4. Kidney tissues are divided into 2
• renal vascular part and
• renal parenchymal part.
• Renal parenchymal disease refers to the various diseases that occurs
in the substance of the kidney
• Once renal parenchymal disease develops, kidneys lose its ability to
remove the waste products from the blood, causing various
symptoms.
5. GLOMERULONEPHRITIS (GN)
This is an acute or chronic non suppurative inflammatory
lesion involving the glomeruli of both kidneys.
The inflammation may be immune or non – immune mediated
Different forms of GN have been described
These different forms are collectively described as the
glomerulonephritides (plural of GN).
6. VARIABLE MANIFESTATIONS OF GLOMERULONEPHRITIS
HAEMATURIA
WITH NORMAL
KIDNEY FUNCTION
PROTEINURIA
WITH NORMAL
KIDNEY FUNCTION
PROTEINURIA
HAEMATURIA OR
WITH ABNORMAL KIDNEY FUNCTION
PROTEINURIA
HAEMATURIA +
WITH ABNORMAL KIDNEY FUNCTION
PROTEINURIA
HAEMATURIA +
WITH NORMAL KIDNEY FUNCTION
7. Proteinuria [Transient, Recurrent, Persistent, Sub-nephrotic or Nephrotic]:
≥ 1+ (≥ 30 mg/dL) by dipstick
or > 4 mg/m2/hr (or UPCR ≥ 20 mg/mmoL) by quantitative assessment
And/ Or
Haematuria [Transient, Recurrent, Persistent]:
– Gross
– Microscopic: dysmorphic or fragmented red blood cells
RBC/Haemgranular casts
With or Without
Oedema
Hypertension
Azotaemia
Elevated plasma creatinine
Reduced GFR
Reduced kidney sizes on ultrasound
DIAGNOSTIC INDICES OF GLOMERULONEPHRITIS
13. Autoimmunity in glomerulonephritis
• failure of tolerance
• trigger e.g. infection
• activated T-cell
• alteration of host protein
• molecular mimicry
14. Factors favouring immune deposits
• persistence of antigenaemia
e.g Hepatitis B & C
• impaired clearance of immune deposits
e.g defective binding to C3b receptor
on rbc.
15. In-situ formation of immune deposits
• antibody to alpha-3 chain of type IV collagen in anti-GBM
disease
• antibody to podocyte antigens in some forms of idiopathic
membranous nephropathy
• antibody to microbial or food antigen on glomerulus
16. Non-immune deposit mediated GMN
• Minimal change disease
• some forms of crescentic GMN
• focal segmental glomerulosclerosis
17. Mechanisms of proteinuria
• loss of charge barrier
( heparin sulphate proteoglycans,
sialoproteins)
• breaching of size barrier
( tight collagen meshwork in GBM &
interdigitating foot processes)
18.
19. Pathogenesis of crescents
• severe acute glomerular injury
• cell mediated
• extravasation of plasma constituents into Bowman’s space
• cytokine driven proliferation of parietal epith cells
• infiltration by activated leucocytes, macrophages
• formation of fibrin
26. Classification - histologic
use of after light microscopy and or IF and electron microscopy
• proliferative or non-proliferative
• diffuse or focal
• global or segmental
40. Treatment
• Self-limiting in some
• Spontaneous remission
MCD, MN
• Treatment of oedema
• Treatment of hypertension
• Treatment of associated /intercurrent disease
• Disease specific therapy
41. Minimal change disease
• Prednisolone 1mg/Kg/day for 8-16 weeks,
then
on alt days for 4 more weeks
• Repeated for first relapse
• For second relapse, cyclophosphamide
2mg/Kg/day
with prednisolone alt die for 12 weeks
• others: cyclosporine, lavamisole
• azathioprine not used
42. Membranous nephropathy
• More effective if serum creatinine < 3mg/dL
• cyclophosphamide 1-2mg/Kg/day with
prednisolone 0.5 mg/Kg/day for 6 months
• Alternating monthly:
oral chlorambucil 0.1-0.2mg/Kg/day for 1
month
and
methylprednisolone 1g i.v, then prednisolone
0.4-0.5mg/Kg/day for 27 days.
43. Focal segmental glomerulosclerosis
Week methylpred prednisolone
• 1 30mg/kg alt die x 3 none
• 2 ,, ,,
• 3-10 30mg/Kg wkly 2mg/Kg alt die
• 11-18 30mg/Kg alt wks ,,
• 19-52 30mg/Kg monthly ,,
• 53-78 30mg/Kg alt month ,,
44. Prognosis
• MCD : good, >95% remission
• MN : rule of thirds; remission, partial,
progression
• FSG : up to 50% remission with therapy
but steroid dependent
• MCGN ; 40-50% ESRF in 10 years.
45. Poststreptococcal glomerulonephritis
• Sporadic or in epidemics
• Pharyngeal or skin infection, usually Lancefield group A Streptococci
• Circulating immune complexes
• Plasmin receptor protein, Streptococcal zymogen
• Acute nephritic syndrome typically
• Diffuse proliferative GN. C3 and IgG staining
• characteristic subepithelial humps later.
• Serology for Streptococcal antigens
46. Malaria
• Giglioli, 1920
• P. malariae mostly, also P. falciparum
• Commoner in children
• Acute nephritis, nephrotic syndrome, CRF
• Typically, basement membrane thickening with
expansion of the mesangium
• Immune deposits in capillary wall and mesangium
IgG, C3
47.
48. Schistosomiasis
• Particularly hepatosplenic mansoni infections
• Nephrotic syndrome
• Mesangiocapillary GN; less often MPGN, MN.
• Predominant IgA deposition in capillaries
• Usually progressive
49. Hepatitis-B virus infection
• Common in developing countries,
• 6-20% seropositivity in W. Africa.
• May follow acute hepatitis or be asymptomatic
• Generally, HbsAg and anti-core positivity
• HbeAg positivity common with membranous nephropathy
• Immune complex disease
• Membranous nephropathy, polyarteritis nodosa, membranoproliferative
GN
50. Hepatitis-C virus infection
• Worldwide problem
• Usually asymptomatic liver disease
• Nephrotic syndrome in about 2/3
• Cryoglobulinaemia with mesangiocapillary GN typical
• Others include MN, mesangial proliferative GN
• Low C3, C4, raised rheumatoid factors in serum.
51. HIV associated nephropathy
• Rising incidence likely
• May be first manifestation of HIV infection
• Nephrotic syndrome with CRF
• Large kidneys
• Focal segmental glomerulosclerosis
• Microcystic dilatation of tubules, inclusion bodies
