NEPHROTIC and NEPHRITIC SYNDROMES

Disease Most Frequent Pathogenesis Light Microscope F.M. Age Group Affected Treatment and
Clinical Presentation (Fluorescence
Microscope) Outcome

E.M. (Electron
Microscope)

Minimal Change Disease • Selective • Loss of foot Normal F.M. = negative #1 cause of Nephrotic Responds well to
proteinuria (Albumin) processes Syndrome in children, corticosteroids.
(Lipoid Nephrosis) • Loss of GBM Lipid in tubules esp. boys younger than
polyanionic sites E.M. = loss of foot 6 yrs. old.
• Appearance of villi processes, lipid No progression
on epithelial cells vacuoles into chronic renal
failure

• Focal and F.M. = IgM, C3

segmental sclerosis
• Non-selective • Idiopathic Does not respond
• Hyalinosis
proteinuria • Lower renal mass Majority occur in older to
Focal Segmental • Adhesions to E.M. = Loss of
• Hypertension (in obese) children. Also occurs corticosteroids.
Glomerular Sclerosis Bowman's Capsule foot processes,
• Microscopic • 2 causes: heroin use, in adults. Leads to renal
• Hypercellular detachment of
hematuria HIV failure.
mesangium epithelium from
• Thick B.M. B.M.

F.M. = "Spike and

Dome." Granular
• Glomeruli are
• Idiopathic IgG, C3
Membranous enlarged yet
• 2 causes:
Nephropathy normocellular Benefit of
• Persistent carcinomas, SLE, #1 cause of Nephrotic
• No cellular corticosteroids is
proteinuria hepatitis, Diabetes E.M. = syndrome in adults
proliferation unknown.
(Glomerulonephritis) Mellitus, thyroiditis, Subepithelial
• B.M.
drugs. immune deposits
Thickening
in B.M., thickened
B.M.

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 • Diabetic
microangiopathy
• Thickened B.M. F.M. = negative
Diabetic Nephropathy • Kimmelstiel-Wilson
• Massive mesangial
• Proteinuria Nodules are
growth Progresses to renal
pathognomonic. Diabetics
(Diabetic • No hematuria • "Kimmelstiel E.M. = massive failure
• Massive mesangial
Glomerulosclerosis) Wilson" nodular mesangial growth,
hypercellularity.
glomerulosclerosis thickened B.M.
• Diffuse
glomerulosclerosis

• Amyloid deposits
are initially mesangial, F.M. = negative
producing mesangial
Subendothelial and widening without Severe amyloid
Reoidosisnal Amyl mesangial amyloid hypercellularity. E.M. = Any age group infiltration leads to
deposits • Later, the amyloid characteristic criss- renal failure
obliterates the lumen cross fibrillary
• PAS(-) proteins.
• Congo-Red (+)

Alport Syndrome • Recurrent Structural defect in Looks normal F.M. = negative Symptoms appear Progresses to
hematuria before age Collagen IV leads to before age 20 renal failure
(Hereditary Nephritis) 20 leaky basement
• Hypertension membranes. E.M. = glomerular
• Deafness and B.M. splitting
ocular problems

• Recurrent F.M. = negative

Benign Familial hematuria
Hematuria • Most frequent Reduced thickness of
Looks normal
cause of glomerular B.M. E.M. = reduced
(Thin B.M. Disease) asymptomatic glomerular B.M.
hematuria. thickness

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 F.M. = "lumpy-
• Glomerular bumpy" granular Return to normal
• Immune-complex
hypercellularity deposits of IgG in 8 weeks.
mediated (Type-III and C3
• Increase in
hypersensitivity)
• Acute nephritis endothelial cells,
Acute (Post- • Occurs after
• Abrupt oliguria, mesangial cells, Common renal disease Complete
Streptococcal) Streptococcal
hematuria, facial and PMN's. E.M. = in childhood recovery without
Glomerulonephritis pharyngitis or
edema, hypertension. • No increase in Subepithelial (not treatment
Hepatitis-B
epithelial cells. subendothelial) (especially in
• High ASO-titer, low
• No B.M. "humps," kids) within 3
C3
thickening otherwise normal years.
appearing B.M.

• WHO I: Normal
• WHO II:
Increased
mesangial matrix F.M. = IgM, IgG +
• WHO III: Focal C3
Degree of kidney proliferation • Type-I:
involvement Anti ds-DNA • WHO IV: Granular
SLE Nephropathy
correlates with antibodies. Diffuse appearance
prognosis in SLE. proliferation, • Type-II:
worst. Pseudo-linear
• WHO V: appearance
Identical to
Membranous
Nephropathy

F.M. = Granular
IgA Nephropathy appearance, IgG +
(Berger's Disease): Circulating IgA + C3
• Mesangial cell
Focal Segmental Most common fibronectin (due to Young men 15-30
proliferation
Glomerulonephritis primary chronic liver disease)
glomerulonephritis E.M. = Mesangial
deposits

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 F.M. = Granular
Same as above, plus appearance, IgG +
systemic disease: C3
• Mesangial cell
Henoch-Schonlein purpura of
proliferation, more Children
Purpura extremities, arthritis,
serious than above.
colicky abdominal
pain. E.M. = Mesangial
deposits

Kidney disease
• Subepithelial F.M. = Granular
Endocarditis S. Aureus resolves when
immune deposits appearance, IgG + C3
infection is cured.

• Cells accumulate in
F.M. = Pauci-
Bowman's Capsule immune. Irregular
• Wegener's: kidney + • Fibrin trapped in
Rapidly Progressive • Inflamed Must be treated or it
upper respiratory tract. glomeruli
Crescentic glomerular capillaries will go to renal failure
• Anuria • Epithelial cell
Glomerulonephritis • ANCA (+) E.M. = wrinkling, within weeks.
• Oliguria proliferation
• Macrophage, PMN discontinuity of
B.M.
infiltrates

F.M. = Linear
pattern, IgG + C3
Goodpasture Syndrome Responds to
Anti-B.M. antibodies, Similar to Crescentic
Lung (hemoptysis) + immunosuppressive
against Type-IV glomerulonephritis, as Males 25-30
(Anti-BM Antibody kidneys (hematuria) therapy and
collagen above. E.M. = No
Disease) plasmapheresis
immune complex
deposits

• B.M. thickening and

Membranoproliferative E.M. = "Tram-
cellular proliferation
Glomerulonephritis track" appearance,
• Mesangial
resulting from
expansion makes double-layer
(Mesangiocapillary glomerular B.M. appearance of
Glomerulonephritis) appear as though it glomerular B.M.
were in two layers

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