Glomerular disease is a group of diseases that affect the glomeruli in an inflammatory manner. They can be primary, arising from issues in the glomeruli themselves, or secondary, arising from other systemic diseases. Primary glomerular diseases include minimal change disease, membranous glomerulonephritis, and IgA nephropathy. Secondary glomerular diseases are often caused by systemic lupus erythematosus, diabetes, or amyloidosis. Glomerular diseases can present as nephrotic syndrome, with heavy proteinuria and edema, or nephritic syndrome, with hematuria and reduced kidney function. Rapidly progressive glomerulonephritis is characterized by a severe loss

1. GLOMERULAR DISEASE
Yousaf Khan
Lecturer Renal Dialysis
IPMS-KMU

2. GLOMERULAR DISEASE
 Group of disease
 Affect of glomerular and inflammatory in nature
 Immunologically mediated
 It may be primary or secondary.

3. PRIMARY GLOMERULAR DISEASE
 Minimal change glomerular disease
 Membranous glomerulonephritis
 Membranoproliferative glomerulonphritis
 IgA nephropathy
 Acute diffuseproliferative glomerulonephritis

4. SECONDARY GLOMERULAR NEPHRITIS
Common
 SLE
 Polyarteritisnodosa
 Diabetes mellitus
 Amyloidosis
 Malarial nephropathy
 Uncommon:
 Sarcoidosis
 Rheumatoid arthritis
 Hemolytic uremicsyndorm
 AIDS nephropaty

5. PATHOGENESIS
1. Circulating immune complex deposition:
Antigen + Antibody – deposition in glomeruli – binding with
complement – inflammation – glomerular injury.
 Antigen may be exogenous or endogenous
2. Antibodies directed against antigen on glomerular
capillary membrane:
 Anti – GBM antibody disease – antigen fixed in the GBM e.g
good pasture syndrome
 Antibodies against non GBM antigen

6. NEPHROTIC SYNDROME
Clinical complex characterized by
 Heavy proteinuria (3.5 g/day)
 Hypoalbuminemia
 Edema
 Hypelipidemia
 Hyperlipiduria
Proteinuria:
 daily loss of protein 3.5 gm or more of protein
 Injury to the capillary wall of the glomeruli result – increase
permeability to the plasma protein – allow to – escape from
plasma

7. PATHOGENESIS
Hypoalbuminemia:
 Proteinuria – decrease serum albumin level
Generalized edema:
 Hypoalbuminemia – result decrease colloid osmotic pressure
Hyperlipidemia:
 Hypoalbuminemia triggers increase sysnthesis of all form of
plasma protein including lipoprotein – hyperlipidemia.
Hyperlipiduria:
 Hyperlipoproteinemia – increase permeability results in
hyperliduria

8. ETIOLOGY OF NEPHROTIC SYNDROME
Primary glomerular disease:
 Minimal change nephropathy
 Focal segmental glomerulosclerosis
 Membranous GN
Secondary GN associated with systemic disease:
 Diabetic nephropathy
 Amyloidoisis
 Drugs: penicillamine, gold, mercury, cadmium
 Allergic reaction

9. CLINICAL FEATURES
Edema:
 Upper and lower limb
 Children more obvious on the face
 Intense edema of scrotum or vulva may occur
 Bilateral hydrothorax
 Edema of intestine causes anorexia, diarrhea and vomiting.
Malnutrition:
 Malnutrition may be due to protienuria, frequent infection and
muscle wasting.
Hypercoagulability:
 Hypercoagulability manifest as peripheral arterial or venous
thrombosis renal vain thrombosis and pulmonary embolism

10. INVESTIGATION
 Urine D/R – Proteinuria
 24 hr urinary protien - > 3 g/day
 Serum albumin – less than 3 g/dl and total serum protein < 6
mg/dl
 Low- density lipoprotien is elevated but HDL is usually normal.
 Raised ESR due to increase serum fibrinogen
 Blood sugar for diabetes and antinuclear factor for SLE.
 Serology and renal biopsy.

11. COMPLICATION AND MENAGEMENT
 Protein malnutrition
 Hypercoagulabilty – due to rise in many clotting factors
 Impaired resistance to infection
 Sepsis, blood loss and hpovolemia may lead to acute oliguric
renal failure
Management:
 Diet
 Diuretics
 Hypercholesterlemia
 Hypercoagulability
 Oliguric renal failure

12. MEMBRANOUS GLOMERULONEPHRITIS
 Slowly progressive disease
 Most common between 30 to 50 year
 Characterized by diffuse thickening of GBM
 Cause by deposition of immune complex on the
epithelial side of the GBM.

13. ETIOLOGY
 Primary 85% membranous nephropathy caused by
autoantibodies that cross-react with antigens expressed
by podocytes.
Secondary causes
 Infections (chronic hepatitis B, syphilis, malaria)
 Malignant tumors, particularly carcinoma of the lung and
colon and melanoma
 Systemic lupus erythematosus and other autoimmune
conditions
 Exposure to inorganic salts (gold, mercury)
 Drugs (penicillamine, captopril, nonsteroidal
antiinflammatory agents)

14. Pathogenesis:
 Membranous glomerulonephritis is a form of chronic immune
complex nephritis
Morphology:
Feature of light microscope
 Diffuse thickening of glomerular basement membrane
Feature of electron microscope:
 Apparent thickening of GBM is caused by subepitheial
deposits that are separated from each other by small spike in
GBM matrix.

15. CLINICAL FEATURE OF MEMBRANOUS GN
 Insidious development of nephrotic syndrome.
 In contrast to minimal change disease the proteinuria is non
selective (albumin and globulin both are excreted)
 Usually does not response to corticosteroid therapy
 About 40% lead to renal failure after 2- 20 years
 60% although proteinuria persist yet they do not progress to
renal failure

16. NEPHRITIC SYNDROME
 Inflammatory process causing renal dysfunction
 Over days to week that may or may not resolve.
 More than 50% loss of nephron function
Characterized by
 Hematuria with RBC casts
 Proteinuria (usually non rephrotic range)
 Hypertension
 Edema
 Oliguria
 uremia

17. Glomerual disease with nephritic presentation
 Post- Streptococcal GN
 IgA nephropaty
 Goodpasteur sysndrom
 Polyarteritits nodosa
 Acute interstitial nephritis

18. Investigation:
Urinalysis
 Dysmorphic red cell
 Red cell cast
 Proteinuria
Serum chemistries
Renal biopsy
Treatment:
 Reduction of hypertension
 Salt water restriction
 Diuretics

19. RAPIDLY PROGRESSIVE
GLOMERULONEPHITIS
Yousaf Khan
Lecturer Renal Dialysis
IPMS-KMU

20. RPGN
 Clinical syndrome
 Characterized by loss of renal function
 Laboratory finding – nephritic syndrome – severe oliguria
 About 50% cases are idiopathic while 50% are related to the
systemic disease.
 Histological finding associated with RPGN is the presence of
cresents

21. TYPES OF RPGN
Type I RPGN:
Anti-GBM disease
 Characterized by deposition of IgG and C3 on GBM
 anti-GBM antibodies cross react with pulmonary alveolar
basement membrane –to produce clinical picture of pulmonary
hemorrhage along with renal hemorrhage – good pasture
syndrome.
 Type II RPGN (Immune – complex mediated disease)
 Complication of any of immune complex nephritis such as
poststrptococcal GN, SLE, IgA nephropathy ets
 Type III:
 Characterized by lack of anti GBM antibodies or immune
complex by immunoflurescent and electron microscope.
 In serum antineutrophilic cytoplasmic antibody
 Associated with some systemic vasculitis

22. MORPHOLOGY
 Presence of crescents in most of the glomeruli
 Crescents are formed by proliferation of the parietal epithelial cells of
bowman capsule
 Crescents eventually obliterate the bowman space and compress the
glomeruli resulting oliguria

23. CLINICAL FEATURE
 Like nephritic syndrome
 But more marked oliguria and azotemia
 90% patient required dialysis and transplantation.

24. Thank You