A 10-year-old boy presented to the office with a 2-day history of “tea-colored” urine. Two weeks prior to this presentation, he had an upper respiratory infection that resolved without treatment. Two years ago, he had a similar episode of gross hematuria that developed after a viral infection, and at that time the diagnosis of IgA nephropathy was entertained. His urine now reveals hematuria (Figure 64-1) but no proteinuria.

Examination of the urinary sediment is a test frequently done for evaluation of patients with suspected genetic/intrinsic (e.g., systemic lupus nephritis, sickle cell disease, glomerulonephritis, interstitial nephritis), anatomic (e.g., arteriovenous malformation), obstructive (e.g., posterior urethral valves, kidney stones), infectious, metabolic (e.g., coagulopathy), traumatic, or neoplastic disease of the urinary tract. Potential findings of red or white blood cells, casts, bacteria, or neoplastic cells help in directing further evaluation of a patient’s problem.

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  Although there is no consensus on the definition of microscopic hematuria in children, 5 to 10 RBCs/HPF are considered significant.¹

  
  
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  Based on an older study (N = 8,954 unselected children ages 8 to 15 years), the incidence of microscopic hematuria found in one or more of four urine specimens was 4.1 percent; the incidence was 1.1 percent for hematuria present in two or more specimens.²

  
  
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  Macroscopic (visible) or gross hematuria among children has an estimated incidence of 1.3/1000.³

  
  
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  Isolated pyuria (>2 to 10 white blood cells per high-power field [WBCs/HPF]) is not uncommon in sick neonates and febrile children.

  
  
  
  
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    In a study of 110 consecutive infants admitted to a neonatal intensive care unit in Karachi, 35 had pyuria, of who 71.4 percent had no growth in urine cultures.⁴

    
    
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    In a case series of children with Kawasaki disease (KD; N = 210), 29.5 percent (N = 62) had pyuria including 34 with sterile pyuria and eight with bacterial pyuria.⁵

    
    
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    In another case series of children with acute KD compared to children with other febrile illnesses, 79.8 percent of KD and 54.0 percent of febrile children without KD had pyuria.⁶ The median number of white blood cells in the urine was higher for children with KD (42 WBC/microL vs. 12 WBC/microL in febrile children).

  
  
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  Urinary tract infections (UTIs) are common in children (8% of girls and 2% of boys by age 7 years) and WBCs on microscopy have 73 percent sensitivity and 81 percent specificity for the diagnosis.⁷

  
  
  
  
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    About 60 percent of children who have a febrile UTI are found to have defects on renal cortical scintigraphy (RCS) indicating acute pyelonephritis; of these, 10 to 40 percent will have permanent renal scarring.⁸

  
  
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  In a laboratory study of greater than 11,000 urinalyses from 88 institutions, 62.5 percent of the tests received a manual microscopic evaluation of the urinary sediment, usually triggered by an abnormal urinalysis.9 New information was obtained 65 percent of the time as a result of the manual examination.

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  Hematuria (Figure 64-1) has many causes including:¹

  
  
  
  
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    Idiopathic.

    
    
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    Glomerular disease (e.g., immunoglobulin [Ig]A nephropathy, post-streptococcal glomerulonephritis, membranoproliferative glomerulonephritis [MPGN]).

    
    
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    Interstitial and tubular disease (e.g., acute pyelonephritis, tuberculosis, hematologic disorders such as sickle cell, or thrombocytopenia).

    
    
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    Structural or congenital abnormalities (e.g., polycystic kidney disease).

    
    
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    Urinary tract (collecting system, ureters, bladder, or urethra) disease (e.g., bladder infection [Escherichia coli in about 85%],⁷ stone, trauma [including recent catheterization], tumors, or exercise).

    
    
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    Metabolic abnormalities including hypercalcemia and hyperuricemia.

    
    
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    Medications (e.g., aminoglycosides, anticonvulsants, or aspirin).

    
    
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    Toxins (e.g., lead, turpentine).

    
    
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    Contamination (menstruation or bloody diarrhea).

    
    
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    The most common causes of hematuria in children are idiopathic, benign familial, idiopathic hypercalciuria, IgA nephropathy, and sickle cell trait or anemia.¹ In the Vehaskari et al. study, of 28 children with hematuria (6 or more RBC/0.9 mm³ or more than 100,000 RBC/hour) on two occasions who underwent renal biopsy, 12 children had normal biopsies, two children were diagnosed with IgA-IgG nephropathy, one with focal segmental sclerosis, one with extracapillary glomerulonephritis, and one with possible hereditary nephritis.²

    
    
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    The source of bleeding in children is most commonly glomerular (vs. urinary tract); RBCs cross the glomerular endothelial-epithelial barrier entering the capillary lumen through discontinuities in the capillary wall.¹

    
    
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    A family history of hematuria, hypertension, renal disease (e.g., kidney stones, cystic disease), sickle cell, hemophilia, and dialysis or transplant can be helpful.¹ In one study of 500 children with beta-thalassemia major requiring transfusion, 10.6 percent had hematuria.¹⁰

  
  
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  Hematuria with dysmorphic RBCs or RBC casts (Figure 64-2) and excess protein excretion (>500 mg/dL) suggests glomerulonephritis.

  
  
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  Gross hematuria suggests a postrenal source in the collecting system, although recurrent episodes of gross hematuria occur in 10 to 20 percent of patients with MPGN.¹¹

  
  
  
  
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    Bright red urine and/or visible clots with normal appearing RBCs on microscopy suggest bleeding from the urinary tract.¹

    
    
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    Brownish-colored urine (described as tea or cola-colored) with RBC casts and dysmorphic RBCs suggest glomerular bleeding.¹

  
  
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  Pyuria (Figure 64-3) is often the result of urinary tract infection.

  
  
  
  
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    The presence of bacteria (>10² organisms per mL or >10⁵ using a midstream urine specimen in older children and adults) suggests infection. A urinalysis with 10 bacteria per HPF is highly suggestive (specificity 99%) of infection (positive likelihood ratio [LR+] 85).¹²

    
    
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    Asymptomatic bacteruria is found in 4 to 15 percent of pregnant women, usually Escherichia coli.

    
    
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    The presence of WBC casts (Figure 64-4) with bacteria indicates pyelonephritis.

  
  
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  As previously noted, isolated (sterile) pyuria can also been seen in children with KD or tuberculosis.^5,6,13

  
  
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  WBCs and/or WBC casts can be seen in tubulointerstitial processes like interstitial nephritis, systemic lupus erythematosus, or transplant rejection.

  
  
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  Urinary casts are formed only in the distal convoluted tubule (DCT) or in the collecting duct (distal nephron).

  
  
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  Hyaline casts are formed from mucoprotein secreted by the tubular epithelial cells within the nephrons. These translucent casts are the most common type of cast and can be seen in normal persons after vigorous exercise or with dehydration. Low urine flow and concentrated urine from dehydration can contribute to the formation of hyaline casts (Figure 64-5).

  
  
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  Granular casts are the second most common type of cast seen (Figure 64-6). These casts can result from the breakdown of cellular casts or the inclusion of aggregates of albumin or immunoglobulin light chains. They can be classified as fine or coarse based on the size of the inclusions. There is no diagnostic significance to the classification of fine or coarse.