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Urolithiasis
Phillip Fournier, MD
image BASICS
DESCRIPTION
  • Stone formation within the urinary tract: Urinary crystals bind to form a nidus which grows to form a calculus (stone).
  • Range of symptoms: asymptomatic to obstructive; febrile morbidity if result of infection
EPIDEMIOLOGY
  • The worldwide epidemiology differs according to both geographic area (higher prevalence in hot, arid, or dry climates) and socioeconomic conditions (dietary intake and lifestyle). Radiolucent stones and stones secondary to infection are less influenced by environmental conditions.
  • Vesical calculosis (bladder stones) due to malnutrition during early life is frequent in Middle East and Asian countries.
  • Incidence in industrialized countries seems to be increasing, probably due to improved diagnostics as well as to increasingly rich diets.
  • Increased incidence in patients with surgically induced absorption issues, such as Crohn disease and gastric bypass surgery (1)[B]
Incidence
  • In industrialized countries: 100 to 200/100,000/year (2)
  • Predominant age: Mean age is 40 to 60 years.
  • Predominant sex: male > female (˜2:1) (3)
ETIOLOGY AND PATHOPHYSIOLOGY
  • Supersaturation and dehydration lead to high salt content in urine which congregates.
  • Stasis of urine
    • Renal malformation (e.g., horseshoe kidney, ureteropelvic junction obstruction)
    • Incomplete bladder emptying (e.g., neurogenic bladder, prostate enlargement, multiple sclerosis)
  • Crystals may form in pure solutions (homogeneous) or on existing surfaces, such as other crystals or cellular debris (heterogeneous).
  • Balance of promoters and inhibitors: organic (Tamm-Horsfall protein, glycosaminoglycan, uropontin, nephrocalcin) and inorganic (citrate, pyrophosphate)
  • Calcium oxalate and/or phosphate stones (80%)
    • Hypercalciuria
      • Absorptive hypercalciuria: increased jejunal calcium absorption
      • Renal leak: increased calcium excretion from renal proximal tubule
      • Resorptive hypercalciuria: mild hyperparathyroidism
    • Hypercalcemia
      • Hyperparathyroidism
      • Sarcoidosis
      • Malignancy
      • Immobilization
      • Paget disease
  • Hyperoxaluria
    • Enteric hyperoxaluria
      • Intestinal malabsorptive state associated with irritable bowel disease, celiac sprue, or intestinal resection
      • Bile salt malabsorption leads to formation of calcium soaps.
    • Primary hyperoxaluria: autosomal recessive, types I and II
    • Dietary hyperoxaluria: overindulgence in oxalaterich food
  • Hyperuricosuria
    • Seen in 10% of calcium stone formers
    • Caused by increased dietary purine intake, systemic acidosis, myeloproliferative diseases, gout, chemotherapy, Lesch-Nyhan syndrome
    • Thiazides, probenecid
  • Hypocitraturia
    • Caused by acidosis: renal tubular acidosis, malabsorption, thiazides, enalapril, excessive dietary protein
  • Uric acid stones (10-15%): hyperuricemia causes as discussed earlier
  • Struvite stones (5-10%): infected urine with ureaseproducing organisms (most commonly Proteus sp.)
  • Cystine stones (<1%): autosomal recessive disorder of renal tubular reabsorption of cystine
  • Bladder stones: seen with chronic bladder catheterization and some medications (indinavir)
  • In children: usually due to malnutrition
Genetics
  • Up to 20% of patients have a family history. However, spouses of those who form stones have higher calcium excretion rates than controls, suggesting strong dietary-environmental factors.
  • Autosomal dominant: idiopathic hypercalciuria
  • Autosomal recessive
    • Cystinuria, Lesch-Nyhan syndrome, hyperoxaluria types I and II
    • Ehlers-Danlos syndrome, Marfan syndrome, Wilson disease, familial renal tubular acidosis
RISK FACTORS
  • White > African American in regions with both populations
  • Family history
  • Previous history of nephrolithiasis
  • Diet rich in protein, refined carbohydrates, and sodium, carbonated drinks
  • Occupations associated with a sedentary lifestyle or with a hot, dry workplace
  • Incidence rates peak during summer secondary to dehydration.
  • Obesity
  • Surgically/medically induced malabsorption (Crohn disease, gastric bypass, celiac)
GENERAL PREVENTION
  • Hydration (4)[A]
  • Decrease salt and meat intake
  • Avoid oxalate-rich foods.
Pediatric Considerations
Rare: more common in men with low socioeconomic status
Pregnancy Considerations
  • Pregnant women have the same incidence of renal colic as do nonpregnant women.
  • Most symptomatic stones occur during the 2nd and 3rd trimesters, heralded by symptoms of flank pain/hematuria.
  • Most common differential diagnosis is physiologic hydronephrosis of pregnancy. Use ultrasound to avoid irradiation. Noncontrast-enhanced CT scan also is diagnostic.
  • Treatment goals
    • Control pain and avoid infection, and preserve renal function until birth or stone passage.
    • 30% require intervention, such as stent placement.
image DIAGNOSIS
PHYSICAL EXAM
Tender costovertebral angle with palpation/percussion and/or iliac fossa
DIFFERENTIAL DIAGNOSIS
  • Appendicitis
  • Ruptured aortic aneurysm
  • Musculoskeletal strain
  • Pyelonephritis (upper UTI)
  • Pyonephrosis (obstructed upper UTI; emergency)
  • Perinephric abscess
  • Ectopic pregnancy
  • Salpingitis
DIAGNOSTIC TESTS & INTERPRETATION
  • Urinalysis for RBCs, leukocytes, nitrates, pH (acidic urine <5.5 is associated with uric acid stones; alkaline >7 with struvite stones)
  • Midstream urine for microscopy, culture, and sensitivity
  • Blood: urea, creatinine, electrolytes, calcium, and urate; consider CBC.
  • Parathyroid hormone only if calcium is elevated
  • Stone analysis if/when stone passed
Initial Tests (lab, imaging)
  • Noncontrast-enhanced helical CT scan of the abdomen and pelvis has replaced IV pyelogram as the investigation of choice (5)[A].
    • Stone is found most commonly at levels of ureteric luminal narrowing: pelviureteric junction, pelvic brim, and VUJ.
    • Acute obstruction: Proximal ureter and renal pelvis are dilated to the level of obstruction, and perinephric stranding is possible on imaging.
  • Renal ultrasound may be as effective with lower radiation at diagnosis as well as identifying obstruction (6)[B].
  • X-ray of kidneys, ureter, and bladder to determine if stone is radiopaque or lucent
    • Calcium oxalate/phosphate stones are radiopaque.
    • 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).
  • Ultrasound has low sensitivity and specificity but is often the first choice for pregnant women.
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image TREATMENT
GENERAL MEASURES
  • 75% of patients are successfully treated conservatively and pass the stone spontaneously.
  • Stones that do not pass usually require surgical intervention.
  • 30-50% of patients will have recurrent stones.
  • Increase fluid intake; eliminate carbonated drinks.
MEDICATION
  • Medical expulsive therapy: &agr;1-antagonists (e.g., tamsulosin) and calcium channel blockers (e.g., nifedipine) improve likelihood of spontaneous stone passage with a number needed to treat (NNT) of ˜5 (7).
  • Category C in pregnancy
ISSUES FOR REFERRAL
  • Urgent referral of patients with UTI/sepsis or acute renal failure/solitary kidney
  • Early referral of pregnant patients, large stones (>8 mm), chronic renal failure, children
  • Refer patients if no passage at 2 to 4 weeks or poorly controlled pain.
ADDITIONAL THERAPIES
  • Uric acid stone dissolution therapy
    • Alkalinize urine with potassium citrate; keep pH >6.5.
    • Allopurinol 100 to 300 mg/day PO (for those who continue to form stones despite alkalinization of urine)
  • Cystine stone dissolution/prevention
    • Alkalinize urine with potassium citrate; keep pH >6.5.
    • Chelating agents: captopril, &agr;-mercapto propionylglycine, D-penicillamine
  • Consider altering medications that increase risk of stone formation: probenecid, loop diuretics, salicylic acid, salbutamol, indinavir, triamterene, acetazolamide.
  • Vitamin D supplementation has not been proven to induce stone formation.
  • Treat hypercalciuria with thiazides on an acute basis only
  • Treat hypocitraturia with potassium citrate and high-citrate juices (e.g., orange, lemon).
  • Treat enteric hyperoxaluria with oral calcium/magnesium, cholestyramine, and potassium citrate.
SURGERY/OTHER PROCEDURES
  • Immediate relief of obstruction is required for patients with the following conditions:
    • Sepsis
    • Renal failure (obstructed solitary kidney, bilateral obstruction)
    • Uncontrolled pain, despite adequate analgesia
  • Emergency surgery for obstruction
    • Placement of a retrograde stent (i.e., endoscopic surgery, usually requires an anesthetic)
    • Radiologic placement of a percutaneous nephrostomy tube
  • Elective surgery for stone treatment
    • Extracorporeal shock wave lithotripsy
    • Ureteroscopy with basket extraction/lithotripsy (laser/pneumatic)
    • Percutaneous nephrolithotomy
  • Open surgery is uncommon.
INPATIENT CONSIDERATIONS
Admission-Criteria/Initial Stabilization
  • Analgesia
    • Combination of NSAIDs (ketorolac 30 to 60 mg) and oral opiate
    • Parenteral opioid if vomiting or if preceding fails to control pain (morphine 5 to 10 mg IV or IM q4h)
    • Antiemetic if required or prophylactically with parenteral narcotics
  • Septic patients with urosepsis or pyonephrosis may require IV antibiotics (once blood and urine cultures are taken), IV fluids, and, in severe cases, cardiorespiratory support in intensive care during recovery.
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
  • Patients with ureteric stones who are being treated conservatively should be followed until imaging is clear or stone is visibly passed.
    • Strain urine and send stone for composition.
    • Tamsulosin and nifedipine in selected patients to speed passage
    • Present to the hospital if pain worsens/signs of infection.
    • If pain management is suboptimal or stone does not progress or pass within 2 to 4 weeks, patient should be referred to a urologist and imaging should be repeated.
  • Patients with recurrent stone formation should have follow-up with a urologist for metabolic workup: 24-hour urine for volume, pH, creatinine, calcium, cystine, phosphate, oxalate, uric acid, and magnesium.
DIET
  • Decrease or eliminate carbonated drinks.
  • Patients who form calcium stones should minimize high-oxalate foods such as green leafy vegetables, rhubarb, peanuts, chocolates, and beer.
  • Decrease protein and salt intake.
  • Lowering calcium intake is inadvisable and even may increase urine calcium excretion.
  • Increase phytate-rich foods such as natural dietary bran, legumes and beans, whole cereal (8).
  • Avoid excessive vitamin C and\or vitamin D.
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. Matlaga BR, Shore AD, Magnuson T, et al. Effect of gastric bypass surgery on kidney stone disease. J Urol. 2009;181(6):2573-2577.
2. Tiselius HG. Epidemiology and medical management of stone disease. BJU Int. 2003;91(8):758-767.
3. Scales CD Jr, Curtis LH, Norris RD, et al. Changing gender prevalence of stone disease. J Urol. 2007;177(3):979-982.
4. Qiang W, Ke Z. Water for preventing urinary calculi. Cochrane Database Syst Rev. 2004;(3):CD004292.
5. Worster A, Preyra I, Weaver B, et al. 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.
6. Luyckx F. Who wants to go further has to know the past: a comment upon: ultrasonography versus computed tomography for suspected nephrolithiasis-R. Smith-Bindman et al. N Engl J Med. 2014 Sep 18;371(12):1100-1110. World J Urol. 2015;33(10):1371-1372.
7. Hollingsworth JM, Rogers MA, Kaufman SR, et al. Medical therapy to facilitate urinary stone passage: a meta-analysis. Lancet. 2006;368(9542);1171-1179.
8. Grases F, Costa-Bauza A, Prieto RM. Renal lithiasis and nutrition. Nutr J. 2006;5:23.
Additional Reading
&NA;
  • Penniston KL, Jones AN, Nakada SY, et al. Vitamin D repletion does not alter urinary calcium excretion in healthy postmenopausal women. BJU Int. 2009;104(10):1512-1516.
  • Qaseem A, Dallas P, Forciea MA, et al. Dietary and pharmacologic management to prevent recurrent nephrolithiasis in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2014;161(9):659-667.
See Also
&NA;
Algorithms: Dysuria; Renal Calculi; Urethral Discharge
Codes
&NA;
ICD10
  • N20.9 Urinary calculus, unspecified
  • N20.0 Calculus of kidney
  • N20.1 Calculus of ureter
Clinical Pearls
&NA;
  • Incidence in industrialized countries seems to be increasing, probably due to improved diagnostics as well as to increasingly rich diets.
  • Vesical calculosis (bladder stones) due to malnutrition during early life is frequent in Middle East and Asian countries.
  • Medical expulsive therapy: &agr;1-Antagonists (e.g., terazosin) and calcium channel blockers (e.g., nifedipine) improve likelihood of spontaneous stone passage with NNT of ˜5.
  • Increased fluid intake for life cannot be overemphasized for decreasing recurrence. Encourage 2 to 3 L/day intake; advise patient to have clear urine rather than yellow.
  • Patients who form calcium stones should minimize high-oxalate foods such as green leafy vegetables, rhubarb, peanuts, chocolates, and beer.
  • Decrease protein and salt intake.
  • Lowering calcium intake is inadvisable and even may increase urine calcium excretion.