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Hematuria

Hematuria is defined as the presence of at least 5 red


blood cells (RBCs) per microliter.
In the clinical setting, qualitative estimates are provided
by a urinary dipstick that uses a very sensitive
peroxidase chemical reaction between hemoglobin (or
myoglobin) and a colorimetric chemical indicator
impregnated on the dipstick.
Chemstrip (Boehringer Mannheim), a common
commercially available dipstick, is capable of detecting
3-5RBCs/?L of unspun urine; significant hematuria is
suggested by >50RBCs/?L.

False-negative results can occur in the presence of formalin


(used as a urine preservative) or high urinary
concentrations of ascorbic acid (i.e., in patients with vitamin
C intake >2000mg/ day).
False-positive results may be seen in a child with an alkaline
urine (pH > 9), or more commonly following contamination
with oxidizing agents such as hydrogen peroxide used to
clean the perineum before obtaining a specimen.
Microscopic analysis of 10-15mL of freshly centrifuged
urine is essential in confirming the presence of RBCs
suggested by a positive dipstick.

Heme-positive urine without RBCs is caused by


the presence of either hemoglobin or myoglobin.
Hemoglobinuria without hematuria can occur in
the presence of hemolysis.
Myoglobinuria without hematuria occurs in the
presence of rhabdomyolysis resulting from
skeletal muscle injury and is generally associated
with a 5-fold increase in the plasma
concentration of creatine kinase.

Rhabdomyolysis can occur secondary to viral


myositis, crush injury, severe electrolyte
abnormalities (hypernatremia, hypophosphatemia),
hypotension, disseminated intravascular
coagulation, toxins (drugs, venom), metabolic
disorders of muscles, and prolonged seizures.
Heme-negative urine can appear red, cola colored,
or burgundy, owing to ingestion of various drugs,
foods (blackberries, beets), or food dyes, whereas
dark brown (or black) urine can result from various
urinary metabolites.

Upper urinary tract sources of hematuria originate


within the nephron (glomerulus, convoluted or collecting
tubules, and interstitium).
Lower urinary tract sources of hematuria originate from
the pelvocalyceal system, ureter, bladder, or urethra.
Hematuria from within the glomerulus is often
associated with brown, cola or tea-colored, or burgundy
urine, proteinuria >100mg/dL via dipstick, urinary
microscopic findings of RBC casts, and deformed urinary
RBCs (particularly acanthocytes).

Hematuria originating within the convoluted or


collecting tubules may be associated with the
presence of leukocytes or renal tubular epithelial
cell casts.
Lower urinary tract sources of hematuria may be
associated with gross hematuria that is bright red or
pink, terminal hematuria (gross hematuria occurring
at the end of the urine stream), blood clots, normal
urinary RBC morphology, and minimal proteinuria on
dipstick (<100mg/dL).

Tea- or cola-colored urine, facial or body edema,


hypertension, and oliguria are classic symptoms of
acute nephritic syndrome.
Diseases commonly manifesting as acute nephritic
syndrome include postinfectious glomerulonephritis,
immunoglobulin A (IgA) nephropathy,
membranoproliferative glomerulonephritis, HenochSchonlein purpura (HSP) nephritis, systemic lupus
erythematosus (SLE) nephritis, Wegener
granulomatosis, microscopic polyarteritis nodosa,
Goodpasture syndrome, and hemolytic-uremic
syndrome.

Hereditary glomerular diseases include


hereditary nephritis (Alport syndrome), thin
glomerular basement membrane disease, SLE
nephritis, and IgA nephropathy (Berger
disease).
Other hematuric renal disorders with a
hereditary component include polycystic kidney
disease (PKD) (both autosomal recessive
[ARPKD] and autosomal dominant [ADPKD]),
urolithiasis, and sickle cell disease/trait.

Abdominal masses may be caused by bladder


distention in posterior urethral valves,
hydronephrosis in ureteropelvic junction
obstruction, PKD, or Wilms tumor.
Hematuria seen in patients with neurologic or
cutaneous abnormalities may be the result of
renal cystic disease or tumors associated with
several syndromes, including tuberous
sclerosis, von Hippel-Lindau syndrome, and
Zellweger (cerebrohepatorenal) syndrome.

The most common cause of gross hematuria is bacterial


urinary tract infection.
Urethrorrhagia, which is urethral bleeding in the absence of
urine, is associated with dysuria and blood spots on
underwear after voiding.
Recurrent episodes of gross hematuria suggest IgA
nephropathy, Alport syndrome, or thin glomerular
basement membrane disease.
Dysuria and abdominal or flank pain are symptoms of
idiopathic hypercalciuria, or urolithiasis.

Anemia in this setting may be caused by intravascular dilution


secondary to hypervolemia associated with acute renal failure;
decreased RBC production in chronic renal failure; hemolysis from
hemolytic-uremic syndrome or SLE; or blood loss from pulmonary
hemorrhage, as seen in Goodpasture syndrome, or melena in
patients with Henoch-Schonlein purpura or hemolytic-uremic
syndrome.
Inspection of the peripheral blood smear might reveal a
microangiopathic process consistent with the hemolytic-uremic
syndrome.
The presence of autoantibodies in SLE can result in a positive
Coombs test, the presence of antinuclear antibody, leukopenia,
and multisystem disease.

Thrombocytopenia can result from decreased


platelet production (malignancies) or increased
platelet consumption (SLE, idiopathic
thrombocytopenic purpura, hemolytic-uremic
syndrome, renal vein thrombosis).
Although urinary RBC morphology may be
normal with lower tract bleeding and
dysmorphic from glomerular bleeding, cell
morphology is not reliable to unequivocally
delineate the site of hematuria.

A voiding cystourethrogram is only required


in patients with a urinary tract infection,
renal scarring, hydroureter, or
pyelocaliectasis.
Renal biopsy is indicated for some children
with persistent microscopic hematuria and
most children with recurrent gross
hematuria associated with decreased renal
function, proteinuria, or hypertension.

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