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Hematuria and
Glomerulonephritis
Debbie Gipson
UNC Kidney Cener
debbie_gipson@med.unc.edu
website: www.uncpeds.org
password: pediatriclib
Program Announcements
UNC Nephrology Fellowship
1 position each year
accepting applications for 2007 and 2008
Case 1
A 17 year old previously healthy African
American female presents for a well child
visit.
Dipstick evaluation reveals moderate blood
and 3+ proteinuria. Microscopic
examination of the urinary sediment
reveals 10 RBC/hpf and no casts.
Physical examination is unremarkable
6. Renal ultrasound
Hematuria + Proteinuria
Combination is an indicator of
disease
Gross hematuria may have
associated low grade proteinuria
( Up/c < 0.5)
CASE 2
A six year old girl develops a puffy face and
notices that her urine has turned brown.
No family history of renal disease. A sister
complained of a sore throat one week before
the onset of dark urine.
Physical exam shows generalized edema and a
blood pressure of 135/ 83 mmHg.
Urinalysis contains: large hemoglobin, 2+
protein
Hypercalciuria
Acute Post Strept GN
IgA nephropathy
Membranoproliferative GN
Systemic Lupus Erythematosis
Hypercalciuria
Acute Post Strept GN
IgA nephropathy
Membranoproliferative GN
Systemic Lupus Erythematosis
1.
2.
3.
4.
5.
1.
2.
3.
4.
5.
Post-infectious GN
Classic Group A Streptococci
Anticedent illness
Pharyngitis (7-21 d) or impetigo (14-21 d)
Nephritogenic strain of streptococcus
Rheumatic fever and nephritis rarely concurrent
Peak age 2 to 6 years
Males > females
Epidemics
Attack rates 10-15%
38% Household contacts
Post infectious GN
Hematuria
70% microscopic
30% macroscopic
Proteinuria
common
Hypertension 75%
Edema
Congestive Heart Failure (elderly)
Encephalopathy (children)
Post-infectious GN
Laboratory
Low C3 (x 6-8 weeks)
ASO or streptozyme titers acute rise if Strep.
May increase serum Cr; uncommon renal failure
Hematuria (1 year), Proteinuria, RBC casts
Pathology
Proliferative GN
Acute Postinfectious GN
Subepithelial Humps
1.
2.
3.
4.
1.
2.
3.
4.
CASE 5
A 12 year old girl has a sore throat and that
same day notices that her urine turns brown.
She feels well and without specific symptoms.
She has not had previous urinalyses. There is
no family history of renal disease.
Her examination is normal.
The urinalysis contains large hemoglobin and
1+ protein.
IgA Nephropathy
Mesangial IgA
Mesangial hypercellularity
1. Family history
2. Proteinuria
3. Elevated serum IgA values
4. Low serum complement values
5. Abdominal pain
1. Family history
2. Proteinuria
3. Elevated serum IgA values
4. Low serum complement values
5. Abdominal pain
IgA Nephropathy
(Bergers Disease)
Most common cause of GN world wide
Forms:
Idiopathic
Familial 10%
Secondary (liver disease, chronic lung or GI d/o)
Age 15 - 30 yo
Asian > Caucasian > African Americans
IgA Nephropathy
Clinical Findings
Presentation
40% asymptomatic hematuria
40% gross hematuria (more frequent in children)
10% nephrotic syndrome
10% renal failure (including rare patients with
RPGN)
5% Malignant HTN
IgA Nephropathy
Prognosis
Indicators
- proteinuria > 1 gm
- nephrotic syndrome
- sustained HTN
- male
+ gross hematuria
2%/year progress to ESRD
Overall 20-40% progress to ESRD
IgA Therapy
ACEi (proven)
Corticosteroids
Mycophenolate (trials)
Fish Oil
Lipid control
Next Case
6 year old male
Crampy abdominal pain without
rebound
Rash on buttocks and lower
extremities
Urine with 2+ blood and 2+ protein
Serum Complements are normal
HSP Prognosis
Chronic renal failure 2 to 5%
Indicators
acute nephritis
persistent nephrotic syndrome
older age
glomerular crescents
Therapy
Rapidly progressive GN
The cocktail: steroids/cytoxan/pharesis