GLOMERULAR DISORDERS OF KIDNEY REVISION NOTES BASED ON LECTURE NOTES & HIGH YIELD TOPIC RENAL DISEASES MEDICINE PATHOLOGY REVISION NOTES NEET PG AIIMS

1. Glomerular disorders
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6. 3 layers of glomerular membrane
• Fenestrated endothelium
• GBM
• Foot process of podocytes
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7. • Endothelial pore size 70-100nm
• Filtration slit 
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8. Filtrationslit  20-30nm
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11. Size of
particle
>8nm cannot pass through GBM
<4nm easily filtered
irrespective of charge
4-8nm
• Negatively charged particles are
repelled
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12. Endothelium
• Negative charge is d/t podocalyxin
• Fenestrated endothelium
• Pore size 70-100nm
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13. GBM
• Glomerular basement membranee
• Thickness  350-400nm
• Thin basement membrane  <200nm
• Type IV collagen
• α3 α4 α5
• Electronegativity of GBM Heparin sulphate proteoglycans 
perlecan & agrin
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16. • GBM lined inside by
• Endothelium & mesangium
• Outside GBM lined by
• Podocytes
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17. Jones methylamine silver stain  best stain
for GBM
PAS also may be used to
stain GBM
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18. Podocytes
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19. • Podocytes are terminally differentiated  cannot replicate or
regenerate
• Filtration
• b/w 2 podocytes
• 20-30nm
• Electronegativity is d/t podocalyxin (sialoglycoprotein)
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21. Endothelial filtration barrier
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22. Mesangium
• Foot process of mesangial cells contain actin
microfilaments
• Mesangial cell help in contraction
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23. Juxtaglomerular apparatus
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25. JGA
• Mesangial cells
• Macula densa of distal tubule
• Granular cells of afferent arteriole
secrete renin
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26. Tubuloglomerular feedback
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29. Renin secretion is increased by Renin secretion is decreased by
• Decreased intravascular volume
• Decreased renal perfusion pressure
• Sympathetic stimulation
• PGE2 & PGI2
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30. • Endothelial injury microscopic hematuria
• In post infectious GN
• Injury to GBM  microscopic hematuria + proteinuria
• Alport syndrome
• Injury to mesangial cells  macroscopic hematuria
• IgA nephropathy
• Injury to podocyte  proteinuria
• Membranous ds
• FSGS
• Minimal change ds
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32. Asymptomatic Macroscopic
hematuria
Nephrotis
syndrome
• Asymptomati
c
• Proteinuria
• Microscopic
Hematuria
• Proteinuria
(>3.5gm/24h
r)
• Hypoalbumin
emia
• Edema
• Hypercholest
rolemia
• Lipiduria
Renal biopsy is
required
Renal biopsy is
required
FSGS
Membranous
nephropathy
IgA nephropathy TONY SCARIA 2010
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34. Proteinuria types
•
Overflow
proteinuria
Tubular proteinuria Glomerular
proteinuria
Functional Orthostatic Persistent non
nephrotic
In multiple myeloma • Anxiety
• Stress
Overcomes ability of
proximal tubule to
reabsorb light chains
• <2g/day
• Mostly beta 2
macroglobulin is
lost
• >2g/day
• Mostly albumin
is lost
• Loss of protein
150-500mg
• Proteinurial
alone in standing
position
• <1g/day
• No proteinuria in
lying down
position  early
morning sample
–ve
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35. Nephrotic syndrome
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37. Nephrotic syndrome
• Characterised by
• Albuminuria(proteinuria)
• Hypoalbuminemia
• Edema
• Hyperlipidemia
• lipiduria.
• Hypercoagulability
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38. Protein decreased Effect
Albumin Edema
Transferrin Iron resistant microcytic hypochromic anemia
Thyroxine binding globulin Decreased thyroxine level
Cholecalciferol binding protein Hypocalcemia
Ceruloplasmin
AT III Increased thrombus formation
Nephrotic syndrome is characteristically associated with
increased fibrinogen levels (Hyper fibrinogenemia)d/t
increased hepatic synthesisTONY SCARIA 2010
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39. muerhrckes line in hypoalbuminemia
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40. Nephrotic edema
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41. Causes of NS
Systemic causes Glomerular disease
• Diabetes mellitus (most common cause),
SLE, Amyloidosis
• Drugs: Gold, penicillamine probenecid ,
street heroin, captopril, NSAIDs
• Infections: Bacterial endocarditis ,
hepatitis B , shunt infections, syphilis,
malaria
• Malignancy: Hodgkin’s and other
lymphomas leukemia, carcinoma of
breast and GI tract
• Allergic reactions
• 1. Minimal change disease (90% in
children and 15% in adults)
• 2. Membranous (40% in adults)
• 3. Focal segmental glomerulosclerosis
• 4. Membranoproliferative GN
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44. Mc cause of nephrotic syndrome
In children Minimal change disease
In adults focal segmental glomerulosclerosis (FSGS)
In old age Membranous GN
Over all MC cause FSGS
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45. Minimal change ds
• Lipoid nephrosis
• Most common cause of NS in children (2-7yrs)
• Selective proteinuria of albumin  frothy urine
• Edema
• Hypertension not a feature
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46. Causes of minimal change ds
• Idiopathic
• Drugs – NSAID, rifampicin, IFN – alpha
• Malignancies  Hodgkin’s disease
• HIV
• Routine immunisation
• Respiratory infection
• Atopic disorders
• Allergy
• insect sting TONY SCARIA 2010
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49. MINIMAL CHANGE DS
• No abnormality on electron
microscopy
• Elctron microscopy 
obliteration & fusion of foot
process
• Immunofluroscopy no
immune deposits
• Serum compliment –> normal
level
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51. • Clinical Features-
• Patient usually presents with insidious onset of generalized edema,
without a decrease in urine output.
• Patient may complain of passing frothy urine due to presence of protein.
• Nephrotic syndrome is associated with = ↑LDL, ↑Tg, ↓HDL
• Patient of nephrotic syndrome can develop spontaneous peripheral arterial or
venous thrombosis
• Increased susceptibility to infection
•  MC cause is streptococcus pneumoniae followed by E coli
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52. Minimal change ds not associated with
• HTN
• Microhematuria
• AKI
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53. Proteinuria in GN
• Effacement of foot process (Earlier called fusion of foot process) is
believed to play an important role in causes proteinuria in MCD.
• Proteinuria occur due to.
• 1. Loss of negative charge (Loss of polyanions)
• 2. Disruption of components of slit diaphragm (Demonstrated in congenital
nephrotic syndrome of the Finnish type)
• 3. Loss of actin cytoskeleton
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54. Urine in NS
• Lipoid cast (d/t lipiduria)
• Hyaline cast
• NO RBC
• Mlatese cross appearance 
lipiduria
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55. Hypercoagulability in NS
• Spontaneous thrombosis of limb arteries
• Renal vein thrombosis
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56. Renal vein thrombosis in NS
• More common in membranous nephropathy
• Present with abdominal pain & haematuria
• Renal vein thrombosis due to
• 1. Increase Fibrinogen
• 2. Increase Lipoproteins
• 3. Reduced antithrombin III &protein C
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57. Renal vein thrombosis
• Trauma
• Extrinsic compression (lymph nodes, aortic aneurysm, tumor)
• Invasion by renal cell carcinoma
• Dehydration (infants)
• Nephrotic syndrome specially membranous GN (adults)
• Pregnancy or oral contraceptives
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58. • Common Renal pathologies causing Renal Vein Thrombosis
• Membranous Glomerulonephritis (strongest association)
• Membranoproliferative Glomerulonephritis
• Amyloidosis
• Lupus Nephritis
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59. Congenital NS
• With in first 3 months
• Steroid resistant
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60. Congenital NS
Gene Protein Disease Inheritance
NPHS1 Nephrin in slit
diaphragm
Nephrotic syndrome
of finnish type
(FSGS)
AR inheritance 19p13.1
NPHS2 Podocin in slit
diaphragm
Steroid resistant
NS(FSGS)
AR 1q25
FSGS1 α actinin 4 FSGS Dominant 19p13
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61. Complications of NS
• Infections (pneumococcal peritonitis) MC complication
• Hypercholesterolemia (atherosclerosis, xanthomata)
• 'The lipid profile in Nephrotic syndrome is characterized by elevations in total
plasma cholesterol, VLDL and LDL and often (increases in later stages) triglyceride &
reduced HDL.
• Venous thrombosis and pulmonary embolism (urinary loss of antithrombin
III, low plasma volume, increased Fibrinogen)
• Hypovolemia and renal failure
• Loss of specific binding proteins, e.g. transferrin, thyroid binding globulin.TONY SCARIA 2010
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62. Indications for renal biopy in NS
• To r/o causes other than MCNS
• Age <1yr or > 8 yrs
• Adult is less likely to be MCNS  mandatory renal biopsy
• Gross hematuria
• HTn
• Renal insufficiency
• Low C3
• Initial steroid resistance
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63. Rx
• Salt restriction < 2g/day
• Protein  1g/kg/day
• Target BP
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66. Minimal change ds progressing to AKI
• Generally no features of AKI
• But can occur if
• Severe hypoalbuminemia pre renal failure
• RVT
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67. Membranous GN
• MC of NS in elderly
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68. Membranous GN
• It is characterized morphologically by the presence of subepithelial
immunoglobulin-containing deposits along the GBM.
• Early in the disease, the glomeruli may appear normal by light
microscopy, but well-developed cases show diffuse thickening of the
capillary wall
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69. Membranous GN
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70. Diffuse granular staining of basement
membrane with Ig & complement
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72. Electron microscopy
• Subepithelial GBM
deposits
• Eoimembranous deposits
• Deposition of immune
complexes b/w BM &
podocytes
• effacement of podocytes
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74. Pathogenesis of membranous GN
Primary membranous GN Secondary membranous GN
autoantibodies that cross-react with antigens
expressed by podocytes
Secondary to other systemic ds
Rat model Human model
Ab against megalin Ag
of rat podocyte 
heymann nephritis
Ab against PLA2 receptor of
human podocyte
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75. Primary membranous nephropathy
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76. Causes of secondary GN
Idiopathic (majority) infection: Neoplasia Drugs: Miscellaneous Autoimmunse ds
• Hepatitis B and C
• secondary and
congenital syphilis
• malaria,
• schistosomiasis,
• leprosy,
• hydatid disease,
• filariasis,
• enterococcal
endocarditis
• Carcinoma of the
breast, lung,
colon, stomach,
and esophagus;
• melanoma;
• renal cell
carcinoma;
• neuroblastoma;
• carotid body
tumor
• Gold,
• penicillamine,
• captopril,
• NSAIDs,
• probenecid,
• trimethadione,
• chlormethiazole,
• mercury
1. ​Sarcoidosis
2. Diabetes mellitus
3. Sickle cell disease
4. Crohn’s disease
5. Guillain – Barre
syndrome
• SLE,
• rheumatoid
disease,
• Sjorgren’s
syndrome,
Hashimoto’s
disease,Graves’
disease, mixed
connective tissue
disease, primary
biliary cirrhosis,
• ankylosing
spondylitis,
• dermatitis
herpetiformis,
bullous
pemphigoid,
• myasthenia gravis
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77. CF of membranous GN
• Massive proteinuria
• Hematuria & HTn in 15-35 % cases
• Patients present with edema, nephrotic proteinuria and high BP.
• Renal insufficiency and abnormal urine sediment may develop later.
• Renal vein thrombosis is common.
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79. Focal segmental glomerulosclerosis
• MC overall cause of NS
• MC in adults
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80. FSGS
• sclerosis affecting some but not all glomeruli (focal involvement) and
involving only segments of each affected glomerulus (segmental
involvement)
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81. FSGS
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82. Focal & segmental involvement of glomeruli
in FSGS
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83. Pathogenesis of FSGS
• injury to the podocytes initiating event of primary FSGS
• Lymphocyte produced factor increasing permeability
• The deposition of hyaline masses in the glomeruli represents the
entrapment of plasma proteins and lipids in foci of injury where
sclerosis develops.
• IgM and complement proteins commonly seen in the lesion are also
believed to result from nonspecifc entrapment in damaged glomeruli
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84. Causes of FSGS
• Idiopathic (majority)
• In associated with systemic diseases or drugs:
• 1. HIV infection
• 2. Diabetes mellitus
• As consequence of sustained glomerular capillary hypertension
• Congenital oligo nephropathies
• Unilateral renal agenesis
• Reflux nephropathy
• Glomerulonephritis or tubulointerstitial nephritis
• Sickle cell nephropathy
• Heroin use
• Congenital Nephrotic syndrome
• NPH1
• NPH2
• FSGS1  autosomal dominant FSGS
• Mutation in TRPC6
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85. Mutated TRPC6  adult onset type FSGS
(increasing Ca2+ influx)
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86. APOL1 gene mutation in FSGS
• apolipoprotein L1 gene (APOL1) on chromosome 22 appears to be
strongly associated with an increased risk of FSGS and renal failure
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87. Histologic variants of FSGS
Collapsing
variant
• Worse
prognosis
Glomerular tip
variant
• Best
prognosis
Perihilar
variant
Cellular
variant
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88. Variants of FSGS
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89. • Light microscopy
• increased mesangial matrix,
obliterated capillary lumina, and
deposition of hyaline masses
(hyalinosis) and lipid droplets.
• Electron microscopy
• podocytes exhibit effacement of foot
processes, as in minimal change
disease
• IF
• Nonspecific trapping of Ig (especially
IgM) & complement(C3) TONY SCARIA 2010
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90. Collapsing variant of FSGS
• Worst prognosis
• It is characterized by collapse of
the glomerular tuft and podocyte
hyperplasia
• associated with HIV infection,
drug-induced toxicities, and some
microvascular injuries
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91. • CF:
• Proteinuria is present and is usually nonselective.
• Hypertension, reduced GFR(arteriolar obliteration by sclerosis),
abnormal tubular function and abnormal urinary sediments
(leukocyturia, hematuria) are seen.
• Hyperlipidemia is severe in cases with focal sclerosis.
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92. Relfux nephropathy & FSGS
• FSGS may develop following acquired loss of nephrons from reflux
nephropathy
• Association of reflux nephropathy and proteinuria suggest an
irreversible glomerular lesion most commonly FSGS
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93. Podocytopathies
• a/w podocyte injury
• Minimal change ds
• Membranous GN
• FSGS
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94. Membranoproliferative GN
• Immune mediated injury
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95. Membrano proliferative GN
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96. TONY SCARIA 2010
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97. Type 1 (MC SUBTYPE) Type II Type III
Sub endothelial electron dense deposits lamina densa and the subendothelial
space of the GBM
are transformed into an irregular, ribbon-
like, extremely
electron-dense structure, resulting from
the deposition of
material of unknown composition
DENSE DEPOSIT DISEASE
Double contours of GBM & subendothelial
deposits subepithelial deposits
Subendothelial deposits of occasionally
granular epithelial & mesangial Ig
Intramembranous deposition
Activation of classical & alternate pathway Activation of alternate pathway
• Idiopathic
• Bacterial endocarditis
• SLE
• Hepatitis C
• Mixed cryoglobulinemia
• Hepatitis B
• Cancer: Lung, breast, and ovary
(germinal)
• Idiopathic
• C3 nephritic factor–associated
• Partial lipodystrophy
• Idiopathic
• Complement FACTOR deficiency
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99. Type I MPGN
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100. Type I MPGN
• discrete subendothelial electron-dense deposits
• C3 is deposited in an irregular granular pattern, and IgG and early
complement components (C1q and C4) often are also present,
indicative of an immune complex pathogenesis
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101. Type II MPGN
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102. Type II MPGN
• d/t activation of alternate
complement pathway
• They have C3 nephritic
factor (C3NeF)
• Stabilises C3 convertase 
enhancing C3 activation 
hypocomplementemia
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103. Type III MPGN
• Intramembranous + subendothelial + subepithelial deposit
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105. Light microscopy
• Thickened capillary loops
• Glomerular cell proliferation
• Lobular appearance of glomeruli
• d/t mesngial proliferation
• Duplication of basement
membrane
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107. Subendothelial deposits
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108. Dense intramembranous
deposits
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110. • Compliment levels are normal in
• 1. Minimal change GN
• 2. Membranous GN
• 3. FSGS
Decreased compliment level in MPGN
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111. Nephritic syndrome
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112. Nephritic syndrome
• a/c glomerulonephritis
• Hypertension,
• Hematuria with red cell cast  high coloured urine
• non nephrotic Proteinuria
• Normal albumin level
• Azotemia & Oliguria a/w AKI
• RBC cast are present in the urine.
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113. nephritic syndromw
Mc cause in
Children Post streptococcal GN
Adults IgA nephropathy
Overall IgA nephropathy
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116. a/c proliferative GN
Post infectious GN
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117. • Postinfectious glomerulonephritis
• occur as a sequela of disease caused by bacteria, viruses, fungi, protozoa,
and helminths
• Post streptococcal GN most common cause of GN in childhood
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118. Nephritis develops 1–3 weeks after pharyngeal (more common in
winter) or cutaneous infection with (more common in summer)
‘nephritogenic’ strains of group A beta – hemolytic streptococci
Group A beta haemolytic
streptococci
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119. Cutaneous streptococcal infection
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120. Pathogenesis of PSGN
• immune complex disease
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125. • Light microscopy
• diffuse  increased cellularity of the glomerular tufts that affects nearly all
glomeruli
• Electron microscopy
• deposited immune complexes arrayed as subendothelial, intramembranous, or, most
often, subepithelial “humps” nestled against the GBM
• Immunofluorescence studies reveal scattered granular deposits of IgG
and complement within the capillary walls and some mesangial areas,
corresponding to the deposits visualized by electron microscopy.
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128. IF deposits  starry sky appaearance in PSGN
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129. CF of PSGN
• sudden onset of hematuria and edema
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130. Lab findings
• Hypocomplementemia
• elevated titers of
• antistreptolysin 0,
• antihyaluronidase, and
• anti-deoxyribonuclease B antibodies
• Unfavourable prognostic factors
• Prolonged persistent heavy proteinuria
• Abnormal GFR
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131. Rx
• Hypertension must be treated aggressively,
• Furosemide or bumetanide is required for the underlying edema-
inducing disease.
• Antibiotic - penicillin.
• Prophylaxis following poststreptococcal glomerulonephritis is not
indicated because recurrences are exceedingly rare.
• Early treatment of pharyngitis does not prevent development of acute GN.
• Immunosuppressive agents or corticosteroids have no therapeutic
role.
• Recurrence is uncommon with PSGNTONY SCARIA 2010
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132. IgA Nephropathy (Berger’s Disease)
• Most common causes of recurrent microscopic or gross hematuria
• MC of GN world wide
• IgA nephropathy is a type of mesangioproliferative
glomerulonephritis with IgA deposition in the mesangium
• Pathogenesis
• Genetic or acquired defects in immune regulation
• Increased IgA1 secretion (only IgA1 is nephritogenic)
• Decreased clearance of IgA
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133. Onset of hematuria occurs 1-4 days after
URTI
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134. Secondary IgA nephropathy
• Celiac ds
• c/c Liver pathology
• HSP
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135. • Light microscopy
• Mesangial proliferation
• Cresents may be present
• Electron microscopy
• Mesangial deposits of IgA IgG or IgM with C3
• Compliment level remain same
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137. TONY SCARIA 2010
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138. IgA nephropathy PSGN
Onset of hematuria after URTI 1-4 days 1-4 weeks
Serum C3 level Normal Transiently decreases for 6-8 weeks
Recurrence Common Rare
Antibody titre Not elevated Elevated ASO titre
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139. Other causes of mesangioproliferative GN
Mesnagioproliferative GN
• IgA nephropathy
• HSP
Proliferation of mesangial cells and
deposition of IgA in matrix
• Hematuria
• Proteinuria
• Hypertension
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140. RPGN
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141. RPGN
• RPGN is defined by 2 criteria
• 1. Presence of epithelial crescents in more than 70% of glomeruli
• 2. Occurrence of rapidly progressive renal failure, End stage disease occurs
within month
• Presents with nephritic syndrome  rapidly progresses to loss of
renal function
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143. TONY SCARIA 2010
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144. RPGN
Crescent
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145. Crescents are features of RPGN
• Crescents are made up of proliferated
parietal epithelial cells fibrin &
leucocyte
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146. TONY SCARIA 2010
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147. Type I RPGN Type II RPGN Type III RPGN
Anti GBM mediated
Ab against α3 chain of collagen IV
Immune complex mediated Pauci immune
ANCA associated
Most common
IF  linear deposits along
basement membrane
IF granular deposits IF  no deposits
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148. TONY SCARIA 2010
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149. Type I RPGN Type II RPGN Type III RPGN
• Idiopathic
• Good pastures syndrome
• Idiopathic
• SLE
• Ig A nephropathy
• MPGN
• Cryoglobulinemia
• Post infectious GN
• Idiopathic
• Granulomatosis with polyangitis
• Microscopic polyangitis
• Best prognosis
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150. Prognosis of RPGN
• The prognosis of RPGN depends upon Number of crescents.
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151. • Diagnosis
• Renal biopsy
• Rx
• Plasmapheresis & immunosuppression
• In immune complex glomerulonephritis, treatment depends on the
individual causative disorder.
• In pauci-immune deposit disease, treatment involves pulse
methylprednisolone and cyclophosphamide.
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152. Good pasture syndrome
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153. Good pasture syndrome
• characterized by formation of Anti GBM antibodies that attack both
pulmonary capillaries and the Glomerulus
• Type II hypersensitivity
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154. Triad of goodpasture syndrome
• Anti GBM ab
• Directed against Non collagenous domain of type α3 collagen
• Glomerulonephritis (usually crescentic)
• Pulmonary hemorrhage (Hemoptysis may precede nephritis).
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155. TONY SCARIA 2010
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156. TONY SCARIA 2010
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157. Ab in good pasture syndrome
• Circulating Anti GBM antibodies (lgG): Positive
• ANCA antibodies: Typically Negative (ANCA negative vasculitis)
• ANA antibodies: usually normal
• C3 levels: Usually normal
• Antibodies against Non collagenous Domain (NCL) of a3 chain of
collagen type IV
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158. CF in good pasture syndrome
• 1. Hemoptysis (Frank)
• 2. Dyspnea
• 3. Hematuria
• 4. Proteinuria
• 5. Edema
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159. Pathology in good pasture
syndrome
• Diffuse crescentic Glomerulonephritis
• Linear IgG staining along basement
membrane on immunofluorescence
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160. B/L pulmonary infiltrates are seen on CXR in good pasture syndrome
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161. • Treatment:
• 1. Plasma exchange may produce remission.
• 2. Prednisolone
• 3. Immunosuppressive therapy
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162. TONY SCARIA 2010
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163. Alport syndrome
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164. TONY SCARIA 2010
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165. TONY SCARIA 2010
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166. Alport syndrome
• X linked dominant form (85 %
case)
• Mutation in α chain
• Autosomal forms
• Mutation in α3 or α4 chain
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167. Eye EAR Kidney
• Anterior lenticonus Sensorineural deafness Hematuria
Proteinuria
Abnormal splitting &
lamination of basement
membrane
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168. ANTERIOR LENTICONUS IN ALPORT
SYNDROME
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169. TONY SCARIA 2010
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170. GBM splitting & lamination  basket weave
appearance
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171. Thin basement membrane
disease
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172. Thin basement membrane ds
• Benign familial hematuria
• Asymptomatic hematuria
• Thickness of GBM <200nm
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173. HSP
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174. TONY SCARIA 2010
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175. HSP
• MC vasculitis of childhood
• Characterised by leukocytoclastic vasculitis & IgA deposition in small
vessels of skin joints GIT & kidney
• Renal involvement hematuria and proteinuria.
• Serum IgA is normal or raised, platelet count is normal.
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176. LAB DIAGNOSIS OF HSP
• Antinuclear antibody (ANA) Negative
• Antineutrophil cytoplasmic Negative
• Antibodies (ANCA) Negative
• Complement (C3, C4) Normal
• Cryoglobulins Negative
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177. CF
• Palpable purpura
• Symmetric mainly on lower extremities & buttocks
• Oligoarticular arthritis & arthralgia
• GI manifestation
• Abdominal pain malena diaarhea
• Renal involvement
• Microscopic hematuria (nephritis)
• Proteinuria
• HTn
• Neurologic
• Seizures
• Cerebral haemorrhage
•
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178. TONY SCARIA 2010
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179. American college of rheumatology Pediatric rheumatology European society criteria
2 of the following
 Palpable purpura
 Age at onset <20 yr
 Bowel angina (post prandial abdominal pain/
bloody diarrhea)
 Biopsy  demonstrating intramuscular
granulocytes in arterioles or venules
Palpable purpura (in absence of coagulopathy or
thrombocytopenia
 Abdominal pain
 Arthritis or arthralgia
 Biopsy  IgA deposition
 Renal involvement
• Proteinuria
• Hematuria
• Red cell cast
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180. TONY SCARIA 2010
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181. TONY SCARIA 2010
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182. Diagnosis
• Leukocytosis thrombocytosis anemia normal platelet count
• Elevated ESR & CRP
• Serum IgA elevated
• Serum albumin levels may be low
• Occult blood
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183. Rx of HSP
• Supportive Rx
• Prednisolone 1mg/kg/day for 1-2 weeks
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184. c/c glomerulonephritis
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185. c/c glomerulonephritis
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186. c/c glomerulonephritis
• poststreptococcal (1% to 2%);  least common chance of progression
• rapidly progressive (crescentic) (90%) most common chance of
progression
• membranous (30% to 50%),
• focal segmental glomerulosclerosis (50% to 80%),
• membranoproliferative GN (50%),
• IgA nephropathy (IgAN, 30% to 50%).
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187. c/c glomerulonephritis
the cortex is thinned
increase in peripelvic fat
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188. c/c glomerulonephritis
• arterial and arteriolar sclerosis
• Marked atrophy of associated
tubules, irregular interstitial
fibrosis, and mononuclear
leukocytic infiltration of the
interstitium
• obliteration of glomeruli,
transforming them into acellular
eosinophilic masses,
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189. Systemic diseases a/w renal
ds
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190. Diabetic nephropathy
• Most important predictor of diabetic nephropathy is duration of
disease
• 20 yrs prediction of nephropathy
• Type 1  30 -40 %
• Type 2 15-20 %
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191. Mechanism of diabetic nephropathy
• Nonenzymatic glycosylation of proteins of basement membrane
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192. • Earliest lab finding in diabetic nephropathy  increase in GFR
• early stages of diabetic nephropathy are characterized by an
increased GFR, increased glomerular capillary pressure, glomerular
hypertrophy, and an increased glomerular filtration area
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193. Lesions seen in diabetic nephropathy
glomerular lesions renal vascular lesions, principally
arteriolosclerosis
pyelonephritis, including
necrotizing papillitis
• capillary basement membrane
thickening (earliest lesion)
• diffuse mesangial
sclerosis(most common
histologic finding)
• nodular glomerulosclerosis
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194. Glomerular lesions
Capillary basement membrane
thickening
Diffuse glomerulosclerosis Nodular glomerulosclerosis
• Earliest lesion • diffuse increase in mesangial
matrix along with mesangial cell
proliferation and
• Glomerular lesion made
distinctive by ball-like deposits
of a laminated matrix situated in
the periphery of the glomerulus
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195. TONY SCARIA 2010
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196. Nodular glomerulosclerosis
• Most specific &
pathognomonic
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197. Fibrin cap & capsular drop in diabetic
retinopathy
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198. Hyaline arteriolar sclerosis
• Affecting afferent & efferent arteriole
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199. Armanni ebstein cells
• In poorly controlled diabetics
• Proximal tubular cells filled glycogen laden
vacuole
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200. Causes of papillary necrosis
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201. TONY SCARIA 2010
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202. Papillary necrosis
• DM  commonest cause
• Analgesic nephropathy
• Sickle cell anemia
• c/c alcoholism
• Urinary tract obstruction
• a/c pyelonephritis
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203. TONY SCARIA 2010
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204. TONY SCARIA 2010
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205. TONY SCARIA 2010
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206. • Ball-on-tee appearance: Contrast material filling central excavations in the
papilla of the interpolar region gives ball-on-tee appearance.
• Lobster claw sign: Excavation extending from the caliceal fornices produces
the lobster claw deformity.
• Signet ring sign: The necrotic papillary tip may remain within the excavated
calyx, producing the signet ring sign when the calyx is filled with contrast
material.
• Club shaped saccular calyx: Due to sloughed papillaTONY SCARIA 2010
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207. TONY SCARIA 2010
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208. Hepatitis C • Cryoglobulinemic glomerulonephritis
• Membranous glomerulonephritis (MGN)
• Membrano prolferative glomerulo
nephritis(MPGN)
Hepatitis B • In children  MGN
• In adults  MPGN
• Over all  MGN
Toxoplasmosis • MPGN
Syphilis
Schistosomiasis
• MGN
Leprosy • Secondary amyloidosis
• Mesangiocapilalry GN
• MPGN1
• Membranous GN
Malaria • Plasmodium malaria  NS
• Plasmodium falciparum  renal failure
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209. Essential mixed cryoglobulinemia
• Cold precipitable monoclonal or polyclonal immunoglobulins
• It causes cutaneous vasculitis synovitis palpable purpura
• It causes proliferative GN most commonly MPGN type 1
• a/w hepatitis C
• Hypocomplimentinemia
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210. Fibronectin nephropathy
• Autosomal dominant
• d/t accumaltion of plasma fibronectin
• Presents with Massive proteinuria
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211. Mesangial
fibronectin
•Cellular
fibrinopectin
•Nonpathogenic
Liver fibronectin
•Produced by
hepatocytes
•Pathogenic
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212. Morphology
• Light microscopy
• Glomerular enlargement & lobulation d/t mesangial proliferation & mesangial
deposits
• PAS & trichrome positive
• Renal tubules interstitium blood vessels are not affected
• Immunofurescence
• No immunoglobulin & compliment deposits are seen
• Electron microscopy
• Mesangial & subendothelial deposits
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