UROLITHIASIS

UROLITHIASIS - Alison H. Blatt, MD
BASICS
DESCRIPTION
• Stone formation within the urinary tract: Urinary crystals bind to form a nidus, which grows to form a calculus (stone).
• Calculus may be asymptomatic or obstructive, or may be a source of chronic infection.
GENERAL PREVENTION
Increased water intake reduces the risk of recurrence and time to recurrence of urinary calculi.
ALERT
Pediatric Considerations
Rare; more common in males; low socioeconomic status
Pregnancy Considerations
• Pregnant women have the same incidence of renal colic as do nonpregnant women.
• Diagnosis is challenging: Most common differential is physiological hydronephrosis of pregnancy.
• Ultrasound; avoid irradiation
• Aim of treatment is pain control, renal function preservation and aseptic urine until birth or stone passage. Only 30% require some form of intervention.
• NSAIDs must be avoided; therefore, acetaminophen  codeine is the mainstay.
EPIDEMIOLOGY
• Predominant age: Mean age is 40-50 years
• Predominant sex: Male > Female (~2:1)
• High frequency of urolithiasis worldwide although rare in a few parts of the world (e.g., in Greenland in the coastal areas of Japan)
• The worldwide epidemiology differs according to both geographical area and socioeconomic conditions (dietary intake and lifestyle).
- Radiolucent and infection stones are less influenced by environmental conditions.
• Vesical calculosis (bladder stones), due to malnutrition in early life, is frequent in Middle Eastern and Asian countries. The incidence is improving as social conditions gradually improve.
• Incidences in industrialized countries appear to be increasing, probably due to improved diagnostics, as well as increasingly rich diets and altered environmental conditions.
Incidence
In industrialized countries: 100-200 per 100,000
Prevalence
In industrialized countries: 5-10%
RISK FACTORS
• White > African American in regions with both populations
• Family history
• Diet rich in protein, refined carbohydrates, and sodium
• Occupations associated with a sedentary lifestyle or with a hot, dry workplace
• Incidence rates peak in summer.
Genetics
• Up to 20% of patients have a family history. However, spouse of stone formers have higher calcium excretion rates than controls, suggesting strong dietary-environmental factors.
• Autosomal dominant: Idiopathic hypercalciuria
• Autosomal recessive: Cystinuria, Lesch-Nyan syndrome, hyperoxaluria types I and II
• Ehler-Danlos syndrome, Marfan syndrome, Wilson disease, familial renal tubular acidosis
PATHOPHYSIOLOGY
• Supersaturation and dehydration
• Stasis of urine
- Renal malformation (e.g., horseshoe kidney)
- Incomplete bladder emptying (e.g., neuropathic bladder, prostate enlargement)
• Nucleation and epitaxy: Crystals may form in pure solutions or on existing surfaces (other crystals, cellular debris, etc.).
• Balance of promoters and inhibitors: Organic (Tamm-Horsfall protein, GAG, uropontin, nephrocalcin) and Inorganic (citrate, pyrophosphate)
ETIOLOGY
• Calcium oxalate and/or phosphate stones (80%)
- Idiopathic hypercalciuria
 Autosomal dominant trait; present in 50% of calcium stone formers and 10% of the normal population
 Absorptive hypercalciuria: Increased jejunal calcium absorption
 Renal leak: Increased calcium excretion from renal proximal tubule
 Resorptive hypercalciuria: Subtle hyperparathyroidism
- Hypercalcemia
 Hyperparathyroidism
 Sarcoidosis
 Malignancy
 Pagets disease
 Multiple myeloma
- Hyperoxaluria
 Enteric hyperoxaluria: Bowel disease, acidosis, or hypokalaemia; bile salt malbsorption leads to formation of calcium soaps, thus leaving increased oxalate available for colon absorption and subsequent increased renal excretion
 Primary hyperoxaluria: Autosomal recessive, types I and II
 Dietary hyperoxaluria
- Hyperuricemia
 Seen in 10% of calcium stone formers
 Acidosis, malbsorption, myeoloproliferative diseases, gout, chemotherapy, Lesch-Nyan syndrome (rare autosomal recessive disorder)
 Thiazides, probenicid
- Hypocitraturia
 Caused by acidosis: Infection, malabsorption, thiazides, hypokalaemia, dietary salt and protein
• Uric acid stones (10-15%): Hyperuricemia causes as above
• Struvite stones (5-10%): Infected urine with urease-producing organisms (most commonly proteus)
• Cystine stones (1%): Autosomal recessive disorder of renal tubular reabsorption of cystine
• Bladder stones
- Inadequate bladder emptying in adults
- In children, it is usually due to malnutrition.


DIAGNOSIS
SIGNS AND SYMPTOMS
• Pain
- Renal colic: Acute onset of severe loin to groin pain; typically patient cannot lie still.
- Distal stones may present with referred pain in labia, penile meatus, or testis.
- Tender renal angle and/or iliac fossa
• Microscopic or gross hematuria occurs in 95% of patients.
• Nonspecific symptoms of nausea, vomiting, tachycardia, diaphoresis
• Low grade fever without infection
• High grade fever, cloudy urine. Infection requires urgent treatment (see below).
• Irritative lower urinary tract symptoms such as frequency and dysuria especially occur with stones at the vesico-ureteric junction.
• Asymptomatic. Particularly nonobstructing stones within the renal calyces
TESTS
Lab
• Urinalysis for red cells, leukocytes, nitrates, pH (acidic urine 5.5 is associated with uric acid stones, alkaline >7.0 with struvite stones)
• Midstream urine for microscopy, culture, and sensitivity.
• Bloods: FBC, urea, creatinine, electrolytes, calcium, and urate
• Blood culture if suspect sepsis
• Parathyroid hormone only if calcium elevated
• Stone analysis if/when stone passed
Imaging
• Noncontrast helical CT of the abdomen and pelvis is the investigation of choice where available.
- Stone is most commonly found at levels of ureteric luminal narrowing: The pelvi-ureteric junction, the pelvic brim, and the vesico-ureteric junction.
- If the obstruction is acute, proximal ureter and renal pelvis is dilated to the level of obstruction and perinephric "stranding" is seen.
- If chronic, renal atrophy may be noted.
• KUB is necessary when a stone is diagnosed to determine whether the stone is radio-opaque or lucent (determines treatment as well as type of follow-up imaging).
- Calcium oxalate/phosphate stones are radio-opaque.
- Uric acid stones are radiolucent.
- Staghorn calculi (that fill the shape of the renal calyces) are usually struvite and opaque.
- Cystine stones are faintly opaque ("ground-glass" appearance).
• IVP has been largely replaced by CT in the initial diagnostic workup.
• Ultrasound has no role in diagnosis due to its low sensitivity and specificity; exceptions are pregnancy and pediatrics.
DIFFERENTIAL DIAGNOSIS
• Appendicitis
• Ruptured aortic aneurysm
• Musculoskeletal strain
• Pyelonephritis (upper urinary tract infection)
• Pyonephrosis (obstructed upper urinary tract infection-emergency)
• Perinephric abscess
• Ectopic pregnancy
• Salpingitis
TREATMENT
PRE-HOSPITAL
• Analgesia
- Combination of NSAIDs (indomethacin suppository 100 mg) and acetaminophen-codeine orally
- Parenteral narcotic if above fails to control pain (morphine 5-10 mg IV or IM q4h)
- Antiemetic if required or prophylactically with parenteral narcotics
• Antibiotics only if patient septic and after urine and blood cultures taken
• Pushing fluids during an acute episode is not advised. It increases pain and probably does not improve stone passage rates.
STABILIZATION
Septic patients with pyonephrosis may require intravenous fluids, and in severe cases, cardiorespiratory support in intensive care even after relief of obstruction.
GENERAL MEASURES
• 75% of patients are successfully treated conservatively and pass the stone spontaneously
• Advise patient to strain urine and take regular analgesia. Present to hospital if pain is uncontrolled or fevers develop.
Diet
• Increased fluid intake for life cannot be overemphasized for decreasing recurrence.
- Encourage 2-3 L/d intake; advise patient to have "clear" urine rather than yellow.
• Diet modification has less effect than fluid intake on urine concentrations of stone substrates, and has low compliance rates.
• Calcium stone formers should minimize high oxalate foods such as spinach, rhubarb, peanuts, chocolates, and parsley.
• Decrease protein and salt intake.
• Lowering calcium intake is inadvisable and may even increase urine calcium excretion.
SPECIAL THERAPY
• Uric acid stone dissolution therapy
- Ural sachet 3x/d OR potassium citrate OR sodium bicarbonate to alkalinize the urine; keep pH >6.5
- Allopurinol 100-300 mg/d PO
• Cystine stone dissolution/prevention
- Captopril, D-penicillamine, alkalinizers
• Consider altering medications that increase risk of stone formation: Probenicid, loop diuretics, salicylic acid, salbutamol, indinavir, triamterine, acetazolamide
• Recurrent calcium stone formers may improve with thiazides; however, long-term use is limited by side effects such as hypotension, hypokalemia, weakness, and impotence.
• Orthophosphate is required in large daily doses to significantly reduce urine calcium excretion causing side effects of diarrhea, flatus, and bloating.
SURGERY
• Immediate relief of obstruction is imperative in 2 groups of patients
- Patients with signs of sepsis
- Renal failure (obstructed solitary kidney, bilateral obstruction)
• Uncontrolled pain despite adequate analgesia is the most common indication for semi-urgent endoscopic stenting.
• Emergency surgery to unobstruct kidney
- Placement of a retrograde stent (i.e., endoscopic surgery, usually requiring an anesthetic)
- Radiological placement of a percutaneous nephrostomy tube, usually performed in emergencies under local anesthetic
• Elective surgery for stone treatment
- Extracorporeal shock-wave lithotripsy (ESWL)
- Ureteroscopy with basket extraction orlithotripsy (laser or pneumatic)
- Percutaneous nephrolithotomy (PCNL)
- Open surgery uncommon
FOLLOW-UP
• Patients being treated conservatively with ureteric stones should be followed until imaging is clear (KUB 2nd weekly if stone is visible) or stone is visibly passed.
- These patients should be advised to strain their urine.
- If pain management is suboptimal or stone does not progress or pass within 2-4 weeks, patient should be referred to a urologist.
• Recurrent stone formers should have follow-up with a urologist for a full biochemical screen to identify reversible risk factors.
- 24 hour urine for volume, pH, creatinine, calcium, cystine, phosphate, oxalate, uric acid, magnesium
DISPOSITION
Issues for Referral
• Urgent referral of patients with urine infection/sepsis, or acute renal failure/solitary kidney
• Early referral of pregnant patients, large stones (>8 mm), chronic renal failure, children
• Referral if stone not passing at 2-4 weeks or pain is poorly controlled
• All patients with >1 stone or stone episode require referral for metabolic screening.
PROGNOSIS
• Spontaneous stone passage depends on stone location (proximal vs. distal) and stone size (5 mm 90% pass, >8 mm 10% pass)
• Stone recurrence: 50% of patients at 10 years
REFERENCES
1. Qiang W, Ke Z. Water for preventing urinary calculi. Cochrane Database of Systematic Reviews. 2004;3:CD004292.
2. Tiselius HG. Epidemiology and medical management of stone disease. BJU Int. 2003;91: 758-767.
3. Worster A, Preyra I, Weaver B, Haines T. The accuracy of noncontrast helical computed tomography versus intravenous pyelography in the diagnosis of suspected acute urolithiasis: A meta-analysis. Ann Emerg Med. 2002;40(3): 280-286.