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 LIST

Macroscopic 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

Dark yellow or orange urine

Concentrated urine

Rifampin, Pyridium, Macrodantin

Brown or black urine

Bile pigment

Methemoglobinemia

Homogentisic acid, thymol, melanin, tyrosinosis, alkaptonuria

Alanine, cascara, resorcinol

Red or pink urine

Red blood cells, hemoglobin/myoglobin

Benzene, chloroquine, deferoxamine, phenazopyridine, phenolphthalein

Beets, blackberries, red dye

Urates

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

Others

Dyes (Table 39-1)

Loin pain-hematuria syndrome

Urethrorrhagia

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

Feature	Glomerular	Nonglomerular
History
Burning on micturition	No	Urethritis, cystitis
Systemic complaints	Edema, fever, pharyngitis, rash, arthralgias	Fever with UTI; pain with calculi
Family history	Deafness in Alport syndrome, renal failure	Usually negative, except with calculi
Physical Examination
Hypertension	Often	Unlikely
Edema	Sometimes present	No
Abdominal mass	No	Wilms tumor, polycystic kidneys
Rash, arthritis	SLE, HSP	No
Urine Analysis
Color	Brown: tea- or cola-colored	Bright red or pink
Proteinuria	Often	No
Dysmorphic RBCs	Yes	No
RBC casts	Yes	No
Crystals	No	May be informative
HSP, Henoch-Schönlein purpura; RBC, red blood cells; SLE, systemic lupus erythematosus; UTI, urinary tract infection.

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.

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