Download presentation
Presentation is loading. Please wait.
2
ACUTE & CHRONIC GLOMERULONEPHRITIS
BY 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 !
Similar presentations
© 2024 SlidePlayer.com. Inc.
All rights reserved.