History
The first step in the evaluation of hematuria is a detailed review of the history and a thorough physical examination.
The presence or absence of hypertension or proteinuria helps to decide how extensively to pursue the diagnostic evaluation. The initial evaluation should be directed toward important and potentially life-threatening causes of hematuria in any child who has any of the following in addition to hematuria: hypertension, edema oliguria, significant proteinuria (more than 500 mg per 24 hours), or RBC casts. An attempt should be made to distinguish glomerular causes of hematuria from extraglomerular ones, as this helps in prioritizing the investigations.
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A history of passage of clots in urine suggests an extraglomerular cause of hematuria.
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A history of fever, abdominal pain, dysuria, frequency, and recent enuresis in older children may point to a urinary tract infection as the cause of hematuria.
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A history of recent trauma to the abdomen may be indicative of hydronephrosis.
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A history of early-morning periorbital puffiness, weight gain, oliguria, the presence of dark-colored urine, and the presence of edema or hypertension suggests a glomerular cause.
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Hematuria due to glomerular causes is painless.
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A history of a recent throat or skin infection may suggest postinfectious glomerulonephritis.
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A history of joint pains, skin rashes, and prolonged fever in adolescents suggests a collagen vascular disorder.
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The presence of anemia cannot be accounted for by hematuria alone, and, in a patient with hematuria and pallor, other conditions such as systemic lupus erythematosus and bleeding diathesis should be considered. [5]
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Skin rashes and arthritis can occur in Henoch-Schönlein purpura and systemic lupus erythematosus.
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Information regarding exercise, menstruation, recent bladder catheterization, intake of certain drugs or toxic substances, or passage of a calculus may also assist in the differential diagnoses.
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Because certain diseases that present with hematuria are inherited or familial, asking for a family history that is suggestive of Alport syndrome, collagen vascular diseases, urolithiasis, or polycystic kidney disease is important.
Physical Examination
In the general physical examination, the most important step is to measure the blood pressure (with an appropriate-sized cuff) and evaluate for the presence of periorbital puffiness or peripheral edema. [6, 7]
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A detailed skin examination is necessary to look for purpura.
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An abdominal examination is indicated to look for palpable kidneys (Wilms tumor or hydronephrotic kidneys).
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A careful examination of the genitalia is also important.
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A detailed ophthalmological evaluation is helpful in familial hematurias.
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Approach to hematuria.
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Nonglomerular hematuria.
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Microscopy of urinary sediment. Typical appearance in non-glomerular hematuria: RBCs are uniform in size and shape but show two populations of cells because a small number have lost their hemoglobin pigment.
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Microscopy of urinary sediment. Typical appearance of RBCs in glomerular hematuria: RBCs are small and vary in size, shape, and hemoglobin content.
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Microscopy of urinary sediment. A cast containing numerous erythrocytes, indicating glomerulonephritis.
Tables
Condition |
Histology |
History |
Laboratory Data |
Systemic lupus erythematosus |
Mild glomerulitis, proliferative changes, immune complex deposition, crescents, immunoglobulin deposition |
Hematuria, proteinuria, hypertension, joint pains, rashes |
Abnormal C3, C4, ANA, and dsDNA levels; anemia; thrombocytopenia |
IgA nephropathy |
IgA deposition in the mesangium, glomerular sclerosis, proliferative changes, crescents in severe cases |
Gross, intermittent, painless hematuria |
No specific changes, although increased serum IgA levels observed in some patients |
Henoch-Schönlein purpura |
Same as IgA nephropathy |
Purpura, joint pains, abdominal pain, hematuria |
No specific laboratory data |
Alport syndrome |
Some thinning of basement membranes, "basket weave" changes in the glomerular basement membrane on electron microscopy |
Sensorineural hearing loss, corneal abnormalities, hematuria, renal failure |
No specific changes |
Thin basement membrane disease |
Average glomerular basement membranes reported to be 100-200 nm in children in this condition |
Persistent microscopic or gross hematuria, significant family history |
No specific changes |
Mesangiocapillary glomerulonephritis |
Glomerular lobulations, thickening of the mesangial matrix and glomerular basement membranes, crescents |
Hematuria, proteinuria, hypertension |
C3 levels possibly abnormal |
