Hematuria
Rebecca Ruebner
Madhura Pradhan
INTRODUCTION
Hematuria, the medical term for the presence of blood in the urine, is a common pediatric problem. Gross hematuria is the visible presence of blood in the urine, whereas microscopic hematuria is usually detected during a routine urinalysis. The incidence of gross hematuria among children presenting to an emergency department is 1.3 in 1,000, whereas 1% to 2% of school-aged children have microscopic hematuria in two or more urine samples. The American Academy of Pediatrics no longer recommends routine screening urinalysis for school-aged children and adolescents.
Hematuria can originate from the glomerulus or the lower urinary tract. Brown, tea-colored, or cola-colored urine is suggestive of glomerular bleeding, whereas bright red urine or presence of visible blood clots is suggestive of bleeding from the urinary tract. Hematuria is first detected by urine dipstick; however, the dipstick will also be positive in the setting of myoglobinuria or hemoglobinuria. Hematuria is confirmed by the presence of red blood cells (RBCs) on microscopic examination of a spun sediment of urine. Microscopic hematuria is defined by the presence of five or more RBCs per high-power field on at least three occasions over a 3-week period in a spun urine sample (see Table 39-1).
DIFFERENTIAL DIAGNOSIS LISTMacroscopic Hematuria
Glomerular Disease
Acute postinfectious glomerulonephritis (GN)
Immunoglobulin A (IgA) nephropathy—recurrent, gross hematuria
Alport syndrome
Thin basement membrane disease
Systemic lupus erythematosus
Membranoproliferative glomerulonephritis (MPGN)
Henoch-Schönlein purpura
Membranous nephropathy
Vasculitis
Infections
Bacterial urinary tract infection (UTI), viral (adenovirus), tuberculosis
Structural Abnormalities
Congenital anomalies
Polycystic kidneys
Trauma
Vascular anomalies—angiomyolipomas, arteriovenous malformations
Tumors
TABLE 39-1 Causes of Discolored Urine | ||||||
|---|---|---|---|---|---|---|
|
Hematologic
Sickle cell trait/disease
Coagulopathies—hemophilia
Renal vein thrombosis
Hypercalciuria and Nephrolithiasis Exercise Medications
Penicillins, polymyxin, sulfa-containing agents, anticonvulsants, warfarin, aspirin, colchicine, cyclophosphamide, indomethacin, gold salts
Asymptomatic Microscopic Hematuria
Idiopathic
Thin basement membrane disease
Hypercalciuria
IgA nephropathy
Sickle cell trait or disease
DIFFERENTIAL DIAGNOSIS DISCUSSION
Glomerular Disease
GN (Table 39-2) usually presents with some combination of gross hematuria (often tea- or cola-colored), proteinuria, hypertension, RBC casts, acute kidney injury, and oligoanuria. GN can be categorized according to serum complement (C3) levels at presentation. Causes of hypocomplementemic GN include acute postinfectious GN, membranoproliferative GN, and systemic lupus erythematosus nephritis. The remainder of etiologies is associated with normal complement levels. The most common forms of nephritis are acute poststreptococcal glomerulonephritis (APSGN) and IgA nephropathy.
APSGN typically presents 10 to 14 days after an upper respiratory infection with beta-hemolytic streptococci or, in some cases, an episode of impetigo. IgA nephropathy often presents with recurrent hematuria and is commonly associated with a viral prodrome 1 to 3 days before the development of grossly bloody urine.
TABLE 39-2 Distinguishing Features of Glomerular and Nonglomerular Hematuria | |||||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||||||||||||||||||
All patients with suspected GN should have microscopic urinalysis, blood chemistries including serum creatinine, complete blood count, antistreptolysin O (ASO) titer and/or streptozyme, C3, and antinuclear antibody (ANA) when clinically indicated. The presence of RBC casts in the urine is diagnostic of a GN. Renal biopsy may be indicated in some instances, particularly if there is rapidly progressive GN characterized by rapid decline in kidney function.
HINT: C3 levels should return to normal within 6 to 8 weeks after presentation of APSGN; a persistently low C3 level is suggestive of membranoproliferative glomerulonephritis.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
