GLOMERULONEPHRITIS

GLOMERULOPATHY
By

Mohamad A. Sobh, MD, FACP

Prof. & Head of Nephrology
Urology & Nephrology Center
Mansoura University
Egypt
 Glomerulopathies and glomerulo-
nephritis are group of diseases of
inflammatory or non-inflammatory
nature involving primeraly the renal
glomeruli.
 Etiology of Glomerulonephritis
a. Primary or idiopathic
b. Secondary:
n Infection (bacteria, parasite, virus).
n Colagen disease (SLE, PAN, Rhoid).
n Drug (Penicillamin, gold, Asprin,
Paradion, heroin).
n Metabolic diseases (DM, Amyloidosis).
n Malignancy (Hodgkins lymphoma).
n Heredofamilial (Alports Syndrome).
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Histopathology of
Glomerulonephritis
1. Minimal change (nil-change) disease.
2. Focal and segmental glomerulosclerosis
3. Membranous glomerulonephritis
4. Proliferative glomerulonephritis.
 Mesangial proliferative GN.
 Mesangiocapillary
(membranoproliferative) GN.
 Crescentic GN.
 IgA nephropathy.
 Clinical Manifestations of
Glomerulonephritis
1. Nephrotic Syndrome.

2. Acute Nephritic Syndrome.

3. Rapidly Progressive GN.

4. Chronic Nephritic Syndrome.

5. Asymptomatic Urinary Abnormalities.

 Nephrotic Syndrome

1. Insidious onset of massive oedema.

2. Heavy proteinuria.

3. Hypoalbuminaemia.

4. Hyperlipidemia.
 Acute Nephritic
(Acute Nephritis)
1. Rapid onset of oedema, smooky urine,
oliguria and hypertension.
2. Urine shows red cell casts, proteinuria.

3. Serum creatinine may be high, but

albumin and lipids usually normal.
4. Prognosis is usually good and recovery
occurs.
Rapidly progressive Glomerulonephritis
(RPGN)

1. Rapid onset of nephritis with

development of uraemia.
2. Urine shows nephritic sediment.

3. Serum creatinine is high.

4. If untreated aggressively, the

prognosis is poor.
 Chronic nephritic Syndrome
1. Slowly progressive (mon., years)
uraemia.

2. Urine shows proteinuria, hematuria,

broad casts, no urine concentration.

3. Serum creatinine is high as well as

other stegmata of uraemia.
 Asymptomatic Urine
Abnormalities
1. Microscopic hematuria or proteinuria
or both.

2. Serum creatinine is normal.

3. Prognosis is usually excellent.

 Nephrotic Syndrome

A syndrome characterized by:

• Heavy proteinuria (> 3.5 gm/1.73 m2/d.)
• Massive oedema.
• Hypoalbminaemia.
• Hyperlipidaemia.
Etiology of Nephrotic Syndrome
1. Primary (idiopathic) N. S.
2. Secondary N. S.
 Post infection.
 Drug induced
 Metabolic
 Collagen and autoimmune.
 Malignancy.
 Renal vein thrombosis.
 Congenital.
 Pathology of Nephrotic
Syndrome
 Minimal change nephritis.
 Focal and segmental glomerulosclerosis.
 Membranous glomerulonephritis.
 Proliferative glomerulonephritis.
 Mesangial proliferative.
 Mesngiocapillary.
 Crescentic GN.
 IgA nephropathy.
 Pathogenesis of
Hypoalbuminaemia in N. S.
• Protenuria
• Decrease influx from GIT (poor intake
and poor absorption)
• Increased tubular catabolism of
filtered albumin.
• Sometimes decreased rate of hepatic
biosynthesis.
 Glomerular damage
Proteinuria

Hypoalbuminaemia

Decreased plasma oncotic pressure

Water Water
retention Oedema retention
Decreased effective
• increased circulating blood volume • increased
angiotensin, ADH
aldosteron Pathogenesis of Oedema
• Decreased ANP in N. S.
 Hyperlipidemia in N. S.
 ↑ Cholesterol, VLDL, LDL

 triglycerids, ↓ HDL.
 ↑ Hepatic synthesis

 ↓ Peripheral utilization.

 Urinary loss of HDL.

 Hypercoagulability in N. S.
 Venous stasis.

 Abnormal platelets and vascular

endothelium.
 Urinary loss of anti-thrombin III,
protein C, and protein S.
 More in membranous G. N. & MPGN.
 Other Urinary Losses in N. S.
 Transferrin

 TBG

 25-OHD3

 IgG, C1q
 Clinical Features of N. S.
1. Oedema

2. Hypertension

3. Lassitude, anorexia, loss of appitite,

pallor.

4. Manifestations of the etiologic cause.

5. Manifestations of complications.
 Complications of N. S.
1. Subnutritional state.
2. Infection.
3. Clotting episodes (DVT) and pulmonary
embolism.
4. Premature atherosclerosis.
5. Hypovolaemia.
6. Drug related complications.
7. Acute renal failure.
8. Bone disease.
9. Anaemia.
 Investigations of Nephrotic
Syndrome
1. Urine analysis for proteinuria,
microscopic hematuria, pyuria, and casts.
2. Blood analysis for creatinine, albumine
and lipid profile.
3. Investigations for diagnosis of the etiology
in secondary N.S. such as DM, SLE,
malignancy.
4. Kidney biopsy.
 Treatment of N. S.
1. Treatment of the cause in 2ry cases.
2. Treatment of complications.
3. Rest in bed during exacerbations and early
ambulation with remissions.
4. Diet:
 Salt restricted
 Protein content equal 1 g/kg/d plus urinary
losses
5. Diuretics, mainly loop diuretics.
6. Human salt free albumin in certain
situations.
7. Steroid, CsA, and other immunosuppressive
drugs.
 Acute Glomerulonephritis
 Post streptococcal (post infection).

 MPGN, mesangial proliferative G.N.

 IgA nephropathy.

 SLE, systemic vasculitis, cryoglobulinemia

endocarditis, Henoch- Schonlein purpura.
Acute post-Streptococcal GN
 Occurs after infection with
nephritogenic strain of group A, B-
haemolytic streptococci.
 Ether pharyngeal or skin infection.
 Latent period is 1-3 weeks.
 Children are affected more than
adults.
 Clinical Features Of Post-
Streptococcal GN
 1-3 weeks after streptococcal infections
patient presents with acute nephritis
(oliguria, smooky urine, oedema,
headache, high blood pressure, ⇑ S.Cr.).
 20% of cases presents with NS.
 5% of cases present with RPGN.
 Some cases may be asymptomatic.
 Post streptococcal G.N.
(Laboratory)
 Urine:
 Red & White blood cell casts.
 Proteinuria ( < 3 gm./4h. In 75%,
<0.5% gm in 50%).
 Rarely –ve.
 Pharyngeal and skin cultures
 ASLO, AH.

 Hypocomplementemia C3 < C1, C4

CH50
 Postreptococcal G.N.
(Histopathology)
Light microscopy Diffuse proliferative
G.N.
Crescents
I. F. C3, C1q, IgG, IgM, IgA.
E. M. Humps
Complications Of Acute
Nephritis

1. Encephalopathy.

2. Heart failure.

3. Acute renal failure.

 Prognosis
 85% of the cases recover completely.

 5% die-in the acute phase.

 10% develop CRF.

 Signs of bad prognosis.

 Treatment
1. Irradication of infection.
2. Rest
3. salt restricted diet.
4. Hypotensive drugs.
5. Diuretics.
6. Dialysis treatment if renal failure
develop.
7. Steroids and immunosuppressives for
cases with RPGN.
Rapidly Progressive Glomerulonephritis
“Crescentic Glomerulonephritis”
“Extracapillary Proliferative G. N.”
“Subacute Glomerulonephritis”
- Type I • Goodpasture’s syndrome.
• Idiopathic.
- Type II • Postinfection.
• SLE.
• Henoch-Schonlein purpura.
• Systemic vasculitis.
• Cryoglobulinemia.
• Idiopathic.
- Type III
 Asymptomatic Urinary
Abnormalities
 Any type of nephropathy.
 Berger’s disease.
 Mild mesangial proliferative G. N.
 Post infection G. N.
 IgM nephropathy.
 Hereditary nephritis.
 Isolated Proteinuria
 > 150 mg/24 hr., < 3 gm/24 hr, almost
always 1 gm/24 hr, occur in 0.6- 8.8% of
healthy young adults.
 All lab tests and clinically are OK.
 Orthostatic or constant, persistent or
transient.
 70% with persistent, constant isolated
proteinuria have abnormal biopsies, while
in only 10-15% of those with persistent
arthostatic.
 Ten-years prognosis is excellent.
 Isolated Proteinuria

 Also with vigorous exercise,

stress, fever, C. H. F., and
hypertension.