2. ACUTE & CHRONIC GLOMERULONEPHRITISBY
DR WAQAR
MBBS, MRCP
ASSISTANT PROFESSOR

3. DEFINITION The term “glomerulonephritis” means
inflammation of the glomerulus
The term “glomerulopathy” is also used, which includes non-inflammatory lesions of the glomerulus also ( eg minimal change disease)

4. NORMAL GLOMERULUS

5. FILTRATION BARRIER AT THE GLOMERULUS
3 Layers
Capillary endothelium
of glomerulus
Basement memb. of
glomerulus
Visceral epithelium of
Bowman’s capsule
(podocytes w/foot
processes)

6. Clinical presentation of glomerular pathology can be as :
Nephrotic syndrome(too much protein in urine)
Nephritic syndrome (urine protein + blood etc)
Asymptomatic proteinuria/ hematuria or
both.
4) Acute renal failure
5) Chronic renal failure

7. Suspect Glomerular lesion when the urine analysis shows :
1) Protein +
2) RBC casts
specially these 2
3) “Deformed” RBCs

8. THE FINAL DIAGNOSIS OF A GLOMERULAR DISEASE IS, OF COURSE, BY BIOPSY, FOLLOWED BY MICROSCOPY & IMMUNOFLORESCENCE OF THE BIOPSY MATERIAL.

9. NEPHRITIC SYNDROME
The following are the features of Nephritic Syndrome:
Hematuria ( RBC casts & deformed RBC)
Proteinuria ( less than 3.5 g in 24 hrs)
Renal insufficiency ( causing high creatinine)
HTN
Edema

10. In this lecture, we will discuss those
glomerulopathies which cause NEPHRITIC
SYNDROME

11. GLOMERULOPATHIES WHICH CAUSE NEPHRITIC SYNDROME
1) Membranoproliferative GN (MPGN) 2) Post- Streptococcal GN 3) Lupus Nephritis 4) IgA nephropathy/Henoch-Schonlein purpura 5) Pulmonary- Renal syndromes

12. GENERAL PATHOGENESIS OF GLOMERULONEPHRITIS
Ag-Ab complexes are deposited in the glomerulus
These complexes initiate an inflammatory reaction in the glomerulus GN

13. GENERAL TREATMENT OF NEPHRITIC SYNDROME
Treat the cause
For HTN: ACE inhibitors/ ARBs
For edema: salt & water restriction, diuretics
For proteinuria : ACE inhibitors/ ARBs
Monitor & correct fluid & electrolyte problems
If you don’t treat proteinuria in renal diseases, it will damage the kidneys more.

14. Membranoproliferative G.N.
ETIOLOGY: Can be divided into 2 types:
* Primary(idiopathic) no known cause
* Secondary: Associated with another disease
- Hep C ( commonest cause of MPGN)
- HIV
- SLE
- Malignancies

15. MPGN (contd).
2) MICROSCOPIC PICTURE: * Excess cells in the mesangium * “Tram track” appearance of the glomerulus 3) Treatment : a) Treat the underlying cause (hep C etc) b) In idiopathic type, may try immunosuppressive drugs eg (cyclophosphamide azathioprine etc) + Symptomatic Rx of nephritic syndrome as discussed earlier

16. Tram track appearance

17. POST INFECTIOUS G.N. Occurs after an infection
Most commonly occurs after a streptococcal infection in children ( throat or skin infection)
post streptococcal GN (B-Hemolytic strep)
Other infections: Abscess, mumps, malaria
IgG & C3 fuse with Strep.antigen get deposited in glomerulus & start inflammation
Occurs 2-4 wks after a strep. Infection
( plz remember the time period 2-4 wks) !

18. Post strep GN contd. PRESENTATION:
* Smoky / red urine after a strep. infection
* Features of nephritic syndrome ( edema,HTN)
INVESTIGATIONS:
Urine: RBC casts, blood, protein(nephritic pic.)
Evidence of strep.infection ( ASO titers in blood, anti-DNAase B antibody)
Serum C3 & C4 levels are low
Renal biopsy: IgG + C3 deposits are seen

19. Post strep.GN (contd) Prognosis is good.
Spontaneous recovery in 2-4 wks
Treatment is symptomatic ( gen. Rx for nephritic syndrome).Rarely, dialysis may be needed for a short time.
No antibiotics, because it is NOT DUE TO
“active Strep”. infection.

20. LUPUS NEPHRITIS Kidney involvement in SLE is called lupus nephritis.
SLE can cause many types of glomerular lesions, causing either Nephrotic syndrome, nephritic syndrome or combination of both.
W.H.O. classification : It is based on the histologic appearance of the lesion
Class I, II, III, IV, V. Remember only two:
* Class IV: MPGN( nephritic)
* Class V: Membranous nephropathy(nephrotic)

21. Lupus nephritis (contd)
DIAGNOSIS:
* Lupus serology positive(ANA, anti dsDNA,,etc)
* Urine : nephritic picture ( RBC casts, protein) or nephrotic picture, depending which lesion is present
Confirmation : renal biopsy shows IgG & C3 deposits + “tram track appearance”( in case of MPGN) or IgG & C3 deposits + “spike
appearance”( in case of membranous nephro-
-pathy) will discuss in the next lecture

22. Lupus nephritis (contd)
Remember only 2 types of renal lesions in SLE: Membranous Membranoprolifera- nephropathy (MN) -tive GN (MPGN) * Class 5 nephritis * Class 4 nephritis * Causes nephrotic * Causes nephritic syndr. * IgG & C3 deposits * Causes IgG & C3 depos. * Spike pattern * Tram track pattern

23. IgG & C3 deposits are seen in:
* SLE nephritis remember the
* Post Strep.GN two S

24. Treatment of Lupus nephritis
Class I & II : No specific treatment.
2) Class III: A short course of oral prednisone
3) Class IV & V: (severe disease)
* Corticosteroids +
* Immunosuppressive agents
(azathioprine, cyclophosphamide,
mycophenolate)

25. IgA Nephropathy MOST COMMON GLOMERULONEPHRITIS WORLDWIDE (OVERALL).
Epidemiology:
* M:F :1
* Most common GN in Far East ( Japan,
Phillipines) & SouthAsia
* More common in young people

26. IgA (contd) Pathology: IgA & C3 deposited in the glomerulus
leads to glomerulonephritis
Etiology: Unknown
Clinical Features : Varied. Can present as
1) Hematuria
* Classic presentation ( 50% of cases)
* Microscopic or visible. Often episodic (comes &
goes)
* Often found on a routine urine check (asymp.)

27. IgA (contd)
* Hematuria often occurs 2-3 days after an upper resp.tract infection. Hematuria occurring after upper resp. tract infection, think of : *Post strep.GN : Occurs after few “wks.” of infection ( 2-4 wks) * IgA nephropathy: After 2-3 “days” of infec.

28. Clinical presentation of IgA nephropathy (contd)
2) Nephritic syndrome 3) Acute renal failure 4) Chronic renal failure Diagnosis: 1) Clinical suspicion ( young pt. w/ episodic hematuria, hematuria after resp. infec.) 2) Confirmation is by biopsy ( shows IgA & C3 deposits)

29. TREATMENT OF IgA NEPHROPATHY
Most cases with just hematuria, no Rx given.
Just annual F/Up
2) If BP is high, ACE inhibitors
3) If Nephritic syndrome treat accordingly
4) Steroids may help in some severe cases

30. IgA (contd) PROGNOSIS: * Some patients slowly develop CRF after many
years
* Some patients continue to have intermittent
hematuria, w/out getting CRF
* Very few pts get complete remission(cure)

31. Henoch-Schonlein Purpura
*Another disease in which there is deposition of IgA ab. in the glomerulus * It is a type of vasculitis & other blood vessels in the body also affected * Mostly seen in children & young people * Palpable purpura on the abdomen & legs ( purpura are small areas of bleeding under the skin) * Abdominal pain * Arthritis * Hematuria

32. H-S Purpura

33. H-S PURPURA

34. TREATMENT OF H-S PURPURA
Symptomatic & supportive
No specific Rx
Self recovery in few days to wks
Some cases may progress to chronic renal failure

35. RPGN (Rapidly progressing GN)
Rapid decline in renal function ( about 50% decline in GFR in 3 months)
If not treated, then ARF and death occur in a few months
Seen in SLE and IgA nephropathy
Crescent shaped scars seen in glomerulus under the microscope

36. Pulmonary-Renal Syndromes
Vasculitis involving the lungs & kidneys
S/S:
In the lungs: Alveolar hemorrhage
In the kidneys: Nephritic syndrome
Examples:
a) Goodpasture’s syndrome
b) Wegener’s granulomatosis

37. CHRONIC G.N.

38. THANK GOD THE LECTURE IS FINISHED !
THANK YOU
THANK GOD THE LECTURE
IS FINISHED !