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Hematuria
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Hematuria
The main causes of hematuria are urinary tract calculi,
renal tumors, urothelial tumors, and infection. CT
urography is the best single diagnostic examination for
diagnosing all of these pathologies, with the exception
of infection, which is effectively diagnosed in most cases
by microbiological analysis of the urine.
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Urinary calculi are solid particles in the urinary system. They may cause pain, nausea, vomiting,
hematuria, and, possibly, chills and fever due to secondary infection. Diagnosis is based on
urinalysis and radiologic imaging, usually noncontrast helical CT. Treatment is with analgesics,
antibiotics for infection, medical expulsive therapy, and, sometimes, shock wave lithotripsy or
endoscopic procedures.
About 1/1000 adults in the US is hospitalized annually because of urinary calculi, which are also
found in about 1% of all autopsies. Up to 12% of men and 5% of women will develop a urinary
calculus by age 70. Calculi vary from microscopic crystalline foci to calculi several centimeters
in diameter. A large calculus, called a staghorn calculus, can fill an entire renal calyceal system.
Etiology
About 85% of calculi in the US are composed of Ca, mainly Ca oxalate (see Table: Composition
of Urinary Calculi); 10% are uric acid; 2% are cystine; most of the remainder are Mg ammonium
phosphate (struvite).
Ca Oxalate Crystals
Cystine Crystals
Mg Ammonium Phosphate
(Struvite) Crystals
Sulfa Crystals
Percentage of All
Composition Common Causes
Calculi
Hypercalciuria
Hyperparathyroidism
Calcium oxalate 70
Hypocitruria
Hyperparathyroidism
Calcium phosphate 15
Hypocitruria
General risk factors include disorders that increase urinary salt concentration, either by increased
excretion of Ca or uric acid salts, or by decreased excretion of urinary citrate.
For Ca calculi, risk factors vary by population. The main risk factor in the US is hypercalciuria,
a hereditary condition present in 50% of men and 75% of women with Ca calculi; thus, patients
with a family history of calculi are at increased risk of recurrent calculi. These patients have
normal serum Ca, but urinary Ca is elevated > 250 mg/day (> 6.2 mmol/day) in men and > 200
mg/day (> 5.0 mmol/day) in women.
Hypocitruria (urinary citrate < 350 mg/day [1820 mol/day]), present in about 40 to 50% of Ca
calculi-formers, promotes Ca calculi formation because citrate normally binds urinary Ca and
inhibits the crystallization of Ca salts.
About 5 to 8% of calculi are caused by renal tubular acidosis. About 1 to 2% of patients with Ca
calculi have primary hyperparathyroidism. Rare causes of hypercalciuria are sarcoidosis, vitamin
D intoxication, hyperthyroidism, multiple myeloma, metastatic cancer, and hyperoxaluria.
Hyperoxaluria (urinary oxalate > 40 mg/day [> 440 mol/day]) can be primary or caused by
excess ingestion of oxalate-containing foods (eg, rhubarb, spinach, cocoa, nuts, pepper, tea) or by
excess oxalate absorption due to various enteric diseases (eg, bacterial overgrowth syndromes,
chronic pancreatic or biliary disease) or ileojejunal (eg, bariatric) surgery.
Other risk factors include taking high doses of vitamin C (ie, > 2000 mg/day) , a Ca-restricted
diet (possibly because dietary Ca binds dietary oxalate), and mild hyperuricosuria. Mild
hyperuricosuria, defined as urinary uric acid > 800 mg/day (> 5 mmol/day) in men or > 750
mg/day (> 4 mmol/day) in women, is almost always caused by excess intake of purine (in
proteins, usually from meat, fish, and poultry); it may cause Ca oxalate calculus formation
(hyperuricosuric Ca oxalate nephrolithiasis).
Uric acid calculi most commonly develop as a result of increased urine acidity (urine pH < 5.5),
or rarely with severe hyperuricosuria (urinary uric acid > 1500 mg/day [> 9 mmol/day]), which
crystallizes undissociated uric acid. Uric acid crystals may comprise the entire calculus or, more
commonly, provide a nidus on which Ca or mixed Ca and uric acid calculi can form.
Mg ammonium phosphate calculi (struvite, infection calculi) indicate the presence of a UTI
caused by urea-splitting bacteria (eg, Proteus sp, Klebsiella sp). The calculi must be treated as
infected foreign bodies and removed in their entirety. Unlike other types of calculi, Mg
ammonium phosphate calculi occur 3 times more frequently in women.
Rare causes of urinary calculi include indinavir, melamine, triamterene, and xanthine.
Analgesia
Facilitate calculus passage, eg, with -receptor blockers such as tamsulosin (described as
medical expulsive therapy)
Analgesia
Renal colic may be relieved with opioids, such as morphine and, for a rapid onset, fentanyl.
Ketorolac 30 mg IV is rapidly effective and nonsedating. Vomiting usually resolves as pain
decreases, but persistent vomiting can be treated with an antiemetic (eg, ondansetron 10 mg IV).
Although increasing fluids (either oral or IV) has traditionally been recommended, increased
fluid administration has not been proven to speed the passage of calculi. Patients with calculi < 1
cm in diameter who have no infection or obstruction, whose pain is controlled with analgesics,
and who can tolerate liquids can be treated at home with analgesics and -receptor blockers (eg,
tamsulosin 0.4 mg po once/day) to facilitate calculus passage. Calculi that have not passed within
6 to 8 wk typically require removal. In patients with infection and obstruction, initial treatment is
relief of obstruction with a ureteral stent and treatment of the infection followed by removal of
calculi as soon as possible.
Calculus removal
The technique used for removal depends on the location and size of the calculus. Techniques
include shock wave lithotripsy and, to ensure complete removal or for larger calculi, endoscopic
techniques. Endoscopic techniques may involve rigid or flexible ureteroscopes (endoscopes) and
may involve direct-vision removal (basketing), fragmentation with some sort of lithotripsy
device (eg, pneumatic, ultrasonic, laser), or both.
For symptomatic calculi < 1 cm in diameter in the renal pelvis or proximal ureter, shock wave
lithotripsy is a reasonable first option for therapy. For larger calculi or if shock wave lithotripsy
is unsuccessful, ureteroscopy (done in a retrograde fashion) with holmium laser lithotripsy is
usually used. Sometimes removal is possible using an endoscope inserted anterograde through
the kidney. For renal stones > 2 cm, percutaneous nephrolithotomy with insertion of a
nephroscope directly into the kidney, is the treatment of choice.
For midureteral calculi, ureteroscopy with holmium laser lithotripsy is usually the treatment of
choice. Shock wave lithotripsy is an alternative.
For distal ureteral calculi, endoscopic techniques, such as direct removal and use of
intracorporeal lithotripsy (eg, pneumatic, electrohydraulic, laser), are considered by many to be
the procedures of choice. Shock wave lithotripsy can also be used.
Calculus dissolution
Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged
alkalinization of the urine with K citrate 20 mEq po bid to tid, but chemical dissolution of
calcium calculi is not possible and of cystine calculi is difficult.
Urinary calculi may remain within the renal parenchyma or renal pelvis or be passed into the
ureter and bladder. During passage, calculi may irritate the ureter and may become lodged,
obstructing urine flow and causing hydroureter and sometimes hydronephrosis. Common areas
of lodgment include the ureteropelvic junction, the distal ureter (at the level of the iliac vessels),
and the ureterovesical junction. Larger calculi are more likely to become lodged. Typically, a
calculus must have a diameter > 5 mm to become lodged. Calculi 5 mm are likely to pass
spontaneously.
Even partial obstruction causes decreased glomerular filtration, which may persist briefly after
the calculus has passed. With hydronephrosis and elevated glomerular pressure, renal blood flow
declines, further worsening renal function. Generally, however, in the absence of infection,
permanent renal dysfunction occurs only after about 28 days of complete obstruction.
Secondary infection can occur with long-standing obstruction, but most patients with Ca-
containing calculi do not have infected urine.