eMedicine Specialties > Radiology > Genitourinary

Nephrolithiasis/Urolithiasis

Author: J Kevin Smith, MD, PhD, Vice Chairman for Veterans Affairs, Associate Professor, Department of Diagnostic Radiology, University of Alabama at Birmingham
Coauthor(s): Mark E Lockhart, MD, Assistant Professor, Department of Radiology, University of Alabama at Birmingham; Nicole W Berland, BA, Outreach Support for Hurricane Relief, Collat Jewish Family Service; Philip Kenney, MD, Chief of GU Section of Diagnostic Radiology, Professor, Department of Diagnostic Radiology, University of Alabama at Birmingham
Contributor Information and Disclosures

Updated: Feb 21, 2007

Introduction

Background

Passage of a urinary stone is the most common cause of acute ureteral obstruction and affects as many as 12% of the population. The pain may be some of the most severe pain that humans experience, and complications of stone disease may result in severe infection; renal failure; or, in rare cases, death.

Pathophysiology

In patients with stone disease, more than 1 of 3 general mechanisms is likely to be active. These include the following: (1) the possible presence or abundance of substances that promote crystal and stone formation; (2) a possible relative lack of substances to inhibit crystal formation; and (3) a possible excessive excretion or concentration of salts in the urine, which leads to supersaturation of the crystallizing salt. The greater the degree of supersaturation, the greater the rate of growth of the calculi.

Stasis or anatomic factors can also contribute to the development of stone disease. These include ureteropelvic junction (UPJ) obstruction, horseshoe or ectopic kidney, autosomal dominant polycystic kidney disease, and vesicoureteral reflux. Calyceal diverticula, the result of anomalous budding of the calyceal system, is also associated with stone disease. In 10-40% of calyceal diverticula, stones are present. These range from a few large calculi to many tiny seed calculi and to the microscopic "milk of calcium."

Medullary sponge kidney is another common anatomic cause of renal calculi. The pathologic process in medullary sponge kidney is renal tubular ectasia. Calculi form in approximately 50% of patients. The calcifications form in the medulla but frequently pass into the collecting system. They are usually bilateral and diffuse, but they may also be unilateral or segmental. On intravenous urography (IVU), pyramidal clusters of calculi within the dilated tubules classically become obscured or appear enlarged after contrast material surrounds them in the dilated tubules.

Calcium stones account for 75-85% of urinary stones. Approximately one half of calcium stones are composed of a mixture of calcium oxalate and calcium phosphate. They demonstrate intermediate fragility to extracorporeal shock wave lithotripsy (ESWL). Approximately three eighths of calcium stones are formed of only calcium oxalate dihydrate. These may be spiculated, dotted, mulberry, or jackstone in appearance. Usually, these stones are fragile in response to ESWL. The remaining one eighth of stones are composed of calcium phosphate (apatite) or calcium monohydrate. These stones are the densest and, consequently, the least responsive to ESWL.

Calcium stones have numerous causes. Approximately 85% of calcium stones are idiopathic, or primary. Idiopathic hypercalciuria occurs in more than one half of patients with calcium oxalate stones. Most causes of hypercalciuria are absorptive. Increased absorption in individuals after a normal diet causes an elevation of serum calcium levels and a suppression of parathyroid function as an abnormal response to vitamin D. Approximately 10% of cases of primary hypercalciuria are renal in origin. The inability of the kidney to conserve calcium results in low serum calcium concentrations, which stimulate parathormone secretion.

The remaining 15% of calcium stones are secondary to some discernible etiology. Most commonly, they result from hyperparathyroidism, which is found in 5-10% of patients with stones. In this situation, hypercalcemia and increased absorption lead to hypercalciuria. Patients with the stones are treated with surgical removal of the parathyroid adenoma or hyperplasia. Calcium stones can also occur in approximately 15% of patients with sarcoidosis in whom the production of activated vitamin D by macrophages is abnormal.

Renal tubular acidosis (RTA) is an additional fairly common secondary cause of calcium stones. In type I (distal) RTA, kidneys have a decreased ability to lower urine pH levels, which may be primary or secondary to a variety of renal injuries. The injured distal tubule loses the ability to maintain the hydrogen-ion gradient. This, in turn, causes alkaline urine, hypercalciuria, and hyperphosphaturia. Nephrocalcinosis or urolithiasis is seen in as many as 70% of patients with type I RTA. Conversely, type II (proximal) RTA is associated with increased bicarbonate loss, which helps keep stones from forming. Type IV RTA commonly is seen in medical renal disease and does not predispose patients to stone formation.

Immobilization of an individual causes rapid mobilization of the calcium in bones, and this is an important mechanism in patients with spinal cord injury, who may develop stones within weeks to months of immobilization. Hyperoxaluria is another, less common, secondary cause of calcium stone formation and most often results from inflammatory bowel disease, bowel surgery, vitamin C overdose, or renal failure. Primary hyperoxaluria is a rare autosomal recessive disease. Other secondary causes include milk-alkali syndrome, use of steroids, Cushing syndrome, hypervitaminosis D, paraneoplastic phenomenon, and multiple myeloma.

Magnesium ammonium phosphate (struvite) stones account for approximately 10-20% of urinary stones. These stones are lucent but complex with calcium phosphate. On occasion, they enlarge and branch (staghorn). Although they fragment easily, patients with these stones usually are treated with percutaneous fragmentation and extraction because of the large size of the stones and, usually, the presence of infection. Struvite stones are caused by urea-splitting bacteria such as Proteus, Klebsiella, and Pseudomonas species. However, as many as one half of patients have an underlying metabolic cause for stone disease; therefore, metabolic evaluation is indicated. Combined obstruction and infection frequently cause renal destruction and, potentially, renal failure if both kidneys are affected.

Uric acid stones account for 5-10% of urinary stones. These small smooth stones usually appear radiolucent on conventional radiographs but opaque on CT scans. Predisposing factors include acidic concentrated urine, excess urinary uric acid, small-bowel disease or resection, gout, and cell lysis (eg, resulting from treatment of leukemia or from starvation). Treatment and prevention for these stones is alkalinization and dilution of the urine.

Cystine stones account for only approximately 1% of urinary stones. These ground-glass stones, which result from cystinuria (a rare autosomal recessive metabolic disorder), are homogeneous; less opaque; and less fragile than other stones, especially if they are smooth.

Several other less common forms of urolithiasis may produce stones that appear relatively lucent, even on CT scans. Inspissation of indinavir, an antiretroviral protease inhibitor used to treat HIV infection, may cause stones that appear lucent on CT scans. Matrix stones formed from inspissated mucoproteins in patients with a chronic Proteus infection may demonstrate soft tissue attenuation on CT scans. Stones can also be caused by metabolic byproducts and drugs (eg, sulfa drugs, salicylates, triamterene ephedrine).

Frequency

United States

Renal calculi occur in 5-12% of the American population, and they are bilateral in 10-15% of patients. The prevalence of urinary lithiasis is as high as 2-3% in the general population.

International

A slightly lower prevalence of urinary stones is found in less developed countries, possibly because of diets lower in protein.

Mortality/Morbidity

  • Passage of a renal stone is the most common cause of acute ureteral obstruction. When this occurs, pressure in the collecting system and renal blood flow acutely increase, followed by decreased blood flow after 1-2 hours. Hematuria usually occurs. This can be intermittent or persistent and microscopic or gross. However, as many as 10% of patients with acute stones may not have hematuria.
  • Acute ureteral obstruction by stone causes severe, colicky (intermittent) flank pain that can radiate throughout the groin, testicles, back, or periumbilical region. Some patients with renal calculi may have no symptoms at all. Stones smaller than 4 mm pass spontaneously in approximately 80% of patients. Stones that are 4-6 mm pass in approximately 50% of patients, whereas stones larger than 8 mm pass in only approximately 20% of patients.
  • Occasionally, recurrent infection may result in pyelonephritis or abscess. Stones can cause renal scarring, damage, or even renal failure if they are bilateral. In 10% of patients, stones recur within 1 year. This percentage increases to 50% within 10 years.

Race

Urinary stones occur more often in white populations than in black populations. They are also more prevalent in highly developed countries, possibly as a result of a higher protein diet.

Sex

Males are at a greater risk than females, with a male-to-female ratio of 3:1 (except for struvite stones and in black populations).

Age

Stones are uncommon but not unknown in children. The peak age for development is in persons aged 40-60 years.

Presentation

Acute ureteral obstruction by stone causes severe colicky (intermittent) flank pain that can radiate throughout the groin, testicles, back, and periumbilical region. Some patients with renal calculi may have no symptoms at all.

Hematuria usually occurs. It can be intermittent or persistent and microscopic or gross. However, as many as 10% of patients with acute stones may not have hematuria.

Occasionally, recurrent infection may result in pyelonephritis or abscess. Stones can result in renal scarring, damage, and renal failure.

Preferred Examination

The goals of imaging are to determine the presence of stones within the urinary tract, evaluate for complications, estimate the likelihood of stone passage, confirm stone passage, assess the stone burden, and evaluate disease activity.

When acute flank pain suggests the passage of a urinary stone, many methods of examination can be used. Often, conventional radiography is initially used to screen for stones, bowel abnormalities, or free intra-abdominal air. Radiographs can also be used to monitor the passage of visible stones.

IVU (excretory urography) provides important physiologic information regarding the degree of obstruction. Ultrasonography (US) is useful in young or pregnant patients and in patients allergic to iodinated contrast material. US is also helpful in problem solving.

All of these methods have become less useful with the advent of more sensitive and specific nonenhanced CT scanning. When CT is available, it is now considered the examination of choice for the detection and localization of urinary stones. Almost all studies conducted to date show that IVU provides no additional clinically important information after nonenhanced CT is performed. As a result of the higher radiation dose of CT, conventional or digital radiography should be used to monitor the passage of stones if radiographic follow-up studies are indicated and if the stone is visible on conventional radiographs.

Limitations of Techniques

Because of the higher radiation dose with CT, conventional or digital radiography should be used to monitor the passage of stones if radiographic follow-up is believed to be indicated and if the stone is visible on conventional radiographs. Pregnant or pediatric patients may be imaged with US first to avoid radiation exposure. The rare false-negative finding is usually due to reader error or a protease-inhibitor CT-lucent stone. False-positive results are usually due to phleboliths adjacent to the ureter. In some cases, intravenous contrast material may be needed to opacify the ureter.

US has limited sensitivity for smaller stones, and does not depict the ureters well. It should be used mainly in patients who are young, those who are pregnant, or those undergoing multiple examinations (eg, patients with spine injury).

IVU is the traditional examination for the assessment of urinary stone disease, and it does provide physiologic information related to the degree of obstruction. The radiation dose is generally smaller than that of CT, but it is of the same order of magnitude. Intravenous contrast is required, with resultant risks of an allergic reaction or nephrotoxicity. IVU is less sensitive than CT, especially for small or nonobstructing stones.

Differential Diagnoses

Appendicitis
Pancreatitis, Chronic
Cholecystitis, Acute
Papillary Necrosis
Cholelithiasis
Pelvic Inflammatory Disease/Tubo-ovarian Abscess
Colon, Diverticulitis
Renal Cell Carcinoma
Congenital Cystic Adenomatoid Malformation
Renal Vein Thrombosis
Crohn Disease
Retroperitoneal Fibrosis
Duodenum, Ulcers
Testicular Torsion
Epididymitis
Transitional Cell Carcinoma
Gastric Ulcer
Tuberculosis, Genitourinary Tract
Gout
Ureterocele
Meckel Diverticulum
Ureteropelvic Junction Obstruction,
Midgut Volvulus
Vesicoureteral Reflux
Nephrocalcinosis
Wilms Tumor
Obstructive Uropathy, Acute
Xanthogranulomatous Pyelonephritis
Ovarian Torsion
Ovarian Vein Thrombosis
Pancreatitis, Acute

Other Problems to Be Considered

Blood clot
Fungus ball
Calcifications in tumors such as renal cell carcinoma
Complicated renal cysts
Infection
Abscess
Infarcts
Hematoma
Malakoplakia
Atherosclerotic calcification
Biliary colic
Ulcer disease
Diverticulitis

More on Nephrolithiasis/Urolithiasis

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References

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Further Reading

Keywords

urinary lithiasis, upper urinary tract stone disease, renal stones, kidney stones, urinary stones, ureteral stones, renal calculi, urinary calculi, kidney calculi, ureteral calculi, renal calculus disease, urinary calculus disease

Contributor Information and Disclosures

Author

J Kevin Smith, MD, PhD, Vice Chairman for Veterans Affairs, Associate Professor, Department of Diagnostic Radiology, University of Alabama at Birmingham
Disclosure: Nothing to disclose.

Coauthor(s)

Mark E Lockhart, MD, Assistant Professor, Department of Radiology, University of Alabama at Birmingham
Mark E Lockhart, MD is a member of the following medical societies: American College of Radiology, American Institute of Ultrasound in Medicine, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

Nicole W Berland, BA, Outreach Support for Hurricane Relief, Collat Jewish Family Service
Disclosure: Nothing to disclose.

Philip Kenney, MD, Chief of GU Section of Diagnostic Radiology, Professor, Department of Diagnostic Radiology, University of Alabama at Birmingham
Philip Kenney, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Uroradiology
Disclosure: Nothing to disclose.

Medical Editor

Steven Perlmutter, MD, FACR, Clinical Associate Professor, Radiology Residency Program Director, Radiology Medical Director, Department of Radiology, University Hospital at Stony Brook
Steven Perlmutter, MD, FACR is a member of the following medical societies: American College of Radiology, American Institute of Ultrasound in Medicine, American Medical Association, American Roentgen Ray Society, Association of Program Directors in Radiology, Association of University Radiologists, Medical Society of the State of New York, Radiological Society of North America, Society of Breast Imaging, Society of Nuclear Medicine, and Society of Uroradiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Joshua A Becker, MD, Professor, Department of Radiology, New York University School of Medicine
Joshua A Becker, MD is a member of the following medical societies: Society of Uroradiology
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

 
 
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