Tutorial Case
Nephrology Division
King Khalid University
tutorial to course441
14 year old Saudi young female
student
C/0 fever- Headache for 10 days
General malaise
Dark urine x 3 days
HPI
Fever intermittent
Muscular joint pain
no skin rash
urine character
edema
PH & Med
antibiotic & NSAID
Social Hx
S. review
FH
Examination
Bp : 160/90 &Pulse 120/MIN
Temp 39 C Resp 25/MIN .pale
Look Sick
Puffiness in face
Head& neck
JVP high
Chest: Bronchial breathing
decrease Breath Rt side
Increase TVF
Increase Dull percussion
S1 increase
S2 N
S3 Positive
pan systolic murmur
radiation to axilla
grade 3
Abd
tend epigastic
tend lions
BS + ve
CNS
Drawsy
M.S
tender joint &muscle
Initial Diagnosis
Fever? Infection
RT lung consolidation
MR
HEAMATURIA:
Renal stone
(ARF –AKI- ATN)
Acute glomerulonephritis (post infection)
GN
RPGN
IgA
Hemolytic anemia
hemolytic uremic syndrome
NSAID
papillary necrosis
Investigation
WBC 15000 cells per
microliter
Hb 100 g/L
Plat 150
g/L
PT normal
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PPT normal
Bl film
Sec
Sec
U&E
Scr 210 μmml

urea 20 mmol/L
K6

mmol/L
Na 125 mmol/L
Ca 1.9 mmol/L

album 28 g/L
Urine Analysis
few RBC
No cast
Protein 1.2g/24h
U/S : kid size ENLARGE 12.2CM
Treatment

Patient receive ceftrixone IV and IV fluid
TREAT HYPERKALEMIA
Follow up:
S cr 300 μmml/L
JVP
Oliguria
Edema
Management:
IV lasix
Repeat urine analysis
RBC CAST
ANCA(P) positive
Kidney Biopsy
RPGN
Final diagnosis microscopic polyangitis
Glomerular Disease –
Acute Glomerulonephritis
Post infectious
glomerulonephritis
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Group A Strep Infection
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Infective endcarditis
Membranoproliferative
glomerulonephritis:
Systemic lupus
erythematosus
Hepatitis C virus
Rapidly progressive glomerulonephritis
Vasculitis (cryoglobulinemia
Type I RPGN (direct antibody)
 Good Posture syndrome
Type II RPGN (immune complex)

Post infectious

Systematic lupus erythematosus

Henoch – Schonlein pupura (IgA)

Others
Type III RPGN (pauci-immune)
o
o
Wegener granulomatosis
Microscopic polyarteritis
Investigations for Glomerulonephritis
Regular Follow-up and U&E
Antistreptolysin O (ASO)
ANA, Anti DNA
C3-C4
ANCA (p, c)
HCV Antibody HBsAg
HIV
RF
Cryoglobulin
Anti-basement Membrane Antibody (With lung hemorrhage)
Acute postinfection Glomerulonephritis
Often associated with group A
B-hemolytic streptococcal type 12 infection
Abrupt onset 10-12 days after strept throat or 14-21
skin infection (impetigo)
Also staphylococcus or viruses
Acute Glomerulonephritis
Symptoms occur 10-21 days after infection
Hematuria
Proteinuria
Decreased GFR, oliguria
Hypertension
Edema around eyes, feet and ankles
Ascites or pleural effusion
Low C3, normal C4, Antistreptolysin O (ASO)
– Kidney biopsy immune complexes and proliferation,
Proliferative GN- poststretococcal
This glomerulus is hypercellular and capillary loops are poorly defined.
This is a type of proliferative glomerulonephritis known as poststreptococcal glomerulonephritis.
Poststreptococcal GN
Post-streptococcal glomerulonephritis is immunologically mediated, and the
immune deposits are distributed in the capillary loops in a granular, bumpy
pattern because of the focal nature of the deposition process.
Post-Streptococcal Glomerulonephritis
CONSERATIVE TREATMENT (acute kidney
injury)
Improves 1-4 weeks, C3 normalizes in 1-3 months,
hypertension improves 1-3 months, intermittent
hematuria x 3 years
99% complete recovery in children and 85% in
adult
IgA Nephropathy (Berger's Disease)
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Most common acute glomerulonephritis in US ;South East Asia
Associated with H.S. Purpura
Upper respiratory(50%) IN 1—2 Day(Synpharyngitic hematuria)
Primary versus secondary (IBD, Liver Disease, SLE, vasculitis)
50% risk of CRF
Proteinuria, hypertension, renal insufficiency predict worse prognosis
50% increased IgA, normal compliments
TREATEMENT COSERVATIVE; ACEI
HIGH RISK: patient prednisone & alkylating agent
(cyclophosphamide-azothroprim) &ASA&ACEI&tosilectomy
Rapidly Progressive GN
Develops over a period of days or weeks
Primarily adults in 50’s and 60’s
Progresses to renal failure in a few weeks or months
Hematuria is common, may see proteinuria, edema or
hypertension
Rapidly Progressive (Crescentic)
Glomerulonephritis
Morphology
crescent formation
crescents are formed by proliferation of parietal cells
infiltrates of WBC’s & fibrin deposition in Bowman’s
space
EM reveals focal ruptures in the GBM
MICROSCOPIC POLYANGITIS
Necrotizing vasculitis of small- and medium- sized
vessels in both the arterial and venous circulations
Frequently involves the lung and the kidneys with
typical
complications
of
hemorrhage
and
glomerulonephritis
Associated with ANCA in three-fourths of all cases,
usually anti-myeloperoxidase antibodies (MPO-ANCA)
that cause a P-ANCA pattern on immuno-flourescence
testing. ANCA directedf againsts proteinae-3 (PR3ANCA) can also be observed in microscopic polyangiitis
Treatment
Initial Therapy
Combination cyclophosphamide-corticosteroid
therapy
A slow steroid taper, with the goal of reaching
20 mg of prednisone per day by the end of
two months and an overall glucocorticoid
course of between 6 and 9 months.
Either daily oral or monthly intravenous
cyclophosphamide.
Treatment
Plasmapheresis
Severe manifestations of pulmonary hemorrhage
on presentation.
Dialysis-dependent renal failure upon
presentation.
Concurrent anti-GBM antibodies.
Goodpasture Syndrome
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Antibody formation against pulmonary and glomerular
capillary basement membranes
Damage glomerular basement membrane
Men 20 - 30 years of age
Pulmonary hemorrhage and renal failure
TREATMENT:
Early treatment is essential
Pulse Steroid (10 mg/ kg/day for 3-5 days)
Cyclophosphamide
Plasmaphorisis
Goodpasture’s syndrome
This immunofluorescence micrograph shows positivity with antibody to IgG
has a smooth, diffuse, linear pattern that is characteristic for glomerular
basement membrane antibody with Goodpasture's syndrome.