease
Is a benign disorder
Frequent cause of nephrotic
syndrome in children
Here the glomeruli shows a diffuse
effacement of podocyte foot
process.

28. 1. MINIMAL CHANGE DISEASE
(LIPOID NEPHPOSIS)
 It is a begin disorder.
 Frequence cause of nephrotic
syndrome.
 Different affacement of
pocodeyti foot processes (they
appear flattened

29. CAUSES
Idiopathic
Systemic disease (hodgkins disease, HIV
infection) & drug therapy (NSAID)
PATHOGONESIS:
Protenuria has been attributed to T cell
derived factor that cause podoeyte
enjury & affacement.
C/F:- Protein Loss
Prognosis – good, Rx is corticosteroids

30. Focal & segmental to slecrosis :
Characterized by sclerosis
affecting some but not all the
glomeruli
CAUSES
Associated with HIV infection
IgA nephropathy
Maladaptation after nephron loss
Congenital malformation in
podocytes

31. PATHOGENS:
Unknown
Investigators have said that FSGS
and MCD are continuous – MCD
may transform into PSGS
C/F:
Variable protunuria
Not responding to corticosteroids
Prognosis:
Poor
Recurs after transplantation

32. 3. MEMBRANOUS NEPHROPATHY
(MENBRANEOUS GN)
Occurs between 30 & 50 years.
Subepithelial deposits
Causing thickening of the capillary wall.
Causes:
idiopathic secondary to
Infections (chronic hepatitis, syphillis,
malaria)
Malignant tumors of lung & colon
SLE & other auto immune disorders
Drugs (NSAID’S)

33. C/F
Heavy protenuria
Does not respond to
cortecosteroids
They may respond to prednisolone.
PROGNOSIS :Variable
30% may have spontaneous
remission

34. Menbranoproliferative FN:Alteration in the GBM &
mesangium
Proliferation of glomerular cell
TYPES:
Mesengial cells are found between
the endothelium & GBM
Immune deposits are found in
subendotheal region
(SLE)
(bacterial endocardites, HIV,
hepatitis

35. TYPE II
Is autoimmune disease called
IgG autoantibodies called c3
nephretic factor
Causing lipodystrophy loss of
subcutaneous fat from the upper
half of the body.

36. IGA NEPHROPATHY :
Affects children
Associated with gross hematuria
Associated with loin pain
Here there is deposition of IgA is
mesangium (due to IgA production
& clearance abnormal)
It is due to some infection is to
respiratory or GI tract.
These activates the alternative
complement pathway
Glomerular injury

37. C/F
Hematuria
Red blood cell cast on urine
analysis.

38. Acute glomerulonephritis

39. PATHOPHYSIOLOGY:
Antigen (group A seta – hemolylic
streptococcus
Antigen – antibody products
Deposition of antigen – antibody
complexes in glomerulers
Increase production of epithelial
cells lining the glonerulus

40. Luekocyte infiltration of
glomerulus
Thickening of the GF membrane
Scarring and loss of glomerular
filtration membrane
Decreased glomerular filtration rate
(GFR)

41. CLINICAL MANIFESTATIONS:
Hematuria
Protinuria
Edema
Azotemia
Hypertension
Abdominal or flank pain
Oliguria
Fever, chills, weakness, pallor,
anorexia, nausea and vomitting
may be present.

42. Elderly patient may experience
circulattory ocurroal, with dyspnea,
engorged nec ceeins, cardionegely
and pulmonary edema.
Hypoalbuninenia and
hyperlipedemia.

43. DIAGNOSTIC STUDIES: History and physical examination
 Urinalysis
 CBC
 BUN, seum creatinine and albunmin
 Complement levels and ASO titre
 Renal biopsy.
 Signs of overload
 Periorbital edema
 Edema and hypertension due to overload
 Crackles
 Elevated jugular venous pressure
 Rashes
 Pallor

44. Physical examination:

45. Lab studies:
Urine analysis
Complement levels
Twenty-four hours urine test for
total protein
Anti sterptolysin O titre
Dipstick test
Imaging studies
Renal biopsy: cellular infiltration,
granular deposits of
immunoglobulin.

46. Treatment:
Antimicrobial therapy:
Penicillin 500000 IU q6 q8 hourly
Loop diuretics:
Frusemide:
Edema: 40-80mg to 20- 40mg 6th
hourly.
Hypertension: 20- 40mg bid PO bid
Vasodilators:
Sodium nitroprusside
0.5-8mcg/kg/mim IV infusion

47. Diet:
Sodium and fluid restriction
Protein restriction 0.6 – 0.75g/kg/wt
Water restriction to 600ml plus the
previous days urine output.
Sodium restriction; 2 to 4g
depending on the degree of edema.
Avoid high sodium food.

48. Chronic
glomerulonephritis

49. Pathophysiology:
Acute GN (repeated episodes)
Cause hardening of renal arteries
Reducing the size
Scar tissue formation (numerous
glomerulus and branches of renal
arteries are thickened)
Severe glomerular damage
End stage renal failure

50. Clinical features:
Hypertension
Elevated BUN
Nosebleed
Edema of the optic disc
General symptoms like malaise,
weight loss, edema, mental
cloudiness,
Gallop rhythm, distended neck
veins, symptoms of heart failure.
crackles

51. Poorly nourished
Mucous membrain pale because of
edema.
Urine analysis shows hematuria,
protienuria, scanty, dark, smoky,
cola coloured,
Peripheral neuropathy
Confusion

52. Diagnostic findings:
History collection
Physical assessment
Urine analysis
Blood investigations
Radiography
Biopsy

53. Treatment:
Medical care:
Drug therapy:
Angiotensin converting enzyme
inhibitors
Eg: enalapril
Dose: 2.5-10 mg orally not to exceed
40mg 1 day)

54. Diuretics:
Fruosimide (lasix)
1-2 mg. 1kg oral/IV/bid not to exceed
600 mg /d
0.1-0.4 mg/kg/hour continuous iv
infusion
Metdazone
5-20 mg orally qd
Calcium channel blockers:
Amlodipine
2.5 – 10 mg qd.

55. Nefidipine
Short acting – 10mg orally tid
Long acting – 30 mg orally qd not
to exceed 120 – 150 mg qd
Beta adrenergic blockers
Metoprolol – 50 mg oral bid
Alpha adrenergic blockers
Clonidine (catapress)
Dose : 0.1 – 0.2 mg orally bid/tid not
to exceed 2.4 mg qid

56. Surgical treatment
Renal replacement therapy
Hemodialysis
Peritoneal dialysis
Renal transplantation
Diet management
Protein restricted diet (0.4 – 0.6 g
1kg/d
Fluid instruction to 600ml

57. Complications
Metabolic acidosis
Pulmonary edema
Pericarditis
Uremic encephalopathy
Uremic nueropathy
Severe anemia & hypocalemia
hyperkelemia

58. NEPHTOTIC SYNDROME
Nephrotic syndrome is a cluster of
clinical findings, including
Marked increase in protein
(particularly albumin) in the urine
(protienuria)
Decreased in albumin in the blood
(hypoalbuminenia)
Edema, hypercholesterolemia &
normal renal function.

59. The causes can be classified also
 Primary glomerulonephrills
 Minimal change disease
 Membranous GN
 Menbranoproliferative GN
 Focal segmental
glomerulosclerosis
 Focal GN
 IgA nephropathy

60. II. systemic disease
 Diabetes mellitus
 Amyloidosis
 SLE
III. Systemic decease
 Viral infection
 Bacterial infection (endocardites,
syphillis, leprosy)
 Protozoa & parasites
(P.falciparum malaria, filariasis

61. IV. Hypersensitivity
Drugs. (heavy metal compounds
like gold & mercury, heroin
addiction,
Bee sting, snake bite, poison ivy
V. Malignancy
Carcinomas
Myeloma
Hodgkins disease

62. VI. Pregnancy
Toxemia of pregnancy
VII. Circulatory disturbance
Renal vein thrombosis
Constructive pericarditis
VIII. Hereditary diseases
Alports disease
Fabry’s disease
Nail patella syndrome

63. Clinical features
Heavy protienuria
Hypolepidemia
Hypoalbumenemia
Edema
lipiduria
Hercoagulability

64. Pathophysiology:
Damage to the glomerular capillary
membrane
Loss of plasma protein
Stimulate synthesis
of liporotiens
hypoalbuminimea
Hyperlipidemia
decreased oncotic press
generalized edema
renin angeotensin
edema