0
Clinical Crossroads | Clinician's Corner

A 44-Year-Old Woman With Kidney Stones

Gary C. Curhan, MD, ScD
[+] Author Affiliations

Author Affiliation: Dr Curhan is Associate Professor of Medicine and Epidemiology, Harvard Medical School and Harvard School of Public Health, Boston, Mass. He divides his time between the Channing Laboratory and the Renal Division at Brigham and Women’s Hospital, Boston, Mass.

More Author Information
JAMA. 2005;293(9):1107-1114. doi:10.1001/jama.293.9.1107
Text Size: A A A
Published online
Figures in this Article
Clinical Crossroads Section Editor: Margaret A. Winker, MD, Deputy Editor.

DR BURNS: Ms P is a 44-year-old woman with a history of morbid obesity and superficial thrombophlebitis who was diagnosed with kidney stones 1 month ago. She recently lost her medical insurance and is applying for free care. She is currently unemployed and lives with her daughter.

While on vacation in Jamaica, Ms P developed severe diarrhea without nausea, vomiting, or fever. After returning to the United States her diarrhea resolved, but she developed brown urine that lasted for several days. She subsequently developed bilateral intermittent low back pain that she treated with acetaminophen and ibuprofen with good relief. She denied any radiation of the pain or any associated weakness or numbness. She had no fever, dysuria, or urinary frequency. She never had similar symptoms in the past. She does not smoke and denies alcohol use.

Ms P contacted her primary care physician who suggested that she be evaluated. At her visit, physical examination was noteworthy for a morbidly obese woman, 370 lb, with right and left upper quadrant tenderness without rebound or costovertebral angle (CVA) tenderness. A urinalysis showed “large blood.”

Ms P was thought to have a kidney stone causing her hematuria and back pain. She was instructed to continue with acetaminophen and ibuprofen for pain. A subsequent computed tomography (CT) scan revealed a 1.2 × 1.6-cm calculus within the right renal pelvis.

The patient was referred to a urologist. At the time of her visit, she had no further discoloration of her urine. She continued to note episodes of colicky low back pain for which she took acetaminophen and ibuprofen as needed. She denied having fever, chills, or dysuria. She had no CVA tenderness on examination. Plain film of the abdomen revealed an 18 × 17-mm calcific density overlying the region of the pelvis of the right kidney, consistent with a calculus.

At the time of her visit, treatment options were discussed, including extracorporeal shock wave lithotripsy (ESWL) vs ureteroscopy. The plan was to proceed with ESWL when her free care application was approved. In the interim, the plan was to alkalinize her urine to try to shrink the stone and minimize the number of potential future invasive procedures if ESWL failed.

Ms P wonders whether she was being treated differently because of her size and lack of insurance and what is the best way to proceed.

I was having some pain, but I didn’t make much of that because I was on vacation and having a good time. When my urine got a little cloudy, I was concerned as I thought that was unusual. So that made me go in to see the doctor, and she scheduled me for a CAT scan and that’s when they saw it immediately.

They told me right away it would not pass on its own and I would probably need an invasive procedure. Unfortunately, any procedure would need to wait until my free care application was approved. Until then I was told to take a medication that I could not afford and so it was switched to baking soda and water.

The baking soda hasn’t done much that I’ve noticed. I mean maybe I’m not supposed to, maybe it works subtly, I don’t know. And I don’t know if it’s breaking it up, because again I don’t know what I’m supposed to be looking for. No one tells me; am I supposed to have pain once it starts? Will I notice that it’s breaking? I don’t know.

If I had health insurance, what would you have recommended be done immediately? Was the treatment I received dictated by my lack of health insurance? Being the woman of size that I am, how does my treatment differ?

What is the epidemiology and underlying pathophysiology of renal stones? How do patients typically present and what are common examination and laboratory findings? What is the differential diagnosis? What workup, if any, is indicated for a first stone? How effective are medical treatment options? What is the role of the urologist and what are the surgical treatment options, both invasive and noninvasive? What are the pros and cons of these treatments, especially in someone who is morbidly obese? What is the rate of recurrence? What evaluation should be undertaken to prevent future episodes and what are the treatment options? What does the future hold? What would you recommend for Ms P?

DR CURHAN: Ms P was recently diagnosed with her first kidney stone. She continues to have lower back pain and microscopic hematuria, but there is no evidence of urinary tract infection. She is considering her options for treatment, which are limited by her obesity and current lack of insurance.

Epidemiology

The prevalence of nephrolithiasis is increasing in both men and women and in whites and blacks.1 The lifetime risk of stone formation is estimated to be about 12% in men and 6% in women.1 - 2

In men, the first episode of renal colic is most likely to occur between the ages of 30 and 60 years.2 - 4 The incidence for men who have never had a stone is 3 to 4 cases per 1000 men per year between the ages of 30 to 60 years and then slowly declines with age. For women, the incidence is highest between the ages of 20 and 30 years (approximately 2 per 1000 women per year) and then declines to about 1 per 1000 women per year for the next 4 decades.2 ,4 - 6

The risk of recurrent stone formation after the incident stone in untreated patients remains controversial. Early studies reported frequencies of stone recurrence ranging from 30% to 50% at 5 years.2 ,7 - 8 Recurrence rates in men were reported to be approximately 3 times higher than in women.2 ,7 ,9 However, data from the control groups of recent randomized controlled trials suggest substantially lower rates of first recurrence after an incident calcium oxalate stone, ranging from less than 2 per 100 person-years10 to slightly more than 5 per 100 person-years.11 Unfortunately, sex-specific rates are not available from the randomized trials of incident stone formers.

Physician office visits for kidney stone disease nearly doubled from 950 000 visits in 1992 to 1 825 000 in 2000.12 However, the estimated total health costs for nephrolithiasis have remained stable at about $2 billion per year, likely due to the shift from inpatient to outpatient procedures.12

Pathophysiology

There are a variety of types of kidney stones. Approximately 85% of stones in men and 70% in women contain calcium,2 ,13 most commonly as calcium oxalate. Overall, urinary tract infection or systemic disorders, such as primary hyperparathyroidism, are responsible for less than 10% of stones in men and 25% in women.13 The other stone types, such as cystine, uric acid, and struvite, are much less common. However, these types of stone also deserve careful attention, because recurrences are common.14 - 16 Based on her history and radiographic findings, Ms P most likely has a calcium-containing stone.

A kidney stone may form when the concentrations of urinary constituents exceed their solubility. The causes of stone formation differ for different stone types. Cystine stones only form in individuals with the autosomal recessive disorder of cystinuria.17 Uric acid stones only form in individuals with persistently acid urine, with or without hyperuricosuria.18 Struvite stones only form in the setting of an upper urinary tract infection with a urease-producing bacterium.19 Stones may occasionally result from precipitation in the urinary tract of medications such as acyclovir and indinavir.20

Calcium-based stones have multiple causes. Recent work suggests that factors in the renal interstitium might be important.21 However, several risk factors for calcium-based stones have been identified. Calcium phosphate stones form in the setting of hypercalciuria, hypocitraturia, and alkaline urine,13 often the result of systemic conditions such as renal tubular acidosis and primary hyperparathyroidism.13 Calcium oxalate stones form when concentrations of calcium, oxalate, or uric acid are increased or urine citrate is decreased.13 The remainder of this article will focus on calcium oxalate stones except where noted.

Risk Factors

The likelihood of stone formation is influenced by urinary, dietary, and genetic factors as well as the presence of other medical conditions ( Article ).The concentrations, not just the total amount, of relevant urinary factors are the key determinants of stone formation. The significance of concentration emphasizes the importance of fluid intake and thereby urinary volume. However, stone formation cannot be perfectly predicted by urinary composition. A number of dietary factors have been associated with a reduced risk of stone formation, including higher intakes of dietary calcium, potassium, and phytate and lower intakes of animal protein, sodium, and sucrose.3 ,5 - 6 Systemic factors also influence risk independent of dietary intake, including higher body mass index22 - 23 (particularly in women), gout,24 and primary hyperparathyroidism.13 Based on the limited information available, Ms P’s obesity may have put her at higher risk for stone formation.

Box. Risk Factors for Calcium Oxalate Stone Formation

Urinary Risk Factors

Increased risk with increasing

  • Calcium

  • Oxalate

  • Uric acid

Decreased risk with increasing

  • Citrate

  • Total volume

Dietary Risk Factors

Increased risk with increasing intake of

  • Animal protein

  • Sucrose

  • Sodium

  • Supplemental calcium

  • Oxalate (?)

  • Vitamin C (?)

Decreased risk with increasing intake of

  • Dietary calcium

  • Potassium

  • Phytate

  • Fluid

  • Fruits and vegetables

Genetic Predisposition

  • Family history

  • Primary hyperoxaluria

Systemic Medical Conditions

  • Gout

  • Obesity

  • Hypertension

  • Primary hyperparathyroidism

  • Complete or incomplete renal tubular acidosis

  • Inflammatory bowel disease or other conditions with gastrointestinal malabsorption

Examination and Laboratory Findings

The typical presentation is sudden-onset unilateral flank pain of sufficient severity that the individual usually seeks medical attention, often at an emergency department.25 Although the term “colic” is used, this is a misnomer because the pain does not completely remit but rather waxes and wanes.26 The pain is often accompanied by nausea and occasionally vomiting. The pain can radiate to a variety of locations depending on the location of the stone: when the stone is in the upper ureter, pain may radiate anteriorly to the abdomen; when the stone is in the lower ureter, pain can radiate to the ipsilateral testicle in men or ipsilateral labium in women; if the stone is lodged at the ureterovesical junction, the major symptoms may be urinary frequency and urgency. A less common acute presentation is gross hematuria without pain. Ms P’s bilateral intermittent low back pain and its relief with acetaminophen are not consistent with pain from a renal or ureteral stone.

Although the physical examination alone will rarely make the diagnosis, there are clues to help guide the evaluation. The patient will typically be in obvious pain and cannot find a comfortable position. There may be ipsilateral CVA tenderness or, in cases of obstruction with infection, signs and symptoms of sepsis may be present. The examination may reveal findings of systemic conditions associated with stone formation, but this will rarely be diagnostic for stone disease.

The serum chemistries are typically normal, but leukocytosis may be present due to stress or infection.27 The urinalysis classically reveals red and white blood cells and occasionally may have crystals.27 If the ureter is completely obstructed due to the stone, there may be no red blood cells, as no urine will be flowing from that ureter into the bladder. A study of 397 patients presenting acutely with urolithiasis found that 9% did not have hematuria.28 Clinically, patients with an asymptomatic renal stone often have microscopic hematuria. Ms P’s hematuria is very likely due to the large renal stone.

Helical CT is the imaging modality of choice because of its sensitivity, ability to visualize uric acid stones (traditionally considered “radiolucent”), and lack of need for radiocontrast.29 Helical CT can detect small stones that may be missed by intravenous urography (Figure), which requires intravenous radiocontrast.30 - 31 Published studies comparing CT and intravenous urography have generally included fewer than 40 subjects and had no definitive gold standard; thus, sensitivity and specificity values are not available. Few data are available that compare CT and ultrasound, but in the acute setting with patients presenting with presumed renal colic, the sensitivity of CT was 96% compared with 61% for ultrasound; the specificity for each was 100%.32 Typically, CT will show a ureteral stone or evidence of recent passage (eg, perinephric stranding or hydronephrosis), whereas plain abdominal x-ray (kidney-ureters-bladder [KUB]) can miss a stone in the ureter or kidney, even if radiopaque, and provides no information on obstruction. For the evaluation of residual stone fragments in patients who have undergone percutaneous nephrostolithotomy, CT is more sensitive than KUB (100% vs 46%) but less specific (62% vs 82%).33 Ultrasound has the advantage of avoiding radiation but can only image the kidney and possibly the proximal ureter; thus, ureteral stones are typically not seen by ultrasound. A retrospective study comparing 123 examinations with ultrasound vs CT found that the sensitivity for ultrasound was 24% and the specificity was 90%; ultrasound may also miss renal stones less than 3 mm in size.34 The discrepancy in stone size between Ms P’s KUB and CT scan is common33 ; it is unlikely, although possible, that the stone grew over the 3-week period between the 2 studies.

Figure. Helical Computed Tomographic Scan of the Upper Abdomen
Grahic Jump Location

High-resolution helical computed tomographic image demonstrating a stone in the right renal pelvis and a smaller stone in the left kidney (arrowheads). There is no hydronephrosis.

Differential Diagnosis

Stone disease is common, so the presence of a renal stone does not clinch the diagnosis of a patient presenting with acute abdominal or flank pain.27 In addition, a stone may mimic a number of other acute conditions. A stone lodged at the right ureteropelvic junction may mimic acute cholecystitis; in the lower right ureter, it may mimic acute appendicitis; at the ureterovesical junction, it may mimic acute cystitis; and in the lower left ureter, it may mimic diverticulitis. An obstructing stone with proximal infection may mimic acute pyelonephritis. Note that infection in the setting of obstruction is a medical emergency (“pus under pressure”) that requires emergent drainage either by placement of a ureteral stent or a percutaneous nephrostomy tube.

The differential diagnosis of someone with suspected renal colic includes muscular or skeletal pain, herpes zoster, acute cholecystitis, duodenal ulcer, appendicitis, diverticulitis, pyelonephritis, abdominal aortic aneurysm, gynecological causes, ureteral obstruction due to other intraluminal factors such as a blood clot or sloughed papilla, and ureteral stricture.26 - 27 Extraluminal factors causing compression tend not to present with symptoms of renal colic because these processes tend to have a more gradual onset.

Evaluation of a First Stone

The workup after a solitary stone remains controversial.35 Some authors have argued that cost, low adherence by patients to recommendations, and the relatively low recurrence rate outweigh the potential benefits of evaluating a first-time stone former. However, many experts believe that an evaluation is indicated for several reasons.36 First, relatively simple, safe, and inexpensive interventions, such as increasing fluid intake,11 are available. The selection of which intervention to recommend depends on the findings from the evaluation. However, if the evaluation is not complete, then the recommendations may not be appropriate.37 Second, other systemic conditions that are of clinical importance, such as osteoporosis and primary hyperparathyroidism, may be diagnosed during the evaluation of the stone former.38 Whether evaluation and subsequent prevention is cost-effective is also controversial. One study reported that it would only be cost saving if the recurrence rate for a first-time stone former was substantially higher than currently observed.39 In another study not limited to first-time stone formers, medical prevention was found to be cost saving.40 My decision to evaluate the first stone depends on several factors. First, what is the stone burden? Even though this was the first symptomatic event, an appreciable proportion of patients will have remaining renal stones and thus could be considered “recurrent” stone formers. If the patient had only a KUB or even an intravenous urogram during the acute evaluation, I would order a CT scan to determine if there were residual renal stones. Second, if the initial stone was large (eg, >10 mm), I would recommend proceeding with a metabolic evaluation. Third, the more invasive the intervention required to remove the first stone, the more likely I am to perform an evaluation. Finally, and most importantly, are the patient’s preferences. If the patient is uninterested in making long-term lifestyle changes or taking medication, then I do not proceed with an evaluation. Because of the large stone burden, I would recommend Ms P pursue a metabolic evaluation.

The metabolic evaluations for the first-time and recurrent stone former are identical. The workup should include serum chemistries and two 24-hour urine collections to help guide therapy, even if the chemical content of the stone has been analyzed (see below for details). For Ms P, the evaluation could be postponed until she is able to obtain insurance and after her stone removal procedure if it can be performed within the near future.

Nonsurgical Treatment Options

Renal colic is one of the most excruciating types of pain that a patient will experience; therefore, the first and foremost treatment is pain control. Evidence from many randomized controlled trials suggests that parenteral nonsteroidal anti-inflammatory drugs (NSAIDs) are as effective as narcotics in relieving the pain of renal colic.41 There are no clinically important differences in terms of rapidity of action or magnitude of relief. A variety of types of medications, dosages, and routes of administration have been compared, but there is no one clearly superior approach.41 Local active warming may also be an adjunctive treatment.42 Newer medications that may be effective include antispasmodics,43 α-blockers,44 trigger point injection with lidocaine,45 desmopressin,46 and NSAIDs combined with nitrates.47 However, data on the utility of these newer interventions are limited and more studies are needed. Intravenous fluids are routinely given for volume repletion, and some experts believe this will increase the likelihood of stone passage,48 but no prospective data are available.

Alkalinization of the urine may be effective for acutely treating ureteral uric acid stones,49 but these are not nearly as common as calcium-based stones. For Ms P, alkalinization would not be indicated because her stone was radiopaque and therefore likely calcium-based since pure uric acid stones are radiolucent by KUB. In fact, if the stone included calcium phosphate, alkalinization could actually increase the stone size.13

Treatment algorithms have been published,50 but none are widely accepted at this time.

The Urologist’s Role and Surgical Treatment

The urologist should assist in the conservative management of the patient in the acute care setting. If the stone does not pass rapidly, the patient can be sent home with appropriate oral analgesics and instructions to return for fever or uncontrollable pain. Most urologists wait several days before intervening unless there is evidence of urinary tract infection, low likelihood the stone will pass spontaneously (eg, stone >6 mm), presence of an anatomic abnormality that would prevent passage, or intractable pain.51 The initial approach is not necessarily stone removal, but relieving obstruction. Ureteral stents may be placed cystoscopically but require anesthesia, can be quite uncomfortable, and not infrequently cause gross hematuria. Stents sometimes help with stone passage,52 but the procedure may push the stone back up into the renal pelvis, which may help with subsequent treatment by lithotripsy.53

Options for stone removal are driven by stone size, location, and composition; urinary tract anatomy; availability of technology; and the experience of the urologist. Extracorporeal shock wave lithotripsy is the least invasive; it is most effective for stones that are smaller than 2 cm, located in the renal pelvis, and composed of calcium oxalate dihydrate, apatite, uric acid, or struvite. Results of studies of effectiveness must be compared with caution because the success of treatment is not uniformly defined.51 If available, ESWL for acute ureteral colic may be successful and reduce the morbidity associated with stone passage.54

Cystoscopic stone removal, by either basket extraction or fragmentation, is invasive but effective and can now be used to remove stones even in the kidney.55 Percutaneous nephrostolithotomy is more invasive but is necessary for large stone burdens or stones that cannot be removed cystoscopically; this is the gold standard for making a patient stone free.56 Fortunately, it is quite rare that a patient would require open ureterolithotomy or nephrolithotomy.

The treatment of existing stones in morbidly obese individuals is challenging. The ability to image the urinary tract may be limited if the patient’s size prohibits access to scanning by CT. Extracorporeal shock wave lithotripsy may not be an option, as morbid obesity may impede stone localization and the ability of the shock waves to reach the calculus. Percutaneous approaches can be used but may be more difficult in the morbidly obese patient; thus, the preferred approach is ureteroscopy.57

Selecting Treatment Options

Percutaneous removal is clearly superior56 in terms of efficacy but also is the most invasive of commonly used methods, adding substantially to cost and morbidity. Treatment with ESWL is effective for most stone formers, does not require an overnight hospitalization (and can be done in some urologists’ offices with minimal or no anesthesia), and allows the patient to return to normal functioning within 1 to 2 days. For stones smaller than 2 cm, ESWL may be the most cost-efficient initial therapy58 ; however, the difference likely diminishes as the stone size approaches 2 cm. With the ongoing improvement in cystoscope technology, more urologists are using cystoscopy as the initial approach, as it may reduce the need for retreatment and morbidity of stone passage often seen with ESWL, although no data on efficacy are currently available.

Prevention

Kidney stones are preventable and thus the evaluation should be directed toward determining the cause of stone formation with the goal of devising an appropriate individualized prevention program. The evaluation should include the following: (1) history (stone number and type, interventions, previous treatments); (2) physical examination (although this rarely provides information on etiology of stone formation, it may uncover another cause of chronic pain that is attributed by the patient to nephrolithiasis); and (3) laboratory measurements. In addition to serum chemistries to assess renal function (creatinine level), presence of metabolic acidosis (total carbon dioxide concentration), and a screen for hyperparathyroidism (calcium and phosphorus concentrations), the cornerstone of the evaluation is the 24-hour urine collection. I do not measure parathyroid hormone or vitamin D levels initially; if the patient has a high urine calcium concentration, then I will test for parathyroid hormone level.13

The 24-hour urine collection is an essential component of the evaluation. Because I ask patients to wait at least 6 weeks before performing the collections to allow time for the patient’s diet to revert to the usual after an acute episode of renal colic, I do not give specific dietary advice until after the collections are completed. Too often patients have been put on restricted diets with little or no justification (eg, a low-oxalate diet prescribed for a patient who has a low urine oxalate level on their usual diet). While the patient consumes his/her usual diet, two 24-hour urine collections should be performed because of the substantial day-to-day variability in the values. Just as a single blood pressure reading is insufficient for a diagnosis of hypertension, a single 24-hour urine collection is inadequate for the medical evaluation of nephrolithiasis.37 Although some experts recommend calcium restriction and loading tests, I do not feel this is necessary because it does not influence the recommendations for dietary changes or the choice of medication. Total urine volume, calcium, oxalate, citrate, uric acid, sodium,potassium, phosphorus, pH, and creatinine should be assessed.27 If the stone type is unknown, cystine should be measured as well. Some laboratories will calculate the relative supersaturation based on the measurements of the urine factors; the relative supersaturation values can be used to guide the impact of therapy.59

Treatment recommendations depend on the circumstances of stone formation and test results. Stones can remain asymptomatic for years,60 so it is often impossible to know when the stone that brought the patient to medical attention actually formed. The current metabolic evaluation may be completely normal and, in that setting, I recommend no changes in lifestyle. Because the likelihood of recurrence cannot be predicted perfectly based on the urine chemistries, I do recommend that patients undergo an imaging study annually for several years to make sure the patient is not an active stone former, although no studies have addressed this issue. For patients at risk for stone recurrence, I prefer to attempt lifestyle modification first, tailoring the recommendation according to stone type and urine chemistries. Urinary uric acid can be reduced by decreasing protein intake. Urine citrate can be increased by increasing intake of potential base (fruits and vegetables) and decreasing acid-producing foods such as animal protein. There is no evidence that dietary calcium restriction alone is helpful and substantial evidence that it is harmful.3 ,6 ,61 Based on the urine volume, I prescribe the number of additional 8-oz glasses of fluid to drink each day with the goal of producing about 2 L of urine daily to decrease the risk of stone formation and recurrence.11 ,62 - 63 For individuals who have had a calcium-containing stone and who take calcium supplements, if they wish to continue the supplement, I measure 24-hour urine chemistries on and off the supplement. The attributable risk due to a calcium supplement is low.6

If dietary recommendations are unsuccessful in modifying the urine composition, then medication is indicated. The 3 most commonly used classes of medications for stone prevention are (1) thiazides, used to reduce urine calcium excretion (eg, chlorthalidone, hydrochlorothiazide), (2) alkali, used to increase urine citrate excretion (eg, potassium citrate), and (3) allopurinol, used to reduce urine uric acid excretion. For patients with elevated urinary calcium levels, particularly with low urine volume, and who do not have excessive calcium intake, I recommend starting a thiazide-type diuretic. Thiazides have been demonstrated in randomized controlled trials to reduce the likelihood of stone recurrence by 50%64 and also to help maintain bone density,65 - 66 so patients who have had stones and who have low bone mineral density or are at risk for osteoporosis can benefit from both effects of thiazides. Citrate salts and allopurinol have been shown in small randomized trials to reduce the likelihood of calcium oxalate stone recurrence by about 50% in individuals with low urine citrate67 and hyperuricosuria,68 respectively. Specific medications for cystine stones (eg, tiopronin) and struvite stones (eg, acetohydroxamic acid) are available, but a specialist should prescribe these due to their potential toxicity.69

Long-term adherence with recommendations is suboptimal,70 but this should not discourage attempts to provide appropriate advice.

Future research about this preventable disease should focus on developing detailed information on the oxalate content of foods and improving understanding of the dietary, environmental, and genetic influences on stone formation, the etiology of stone formation including hypercalciuria, and the events involved in the initiation of stone formation.

What Would You Recommend for Ms P?

A stone of the size Ms P has should be removed, but it is not urgent as long as it is not infected or causing intractable pain. It is hard to know whether her back pain is due to the stone or is muscular in origin. Extracorporeal shock wave lithotripsy alone is very unlikely to make her stone free because of the large stone size and the potential difficulty of focusing the shock waves due to her large body size; thus, at least 1 additional intervention would be necessary. A percutaneous approach would be the optimal intervention, but her body size may also preclude this option. Ureterorenoscopy is probably the best initial choice, as this approach is less affected by body size and direct visualization would increase the likelihood of making her stone free. Any passed or retrieved fragments should be collected and sent for chemical analysis.

I would discontinue the alkalinization of her urine, as it is unlikely to helpful and could be harmful. After the stone is removed, she should undergo metabolic evaluation to guide recommendations for prevention of new stone formation. Because higher body mass index is independently associated with an increased risk of stone formation,22 - 23 strategies for weight loss should also be discussed.

A PHYSICIAN: I’ve always been a subscriber to the lore that forcing the patient to have nocturia is a good thing because a patient who forms saturated urine at night is more likely to form stones. Are there any data that substantiate this practice?

DR CURHAN: The short answer is no; however, if you can maintain low urine concentration throughout the day, that’s a good idea. The first morning urine in most people is the most concentrated and if they’re sleeping for 8 hours, then crystals may form. Calcium oxalate crystals, once they form, don’t dissolve. So there is theoretical evidence to suggest this practice would be beneficial. The reasons that I don’t recommend it are several. First, I wouldn’t want to be waking up several times per night to prevent stones for the rest of my life. Second, it’s not clear whether they should just be drinking after meals. For example, after you eat an oxalate load, the level goes up in the blood, peaks, and comes down.71 It may be that the stone-forming periods are right after ingestion of certain meals. But that’s all theoretical at this point.

A PHYSICIAN: Would you comment on stone size and when you would recommend performing a procedure to remove a stone?

DR CURHAN: In acute colic, which is different from our patient, if you have a ureteral stone that is 6 mm or less and not moving, usually the urologist will wait for 48, 72, sometimes 96 hours, assuming there isn’t evidence of infection or intractable pain.51 If the pain can’t be controlled or there’s evidence of infection, they will usually go in right away and either try to take the stone out or insert a ureteral stent to relieve the obstruction.

A PHYSICIAN: Is there any difference between the types of calcium supplementation a woman or a man might take such as calcium carbonate or calcium citrate?

DR CURHAN: There is some evidence that calcium citrate may raise the urine citrate level a little bit more than calcium carbonate, but as far as actual stone formation, I can’t tell you whether one’s different from another. For an individual who has never had a stone, I think that the use of calcium supplements is reasonable if indicated. The absolute risk for a woman who’s never had a stone is 1 per 1000 per year6 ; if you increase a supplement user’s risk by 20%, her absolute risk would increase from 1 per 1000 per year to 1.2 per 1000 per year. So the actual contribution of supplements to the problem of incident stone disease is relatively small. If someone’s had a stone, before I start them on supplementation, I measure the urine chemistries on and off the supplements to see whether it makes a difference. There are some people whose urine calcium values are much higher when taking a calcium supplement. For many people, you’d be surprised that the urine calcium hardly changes at all.

A PHYSICIAN: Why is it important that her stone come out? We sometimes see calcium stones on CT scans. Should we go invade them all?

DR CURHAN: Her stone needs to be removed because of its size. When a stone of this size moves, it may cause obstruction of the ureteropelvic junction and then she’s going to have a medical emergency.51 Even if it does not cause ureteropelvic junction obstruction, other reasons to remove the stone include that it will likely continue to get bigger and become even more difficult to remove. Is there any evidence that it should be removed in a certain period of time? I can’t tell you. There are studies of individuals with asymptomatic stones and how likely they are to become symptomatic.60 Just under half of individuals with asymptomatic stones will become symptomatic over a 5-year period.60 For all the incidental stones that we find, most urologists won’t touch anything that’s asymptomatic if it’s 6 mm or less. If it’s more than that, or certainly if it’s a centimeter or more, most urologists would recommend “prophylactic lithotripsy,” but I can’t provide you with any data that support this plan.

Corresponding Author: Gary Curhan, MD, ScD, Channing Laboratory, 181 Longwood, Third Floor, Brigham and Women's Hospital, Boston, MA 02115 (gcurhan@partners.org).

Financial Disclosures: None reported.

Funding/Support: This Clinical Crossroads is made possible in part by a grant from the Jacqueline and Martin J. Shaevel Charitable Trust. Dr Curhan was supported in part by grant DK59583 from the National Institutes of Health.

Role of the Sponsor: The National Institutes of Health did not participate in the design and conduct of the study; in the collection, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript.

Acknowledgement: We thank the patient for sharing her story. The helical CT image was kindly provided by Drs Peter Mueller and Mukesh Harisinghani at Massachusetts General Hospital, Boston.

This conference took place at the Medicine Grand Rounds of Beth Israel Deaconess Medical Center, Boston, Mass, on March 4, 2004.

Clinical Crossroads at Beth Israel Deaconess Medical Center is produced and edited by Risa B. Burns, MD, Eileen E. Reynolds, MD, and Amy N. Ship, MD. Tom Delbanco, MD, is series editor.

Stamatelou KK, Francis ME, Jones CA, Nyberg LM, Curhan GC. Time trends in reported prevalence of kidney stones in the United States: 1976-1994.  Kidney Int. 2003;631817-1823
PubMed
Johnson CM, Wilson DM, O’Fallon WM, Malek RS, Kurland LT. Renal stone epidemiology: a 25-year study in Rochester, Minnesota.  Kidney Int. 1979;16624-631
PubMed
Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones.  N Engl J Med. 1993;328833-838
PubMed
Hiatt RA, Dales LG, Friedman GD, Hunkeler EM. Frequency of urolithiasis in a prepaid medical care program.  Am J Epidemiol. 1982;115255-265
PubMed
Curhan GC, Willett WC, Knight EL, Stampfer MJ. Dietary factors and the risk of incident kidney stones in younger women (Nurses’ Health Study II).  Arch Intern Med. 2004;164885-891
PubMed
Curhan G, Willett W, Speizer F, Spiegelman D, Stampfer M. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.  Ann Intern Med. 1997;126497-504
PubMed
Coe FL, Keck J, Norton ER. The natural history of calcium urolithiasis.  JAMA. 1977;2381519-1523
PubMed
Williams RE. Long-term survey of 538 patients with upper urinary tract stones.  Br J Urol. 1963;35416-437
PubMed
Ljunghall S, Danielson BG. A prospective study of renal stone recurrences.  Br J Urol. 1984;56122-124
PubMed
Hiatt R, Ettinger B, Caan B, Quesenberry C Jr, Duncan D, Citron J. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones.  Am J Epidemiol. 1996;14425-33
PubMed
Borghi L, Meschi T, Amato F, Briganti A, Novarini A, Giannini A. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study.  J Urol. 1996;155839-843
PubMed
Pearle M, Calhoun E, Curhan GC. Urolithiasis. In: Litwin MS, Saigal, CS, eds. Urologic Diseases in America. Washington, DC: US Dept of Health and Human Services, Public Health Service, National Institute of Diabetes and Digestive and Kidney Diseases; 2004
Coe F, , Parks J, . Nephrolithiasis: Pathogenesis and Treatment. Chicago, Ill: Year Book Medical; 1988
Shekarriz B, Stoller ML. Cystinuria and other noncalcareous calculi.  Endocrinol Metab Clin North Am. 2002;31951-977
PubMed
Rodman JS. Prophylaxis of uric acid stones with alternate day doses of alkaline potassium salts.  J Urol. 1991;14597-99
PubMed
Cohen TD, Preminger GM. Struvite calculi.  Semin Nephrol. 1996;16425-434
PubMed
Scheinman SJ. Nephrolithiasis.  Semin Nephrol. 1999;19381-388
PubMed
Moe OW, Abate N, Sakhaee K. Pathophysiology of uric acid nephrolithiasis.  Endocrinol Metab Clin North Am. 2002;31895-914
PubMed
Rodman JS. Struvite stones.  Nephron. 1999;81(suppl 1)  50-59
PubMed
Nadler RB, Rubenstein JN, Eggener SE, Loor MM, Smith ND. The etiology of urolithiasis in HIV infected patients.  J Urol. 2003;169475-477
PubMed
Evan AP, Lingeman JE, Coe FL.  et al.  Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle.  J Clin Invest. 2003;111607-616
PubMed
Curhan GC, Willett WC, Rimm EB, Speizer FE, Stampfer MJ. Body size and risk of kidney stones.  J Am Soc Nephrol. 1998;91645-1652
PubMed
Taylor EN, Stampfer MJ, Curhan GC. Obesity, weight gain, and the risk of kidney stones.  JAMA. 2005;293455-462
PubMed
Kramer HJ, Choi HK, Atkinson K, Stampfer M, Curhan GC. The association between gout and nephrolithiasis in men: the Health Professionals’ Follow-Up Study.  Kidney Int. 2003;641022-1026
PubMed
Travaglini F, Bartoletti R, Gacci M, Rizzo M. Pathophysiology of reno-ureteral colic.  Urol Int. 2004;72(suppl 1)  20-23
PubMed
Gupta MSM. Acute and chronic renal pain. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:463-500
Asplin J, Chandhoke PS. The stone forming patient. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:773-786
Li J, Kennedy D, Levine M, Kumar A, Mullen J. Absent hematuria and expensive computerized tomography: case characteristics of emergency urolithiasis.  J Urol. 2001;165782-784
PubMed
Vieweg J, Teh C, Freed K.  et al.  Unenhanced helical computerized tomography for the evaluation of patients with acute flank pain.  J Urol. 1998;160679-684
PubMed
Lang EK, Macchia RJ, Thomas R.  et al.  Improved detection of renal pathologic features on multiphasic helical CT compared with IVU in patients presenting with microscopic hematuria.  Urology. 2003;61528-532
PubMed
Wong SK, Ng LG, Tan BS.  et al.  Acute renal colic: value of unenhanced spiral computed tomography compared with intravenous urography.  Ann Acad Med Singapore. 2001;30568-572
PubMed
Sheafor DH, Hertzberg BS, Freed KS.  et al.  Nonenhanced helical CT and US in the emergency evaluation of patients with renal colic: prospective comparison.  Radiology. 2000;217792-797
PubMed
Pearle MS, Watamull LM, Mullican MA. Sensitivity of noncontrast helical computerized tomography and plain film radiography compared to flexible nephroscopy for detecting residual fragments after percutaneous nephrostolithotomy.  J Urol. 1999;16223-26
PubMed
Fowler KA, Locken JA, Duchesne JH, Williamson MR. US for detecting renal calculi with nonenhanced CT as a reference standard.  Radiology. 2002;222109-113
PubMed
Uribarri J, Oh MS, Carroll HJ. The first kidney stone.  Ann Intern Med. 1989;1111006-1009
PubMed
Smith CL. When should the stone patient be evaluated? early evaluation of single stone formers.  Med Clin North Am. 1984;68455-459
PubMed
Parks JH, Goldfisher E, Asplin JR, Coe FL. A single 24-hour urine collection is inadequate for the medical evaluation of nephrolithiasis.  J Urol. 2002;1671607-1612
PubMed
Pak CY, Poindexter JR, Adams-Huet B, Pearle MS. Predictive value of kidney stone composition in the detection of metabolic abnormalities.  Am J Med. 2003;11526-32
PubMed
Chandhoke PS. When is medical prophylaxis cost-effective for recurrent calcium stones?  J Urol. 2002;168937-940
PubMed
Parks JH, Coe FL. The financial effects of kidney stone prevention.  Kidney Int. 1996;501706-1712
PubMed
Labrecque M, Dostaler LP, Rousselle R, Nguyen T, Poirier S. Efficacy of nonsteroidal anti-inflammatory drugs in the treatment of acute renal colic: a meta-analysis.  Arch Intern Med. 1994;1541381-1387
PubMed
Kober A, Dobrovits M, Djavan B.  et al.  Local active warming: an effective treatment for pain, anxiety and nausea caused by renal colic.  J Urol. 2003;170741-744
PubMed
Romics I, Molnar DL, Timberg G.  et al.  The effect of drotaverine hydrochloride in acute colicky pain caused by renal and ureteric stones.  BJU Int. 2003;9292-96
PubMed
Cervenakov I, Fillo J, Mardiak J, Kopecny M, Smirala J, Lepies P. Speedy elimination of ureterolithiasis in lower part of ureters with the alpha 1-blocker-Tamsulosin.  Int Urol Nephrol. 2002;3425-29
PubMed
Iguchi M, Katoh Y, Koike H, Hayashi T, Nakamura M. Randomized trial of trigger point injection for renal colic.  Int J Urol. 2002;9475-479
PubMed
Lopes T, Dias JS, Marcelino J, Varela J, Ribeiro S, Dias J. An assessment of the clinical efficacy of intranasal desmopressin spray in the treatment of renal colic.  BJU Int. 2001;87322-325
PubMed
Kekec Z, Yilmaz U, Sozuer E. The effectiveness of tenoxicam vs isosorbide dinitrate plus tenoxicam in the treatment of acute renal colic.  BJU Int. 2000;85783-785
PubMed
Bihl G, Meyers A. Recurrent renal stone disease—advances in pathogenesis and clinical management.  Lancet. 2001;358651-656
PubMed
Rodman JS, Sosa RE, Lopez MA. Diagnosis and treatment of uric acid calculi. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:973-989
Teichman JM. Acute renal colic from ureteral calculus.  N Engl J Med. 2004;350684-693
PubMed
Curhan GC, Fitzpatrick JM. Nephrolithiasis: lithotripsy and surgery. In: Brady HR, Wilcox C, eds. Therapy in Nephrology and Hypertension. 2nd ed. New York, NY: Elsevier Science; 2003:405-411
Chandhoke PS, Barqawi AZ, Wernecke C, Chee-Awai RA. A randomized outcomes trial of ureteral stents for extracorporeal shock wave lithotripsy of solitary kidney or proximal ureteral stones.  J Urol. 2002;1671981-1983
PubMed
Mueller SC, Wilbert D, Thueroff JW, Alken P. Extracorporeal shock wave lithotripsy of ureteral stones: clinical experience and experimental findings.  J Urol. 1986;135831-834
PubMed
Tligui M, El Khadime MR, Tchala K.  et al.  Emergency extracorporeal shock wave lithotripsy (ESWL) for obstructing ureteral stones.  Eur Urol. 2003;43552-555
PubMed
Rudnick DM, Bennett PM, Dretler SP. Retrograde renoscopic fragmentation of moderate-size (1.5-3.0-cm) renal cystine stones.  J Endourol. 1999;13483-485
PubMed
Albala DM, Assimos DG, Clayman RV.  et al.  Lower pole I: a prospective randomized trial of extracorporeal shock wave lithotripsy and percutaneous nephrostolithotomy for lower pole nephrolithiasis—initial results.  J Urol. 2001;1662072-2080
PubMed
Aso Y, Minowada S. Management of ureteral calculi. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:651-663
May DJ, Chandhoke PS. Efficacy and cost-effectiveness of extracorporeal shock wave lithotripsy for solitary lower pole renal calculi.  J Urol. 1998;15924-27
PubMed
Asplin J, Parks J, Lingeman J.  et al.  Supersaturation and stone composition in a network of dispersed treatment sites.  J Urol. 1998;1591821-1825
PubMed
Glowacki LS, Beecroft ML, Cook RJ, Pahl D, Churchill DN. The natural history of asymptomatic urolithiasis.  J Urol. 1992;147319-321
PubMed
Borghi L, Schianchi T, Meschi T.  et al.  Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria.  N Engl J Med. 2002;34677-84
PubMed
Curhan G, Willett W, Rimm E, Spiegelman D, Stampfer M. Prospective study of beverage use and the risk of kidney stones.  Am J Epidemiol. 1996;143240-247
PubMed
Curhan GC, Willett WC, Speizer FE, Stampfer MJ. Beverage use and risk for kidney stones in women.  Ann Intern Med. 1998;128534-540
PubMed
Coe FL, Parks JH. Medical management of nephrolithiasis. In: Brady HR, Wilcox C, eds. Therapy in Nephrology and Hypertension. 2nd ed. New York, NY: Elsevier Science; 2003:399-403
Reid IR, Ames RW, Orr-Walker BJ.  et al.  Hydrochlorothiazide reduces loss of cortical bone in normal postmenopausal women: a randomized controlled trial.  Am J Med. 2000;109362-370
PubMed
LaCroix AZ, Ott SM, Ichikawa L, Scholes D, Barlow WE. Low-dose hydrochlorothiazide and preservation of bone mineral density in older adults: a randomized, double-blind, placebo-controlled trial.  Ann Intern Med. 2000;133516-526
PubMed
Barcelo P, Wuhl O, Servitge E, Rousaud A, Pak CY. Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis.  J Urol. 1993;1501761-1764
PubMed
Ettinger B, Tang A, Citron JT, Livermore B, Williams T. Randomized trial of allopurinol in the prevention of calcium oxalate calculi.  N Engl J Med. 1986;3151386-1389
PubMed
Williams JJ, Rodman JS, Peterson CM. A randomized double-blind study of acetohydroxamic acid in struvite nephrolithiasis.  N Engl J Med. 1984;311760-764
PubMed
Parks JH, Asplin JR, Coe FL. Patient adherence to long-term medical treatment of kidney stones.  J Urol. 2001;1662057-2060
PubMed
Schwille PO, Hanisch E, Scholz D. Postprandial hyperoxaluria and intestinal oxalate absorption in idiopathic renal stone disease.  J Urol. 1984;132650-655
PubMed

First Page Preview

First page PDF preview

Figures

Figure. Helical Computed Tomographic Scan of the Upper Abdomen
Grahic Jump Location

High-resolution helical computed tomographic image demonstrating a stone in the right renal pelvis and a smaller stone in the left kidney (arrowheads). There is no hydronephrosis.

Tables

Interactive Graphics

Video

Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal

Stamatelou KK, Francis ME, Jones CA, Nyberg LM, Curhan GC. Time trends in reported prevalence of kidney stones in the United States: 1976-1994.  Kidney Int. 2003;631817-1823
PubMed
Johnson CM, Wilson DM, O’Fallon WM, Malek RS, Kurland LT. Renal stone epidemiology: a 25-year study in Rochester, Minnesota.  Kidney Int. 1979;16624-631
PubMed
Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones.  N Engl J Med. 1993;328833-838
PubMed
Hiatt RA, Dales LG, Friedman GD, Hunkeler EM. Frequency of urolithiasis in a prepaid medical care program.  Am J Epidemiol. 1982;115255-265
PubMed
Curhan GC, Willett WC, Knight EL, Stampfer MJ. Dietary factors and the risk of incident kidney stones in younger women (Nurses’ Health Study II).  Arch Intern Med. 2004;164885-891
PubMed
Curhan G, Willett W, Speizer F, Spiegelman D, Stampfer M. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.  Ann Intern Med. 1997;126497-504
PubMed
Coe FL, Keck J, Norton ER. The natural history of calcium urolithiasis.  JAMA. 1977;2381519-1523
PubMed
Williams RE. Long-term survey of 538 patients with upper urinary tract stones.  Br J Urol. 1963;35416-437
PubMed
Ljunghall S, Danielson BG. A prospective study of renal stone recurrences.  Br J Urol. 1984;56122-124
PubMed
Hiatt R, Ettinger B, Caan B, Quesenberry C Jr, Duncan D, Citron J. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones.  Am J Epidemiol. 1996;14425-33
PubMed
Borghi L, Meschi T, Amato F, Briganti A, Novarini A, Giannini A. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study.  J Urol. 1996;155839-843
PubMed
Pearle M, Calhoun E, Curhan GC. Urolithiasis. In: Litwin MS, Saigal, CS, eds. Urologic Diseases in America. Washington, DC: US Dept of Health and Human Services, Public Health Service, National Institute of Diabetes and Digestive and Kidney Diseases; 2004
Coe F, , Parks J, . Nephrolithiasis: Pathogenesis and Treatment. Chicago, Ill: Year Book Medical; 1988
Shekarriz B, Stoller ML. Cystinuria and other noncalcareous calculi.  Endocrinol Metab Clin North Am. 2002;31951-977
PubMed
Rodman JS. Prophylaxis of uric acid stones with alternate day doses of alkaline potassium salts.  J Urol. 1991;14597-99
PubMed
Cohen TD, Preminger GM. Struvite calculi.  Semin Nephrol. 1996;16425-434
PubMed
Scheinman SJ. Nephrolithiasis.  Semin Nephrol. 1999;19381-388
PubMed
Moe OW, Abate N, Sakhaee K. Pathophysiology of uric acid nephrolithiasis.  Endocrinol Metab Clin North Am. 2002;31895-914
PubMed
Rodman JS. Struvite stones.  Nephron. 1999;81(suppl 1)  50-59
PubMed
Nadler RB, Rubenstein JN, Eggener SE, Loor MM, Smith ND. The etiology of urolithiasis in HIV infected patients.  J Urol. 2003;169475-477
PubMed
Evan AP, Lingeman JE, Coe FL.  et al.  Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle.  J Clin Invest. 2003;111607-616
PubMed
Curhan GC, Willett WC, Rimm EB, Speizer FE, Stampfer MJ. Body size and risk of kidney stones.  J Am Soc Nephrol. 1998;91645-1652
PubMed
Taylor EN, Stampfer MJ, Curhan GC. Obesity, weight gain, and the risk of kidney stones.  JAMA. 2005;293455-462
PubMed
Kramer HJ, Choi HK, Atkinson K, Stampfer M, Curhan GC. The association between gout and nephrolithiasis in men: the Health Professionals’ Follow-Up Study.  Kidney Int. 2003;641022-1026
PubMed
Travaglini F, Bartoletti R, Gacci M, Rizzo M. Pathophysiology of reno-ureteral colic.  Urol Int. 2004;72(suppl 1)  20-23
PubMed
Gupta MSM. Acute and chronic renal pain. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:463-500
Asplin J, Chandhoke PS. The stone forming patient. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:773-786
Li J, Kennedy D, Levine M, Kumar A, Mullen J. Absent hematuria and expensive computerized tomography: case characteristics of emergency urolithiasis.  J Urol. 2001;165782-784
PubMed
Vieweg J, Teh C, Freed K.  et al.  Unenhanced helical computerized tomography for the evaluation of patients with acute flank pain.  J Urol. 1998;160679-684
PubMed
Lang EK, Macchia RJ, Thomas R.  et al.  Improved detection of renal pathologic features on multiphasic helical CT compared with IVU in patients presenting with microscopic hematuria.  Urology. 2003;61528-532
PubMed
Wong SK, Ng LG, Tan BS.  et al.  Acute renal colic: value of unenhanced spiral computed tomography compared with intravenous urography.  Ann Acad Med Singapore. 2001;30568-572
PubMed
Sheafor DH, Hertzberg BS, Freed KS.  et al.  Nonenhanced helical CT and US in the emergency evaluation of patients with renal colic: prospective comparison.  Radiology. 2000;217792-797
PubMed
Pearle MS, Watamull LM, Mullican MA. Sensitivity of noncontrast helical computerized tomography and plain film radiography compared to flexible nephroscopy for detecting residual fragments after percutaneous nephrostolithotomy.  J Urol. 1999;16223-26
PubMed
Fowler KA, Locken JA, Duchesne JH, Williamson MR. US for detecting renal calculi with nonenhanced CT as a reference standard.  Radiology. 2002;222109-113
PubMed
Uribarri J, Oh MS, Carroll HJ. The first kidney stone.  Ann Intern Med. 1989;1111006-1009
PubMed
Smith CL. When should the stone patient be evaluated? early evaluation of single stone formers.  Med Clin North Am. 1984;68455-459
PubMed
Parks JH, Goldfisher E, Asplin JR, Coe FL. A single 24-hour urine collection is inadequate for the medical evaluation of nephrolithiasis.  J Urol. 2002;1671607-1612
PubMed
Pak CY, Poindexter JR, Adams-Huet B, Pearle MS. Predictive value of kidney stone composition in the detection of metabolic abnormalities.  Am J Med. 2003;11526-32
PubMed
Chandhoke PS. When is medical prophylaxis cost-effective for recurrent calcium stones?  J Urol. 2002;168937-940
PubMed
Parks JH, Coe FL. The financial effects of kidney stone prevention.  Kidney Int. 1996;501706-1712
PubMed
Labrecque M, Dostaler LP, Rousselle R, Nguyen T, Poirier S. Efficacy of nonsteroidal anti-inflammatory drugs in the treatment of acute renal colic: a meta-analysis.  Arch Intern Med. 1994;1541381-1387
PubMed
Kober A, Dobrovits M, Djavan B.  et al.  Local active warming: an effective treatment for pain, anxiety and nausea caused by renal colic.  J Urol. 2003;170741-744
PubMed
Romics I, Molnar DL, Timberg G.  et al.  The effect of drotaverine hydrochloride in acute colicky pain caused by renal and ureteric stones.  BJU Int. 2003;9292-96
PubMed
Cervenakov I, Fillo J, Mardiak J, Kopecny M, Smirala J, Lepies P. Speedy elimination of ureterolithiasis in lower part of ureters with the alpha 1-blocker-Tamsulosin.  Int Urol Nephrol. 2002;3425-29
PubMed
Iguchi M, Katoh Y, Koike H, Hayashi T, Nakamura M. Randomized trial of trigger point injection for renal colic.  Int J Urol. 2002;9475-479
PubMed
Lopes T, Dias JS, Marcelino J, Varela J, Ribeiro S, Dias J. An assessment of the clinical efficacy of intranasal desmopressin spray in the treatment of renal colic.  BJU Int. 2001;87322-325
PubMed
Kekec Z, Yilmaz U, Sozuer E. The effectiveness of tenoxicam vs isosorbide dinitrate plus tenoxicam in the treatment of acute renal colic.  BJU Int. 2000;85783-785
PubMed
Bihl G, Meyers A. Recurrent renal stone disease—advances in pathogenesis and clinical management.  Lancet. 2001;358651-656
PubMed
Rodman JS, Sosa RE, Lopez MA. Diagnosis and treatment of uric acid calculi. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:973-989
Teichman JM. Acute renal colic from ureteral calculus.  N Engl J Med. 2004;350684-693
PubMed
Curhan GC, Fitzpatrick JM. Nephrolithiasis: lithotripsy and surgery. In: Brady HR, Wilcox C, eds. Therapy in Nephrology and Hypertension. 2nd ed. New York, NY: Elsevier Science; 2003:405-411
Chandhoke PS, Barqawi AZ, Wernecke C, Chee-Awai RA. A randomized outcomes trial of ureteral stents for extracorporeal shock wave lithotripsy of solitary kidney or proximal ureteral stones.  J Urol. 2002;1671981-1983
PubMed
Mueller SC, Wilbert D, Thueroff JW, Alken P. Extracorporeal shock wave lithotripsy of ureteral stones: clinical experience and experimental findings.  J Urol. 1986;135831-834
PubMed
Tligui M, El Khadime MR, Tchala K.  et al.  Emergency extracorporeal shock wave lithotripsy (ESWL) for obstructing ureteral stones.  Eur Urol. 2003;43552-555
PubMed
Rudnick DM, Bennett PM, Dretler SP. Retrograde renoscopic fragmentation of moderate-size (1.5-3.0-cm) renal cystine stones.  J Endourol. 1999;13483-485
PubMed
Albala DM, Assimos DG, Clayman RV.  et al.  Lower pole I: a prospective randomized trial of extracorporeal shock wave lithotripsy and percutaneous nephrostolithotomy for lower pole nephrolithiasis—initial results.  J Urol. 2001;1662072-2080
PubMed
Aso Y, Minowada S. Management of ureteral calculi. In: Coe FL, Favus MJ, Pak CY, Parks JH, Preminger GM, eds. Kidney Stones: Medical and Surgical Management. Philadelphia, Pa: Lippincott-Raven; 1996:651-663
May DJ, Chandhoke PS. Efficacy and cost-effectiveness of extracorporeal shock wave lithotripsy for solitary lower pole renal calculi.  J Urol. 1998;15924-27
PubMed
Asplin J, Parks J, Lingeman J.  et al.  Supersaturation and stone composition in a network of dispersed treatment sites.  J Urol. 1998;1591821-1825
PubMed
Glowacki LS, Beecroft ML, Cook RJ, Pahl D, Churchill DN. The natural history of asymptomatic urolithiasis.  J Urol. 1992;147319-321
PubMed
Borghi L, Schianchi T, Meschi T.  et al.  Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria.  N Engl J Med. 2002;34677-84
PubMed
Curhan G, Willett W, Rimm E, Spiegelman D, Stampfer M. Prospective study of beverage use and the risk of kidney stones.  Am J Epidemiol. 1996;143240-247
PubMed
Curhan GC, Willett WC, Speizer FE, Stampfer MJ. Beverage use and risk for kidney stones in women.  Ann Intern Med. 1998;128534-540
PubMed
Coe FL, Parks JH. Medical management of nephrolithiasis. In: Brady HR, Wilcox C, eds. Therapy in Nephrology and Hypertension. 2nd ed. New York, NY: Elsevier Science; 2003:399-403
Reid IR, Ames RW, Orr-Walker BJ.  et al.  Hydrochlorothiazide reduces loss of cortical bone in normal postmenopausal women: a randomized controlled trial.  Am J Med. 2000;109362-370
PubMed
LaCroix AZ, Ott SM, Ichikawa L, Scholes D, Barlow WE. Low-dose hydrochlorothiazide and preservation of bone mineral density in older adults: a randomized, double-blind, placebo-controlled trial.  Ann Intern Med. 2000;133516-526
PubMed
Barcelo P, Wuhl O, Servitge E, Rousaud A, Pak CY. Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis.  J Urol. 1993;1501761-1764
PubMed
Ettinger B, Tang A, Citron JT, Livermore B, Williams T. Randomized trial of allopurinol in the prevention of calcium oxalate calculi.  N Engl J Med. 1986;3151386-1389
PubMed
Williams JJ, Rodman JS, Peterson CM. A randomized double-blind study of acetohydroxamic acid in struvite nephrolithiasis.  N Engl J Med. 1984;311760-764
PubMed
Parks JH, Asplin JR, Coe FL. Patient adherence to long-term medical treatment of kidney stones.  J Urol. 2001;1662057-2060
PubMed
Schwille PO, Hanisch E, Scholz D. Postprandial hyperoxaluria and intestinal oxalate absorption in idiopathic renal stone disease.  J Urol. 1984;132650-655
PubMed
CME Course for: March 2, 2005: A 44-Year-Old Woman With Kidney Stones


You need to register in order to view this quiz.
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s “Cited By” API will populate this tab (http://www.crossref.org/citedby.html).
Submit a Response

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Topics
PubMed Articles