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Macroscopic - Microscopic
Symptomatic - Symptomless
Transient - Persistent
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Kidney disease
Malignant hypertension
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Use of anticoagulant
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Liver disease
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X-linked dominant
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Autosomal recessive
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Autosomal dominant
Macro /Microhematuria
Proteinuria
Nephrotic syndrome
Hypertension
Renal failure- males
Progressive or juvenile – 20 y
Nonprogressive – 40 y
Urology & Nephrology Center, Mansoura University, Egypt
Hearing defe cts
Sensorineural bilateral
Never congenital
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Hematuria
Proteinuria
Attenuation of the GBM
In children may be Alport
In adults m/p benign disorder
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Following exercise
Febrile disorders
Myoglobinuria.
Ascorbic acid.
Glomerular
- Benign Familial Hematuria
- Alport syndrome
Non-glomerular
- Idiopathic Hypercalciuria
- Polycystic Kidney Disease
- Urolithiasis
- Tumors
In case of haemoglobinuria,
manifestations of haemolysis may be
evident
Urology & Nephrology Center, Mansoura University, Egypt
Eval uation of Hematuri a
History
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Blood picture:
Sickle cell anemia
Lymphoma
leukemia
Transient cause?
• Sexual intercourse • Menstruation Yes RBCs present
Yes • Infection • Vigorous exercise
• GU instrumentation
Repeat UA when NO
condition resolved Persistent hematuria
• Hemoglobinuria
Glomerular etiology? • Myoglobinuria
• Proteinuria > 500 mg/24 hr
Nephrology • UA shows RBC casts +/- dysmorphic RBCs
referral Yes • Renal insufficiency
• Cysto+/-
• Cytology
Evaluation of haematuria
Work-u p o f a chil d wi th
Hematuri a
Phase I:
Urinalysis ( sediment examination )
RBC’s morphology
Urine culture
BUN, Creatinine, Proteins, Electrolytes
Antibodies against strept. & other antigens
Complement, ANF, Immunoglobulins
Renal US
Urinalysis of 1st degree relatives
24h urine collection: Ca, Creat.,Protein, UA
Phase II:
Hearing test
Cystoscopy
Renal biopsy
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Disappearance of hematuria