1. Dr S Chakradhar

2. IgA nephropathy (Berger's disease) :
Is named for the deposits of IgA in the glomerulus (Mesangium)
Commonly seen in children & young adults
It often affects young males within days (24-48hrs) after an upper respiratory tract or gastrointestinal infection.
Microscopic examination
Shows increased number of mesangial cells with increased matrix
Dr S Chakradhar

3. It usually presents as macroscopic haematuria (visibly bloody urine).
Presentation
It usually presents as macroscopic haematuria (visibly bloody urine).
Gross hematuria often associated with URTI
Others present with asymptomatic hematuria accompanied by mild to moderate proteinuria.
Mild proteinuria of less than 1g/d is common, but the NS develops occasionally.
Dr S Chakradhar

4. Serum IgA levels are increased in about 50% of cases but Serum complement is normal.
Immuno-staining is positive for immunoglobulin A deposits within the matrix.
Treatment
Intermittent steroid therapy may reduce the frequency of episodes of gross of hematuria.
Steroids may also result in remissions of proteinuria in those patients with NS.
Dr S Chakradhar

5. Is variable, but tends to progress slowly.
Prognosis
Is variable, but tends to progress slowly.
50% of pts develop ESRF within 25 years of the time of diagnosis.
Poor prognostic indicators include proteinuria, hypertension, and azotemia.
Dr S Chakradhar

6. Henoch-Schönlein purpura :
Is a systemic variant of IgA nephropathy which causes a small-vessel vasculitis and associated glomerulonephritis.
Deposition of immune complexes containing the antibody IgA in the skin and kidney
Dr S Chakradhar

7. Membranoproliferative (MPGN)/ Mesangiocapillary GN :
There is thickening of GBM
Splitting of BM occurs due to inclusion of processes of mesangial cells
Proliferation of glomerular cells & mesangial cells
Types
Primary - Idiopathic
Secondary to SLE, viral hepatitis
Presents clinically as Nephrotic, Nephritic or mild proteinuria with inevitable progression to end stage renal failure
Dr S Chakradhar

8. Minimal change GN :
No changes are visible on simple light microscopy, but on electron microscopy there is fusion of podocytes
This form of GN causes 80% of Nephrotic syndrome in children, but only 20% in adults.
Dr S Chakradhar

9. Focal Segmental Glomerulo sclerosis (FSGS) :
Sclerosis of some but not all glomeruli
And only a segment of an individual glomerulus.
May be
Primary (Idiopathic)
Secondary to reflux nephropathy, Alport syndrome, heroin abuse or HIV.
Presents as a Nephrotic syndrome
With varying degrees of impaired renal function (seen as a rising serum creatinine, hypertension).
Dr S Chakradhar

10. Steroids are often tried but not shown to be effective.
Treatment
Steroids are often tried but not shown to be effective.
50% of people with FSGS continue to have progressive deterioration of kidney function, ending in renal failure.
Normal
Dr S Chakradhar

11. Membranous glomerulonephritis :
Relatively common type of glomerulonephritis in adults,
Microscopically, MGN is characterized by a thickened glomerular basement membrane without a hypercellular glomerulus.
Immunofluorescence demonstrates diffuse granular uptake of IgG.
Etiology
Idiopathic (85%) – taken as autoimmune disease
Secondary to systemic disease
Malignant epithelial tumors – ca of lungs & colon
SLE
Infections – chronic nephritis malaria syphillis, schistosomiasis
Drugs – captopril
Dr S Chakradhar

12. Frequently produces a mixed nephrotic and nephritic picture.
Prognosis follows the rule of thirds:
1/3rd remain with MGN indefinitely
1/3rd remit and
1/3rd progress to end-stage renal failure
The kidney appears to shrink.
Treatment with corticosteroids is attempted if the disease progresses.
Dr S Chakradhar

13. RAPIDLY PROGRESSIVE (crescentic) GLOMERULONEPHRITIS (RPGN)
Crescents are formed in Bowman’s space by proliferating parietal epithelial cells with infiltrating monocytes & macrophage & sometimes neutrophils & lymphocytes
Reaches end stage renal failure within a period of days or weeks
Dr S Chakradhar

14. Good Pasture’s (anti GMB) Disease
Common Causes
Systemic vasculitis
SLE
Good Pasture’s (anti GMB) Disease
Aggressive phase of other inflammatory nephritis ( Ig A nephropathy, post infectious)
Dr S Chakradhar

15. Patient presentation (Goodpasture’s syndrome)
Adults, before the age of 30 years. A male predominance
Onset generally preceded by upper respiratory infection
Renal failure develop rapidly, Severe oliguria
Symptoms like AGN – hematuria , proteinuria
Hypertension is uncommon
Pulmonary – haemoptysis & dyspnoe
Diagnosis is confirmed by detecting anti – GBM antibodies
Dr S Chakradhar

16. Prednisolone plus cyclophosphamise or azathiprin
Treatment
Prednisolone plus cyclophosphamise or azathiprin
Plasma exchange to remove the Antiglomerular basement membrane antibodies in the plasma.
Prognosis
Prognosis depends on the degree of irreversible glomerular damage.
Earlier diagnosis and treatment increases survival.
Dr S Chakradhar

17. Chronic glomerulonephritis (CGN)
Is the final stage of GN when sclerosis has limited many glomeruli & their associated tubules
Persistent urinary abnormalities (proteinuria and/or hematuria)
Hypertension
Progressive loss of functioning Nephrons.
These patients generally progress to ESRD.
Dr S Chakradhar

18. Supportive and symptomatic. No specific treatment
Hypertension and infections should be treated vigorously.
Nephrotoxic agents should be avoided.
Prognosis
Depends upon the nature of the underlying disease and presence or absence of complications, especially hypertension.
Ten, twenty, or more years may elapse from the first discovery of CGN until the development of ESRD.
Dr S Chakradhar