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Nephritic or Nephrotic
Nephritic Urine
RBC casts
Diagnosis
History
Physical Examination
Laboratory Studies
Urinalysis casts, red cells, protein
Serum creatinine
C3 Complement
ASO / AntiDNAse B
ANA Titer
Clues to Diagnosis
Events in Glomerulonephritis
Clinical manifestations
PATHOPHYSIOLOGY
Glomerular injury
Inflammation of glomerular
capillary bed
Decreased glomerular
capillary perfusion
Decreased GFR
Increased Na and
H2O reabsorption
Azotemia,
Inc Uosm, Decr UNa
Decr urinary volume
(Htn, edema, Anemia)
Heart Failure
Encephalopathy
APSGN
Prototypic GN
Streptococcus A specific serotypes
Nephritic presentation, 1-2 weeks after
phayrngitis or 3-6 weeks after a skin infection
Tea-colored urine
Mild to severe hypertension
Less than 5% have nephrotic syndrome
Severe complications include pulmonary edema,
hypertensive encephalopathy, acute renal failure
Treatment is supportive (diuretics, salt
restriction, etc)
Normal Glomerulus
APSGN
DIAGNOSIS PSGN
Pathogenesis of PSGN
Treatment of PSGN
Restrict K if hyperkalemic
Penicillin if + strep culture
Dialysis if usual indication present Rarely
needed
Post-infectious Glomerulonephritis
IgA Nephritis
IgA
IgA
Treatment of IgA GN
Henoch-Schnlein Purpura
Idiopathic small vessel vasculitis affecting mainly:
skin
bowel
joints
kidney
Arthritis
Abd Pain
7
Days
11 13
Nephritis in HSP
Occurs in 20-40% of patients
Rarely presenting complaint
May appear later but rarely after 3 months
Hematuria alone in 20-30%
Hematuria + proteinuria in 50%
Acute nephritis in 10-20%
Acute nephritis + nephrotic syndrome 10-20%
MPGN
Mesangiocapillary
glomerulonephritis and
membranoproliferative glomerulonephritis
20-30% have acute GN at presentation
40% have evidence of a recent strep infection
30-50% may have nephrotic syndrome
50% have low C3 with normal or low C4
Unknown pathogenesis
Histology varies but results in basement membrane
changes that are characteristic
Treatment in children is often alternate day steroids
ESRD may occur in 10-50% of patients
MPGN
MPGN
MPGN
Vasculitis Classification
Large-vessel vasculitis
- Giant-cell arteritis
- Takayasus arteritis
Medium-sized-vessel vasculitis
- Polyarteritis nodosa
- Kawasakis disease
- Primary granulomatous central nervous system vasculitis
Small-vessel vasculitis
- ANCA-associated small-vessel vasculitis
- Microscopic polyangiitis
- Wegeners granulomatosis
- Churg-Strauss syndrome
- Drug-induced ANCA-associated vasculitis
Vasculitis Classification
Small-vessel vasculitis
- Immune-complex small-vessel vasculitis
- Henoch-Schnlein purpura
- Cryoglobulinemic vasculitis
- Lupus vasculitis
- Rheumatoid vasculitis
- Sjgrens syndrome vasculitis
- Hypocomplementemic urticarial vasculitis
- Behets disease
- Goodpastures syndrome
- Serum-sickness vasculitis
- Drug-induced immune-complex vasculitis
- Infection-induced immune-complex vasculitis
- Inflammatory bowel disease vasculitis
Lupus
RPGN
Describes
is individualized by cause
Large IV doses of methylprednisolone + cytotoxic
drug usually
Crescentic GN - SLE
Schistocytes
Renal Pathology: EM
Endothelial cells are swollen
and occasionally detached,
resulting in a translucent
subendothelial space.
Fragmented red cells, an
ultrastructural appearance
characteristic of thrombotic
microangiopathy associated
with the hemolytic-uremic
syndrome.
Hemolytic-Uremic Syndrome:
Acquired
Shigella dysenteriae
E. coli O157:H7
Shiga Toxin
B (binding) subunits A subunit (33 kDa) and five B subunits (7.7 kDa
each)
bind to host cells, A (enzymatic) subunit causes inactivation of 60S
ribosomal subunit.
B subunits specifically bind to glycospingolipid globotriaosyl ceramide
receptor or Gb3.
Once shiga toxin is bound to Gb3, the toxin is internalized and A subunit
is enzymatically active: inhibition of an RNA N-glycosidase.
AGN Summary