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Prevention and Treatment of Kidney Stones

National Institutes of Health
Consensus Development Conference Statement
March 28-30, 1988

Conference artwork, a kidney figure overlaid with fragments of different types of crystals.

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus

This statement was originally published as: Prevention and Treatment of Kidney Stones. NIH Consens Statement 1988 Mar 28-30;7(1):1-23.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Prevention and Treatment of Kidney Stones. NIH Consens Statement Online 1988 Mar 28-30 [cited year month day];7(1):1-23.


Renal stone disease (nephrolithiasis) accounts for about 7 to 10 out of every 1,000 hospital admissions in the United States, and has an annual incidence of 7 to 21 cases per 10,000 persons. Four of every five patients with stones are men, and in both sexes the peak age of onset is between 20 and 30 years, so people are affected during years of prime adult life. The majority of stones, 70 to 80 percent, are composed mainly of calcium oxalate crystals; the rest are composed of calcium phosphate salts, uric acid, struvite (magnesium, ammonium and phosphate), or the amino acid cystine. Occasionally, stones injure kidneys and reduce their function by causing infection or obstruction, but many patients with stones suffer only from the pain of stone passage, urinary infection, and bleeding, which is worrisome though not in itself dangerous, and the inconvenience of hospitalization and discomfort of urological procedures. In essence, nephrolithiasis is a common cause of morbidity rather than of death or renal failure.

The diagnosis of nephrolithiasis is not difficult in most patients. The pain of stone passage, called renal colic, has easily recognized characteristics including location in the flank, sudden onset, extreme severity, radiation down the abdomen toward the groin, association with hematuria, and urinary symptoms of frequency, urgency and dysuria, and relief immediately following stone passage. Stone passage itself or radiographic evidence of the stone and its attendant urinary obstruction make the diagnosis certain.

A stone can form only when urine is supersaturated with respect to its constituent crystals. Supersaturation means that the concentration of a stone forming salt, such as calcium oxalate, exceeds its solubility in urine. Urine of most normal people is supersaturated with respect to calcium oxalate, so--in principle--all people can form such stones. Normal urine is not supersaturated with respect to uric acid, cystine or struvite. Conditions that raise calcium oxalate supersaturation raise the risk of calcium oxalate stones. Hypercalciuria and hyperoxaluria are two main clinical examples, and both can result from many diseases. Hyperparathyroidism, renal tubular acidosis, sarcoidosis, vitamin D intoxication, and "idiopathic" hypercalciuria all are causes of hypercalciuria. Hyperoxaluria may be due to overproduction, from hereditary disorders of metabolism, or be acquired from intestinal disease or diet.

Apart from overexcretion, supersaturation can be increased by abnormal interactions between urine ions. Urine citrate forms a soluble salt with calcium that normally reduces free calcium ion levels appreciably; low urine citrate from bowel disease, renal tubular acidosis, and, perhaps, dietary and hereditary causes can raise calcium oxalate supersaturation and promote stones. Normal women excrete more citrate and less calcium than normal men, perhaps a reason why men form stones more often. Low urine pH from hereditary causes or bowel disease promotes uric acid stones; high pH, from alkali, drugs, or renal tubular acidosis increases calcium phosphate supersaturation. Struvite supersaturation occurs only when urine is infected with microorganisms that possess urease, and are rightly called "infection" stones. Cystine stones occur only in cystinuria, a hereditary disorder of amino acid transport.

Supersaturation creates stone crystals by causing ions in solution to combine with one another into a solid phase, a process called nucleation. Calcium and oxalate ions can orient themselves on surfaces of another crystal, such as uric acid, and such heterogeneous nuclei may promote calcium oxalate stones. Hyperuricosuria, from dietary purine excess or from endogenous overproduction, and low urine pH, can promote stones that are pure uric acid, or mixed calcium oxalate--uric acid stones; hyperuricosuria can promote seemingly pure calcium oxalate stones. Other heterogeneous nucleators may be urine proteins, Tamm- Horsfall protein, the urothelial surface itself, and other crystals.

The disorders that raise supersaturation, and promote heterogeneous nucleation are the presently accepted causes of nephrolithiasis; their diversity, and the diversity of their current treatments complicate clinical management of patients, and offer many opportunities for fruitful research. At the same time, there are other factors that may influence stone forming propensity, such as inhibitors of calcium oxalate crystallization and urothelial surface properties that affect crystal retention; variations of inhibitors and urothelial surface properties may partly explain why only a small fraction of people form calcium oxalate stones even though urinary calcium oxalate supersaturation is almost universal. Assessment of inhibitors and urothelial surface properties are not yet applicable to clinical practice, but may eventually transform it.

New instruments and techniques have improved and simplified the treatment of stones in the kidney or urinary tract. Percutaneous techniques permit surgeons to extract or disintegrate stones that as recently as 5 years ago could be treated only by conventional surgery. Open surgery now is required for treatment of less than 5 percent of the patients. The extracorporeal shock wave lithotriptor was introduced into U.S. practice in 1984; it can disrupt stones into fragments that can be passed with the urine, eliminating the need for most invasive surgery. Worldwide, over 500,000 patients have been treated with this instrument since 1980. These breakthroughs have reduced the risk of stone removal and have affected public assessment of the benefits of medical stone prevention, complicating the question of what is the best way to evaluate and treat patients.

Given the natural complexity of this common disease, the great changes that new technology has made in surgical practice, and the exciting prospects offered by recent scientific discoveries, the National Institute of Diabetes and Digestive and Kidney Diseases and the Office of Medical Applications of Research of the National Institutes of Health convened a
Consensus Development Conference on the Prevention and Treatment of Kidney Stones on March 28-30, 1988. After a day and a half of presentations by experts and discussion by the audience, a consensus panel drawn from specialists and generalists from the medical profession and related scientific disciplines, clinical investigators, and public representatives considered the evidence. The panel agreed on answers to the following key questions:

  1. What are the methods of medical prevention, and how successful are they?
  2. What is the role of lithotripsy, and can it replace medical prevention?
  3. What are clinical and laboratory approaches for the evaluation of patients with stones?
  4. What are the directions for future research?
What Are the Methods of Medical Prevention, and How Successful Are They?

Current medical treatment will not dissolve most stones. Rather it is aimed at inhibiting stone growth and preventing formation of new stones. Medical treatment can be divided into specific and nonspecific. The nonspecific treatment used in all patients with stones is increased fluid intake. Specific treatment regimens are directed to the particular type of stone that is being prevented.

Nonspecific Treatment

Increased fluid intake increases the urinary output, thereby lowering the concentration of the substances involved in stone formation. Although there is no controlled clinical study that examines the effectiveness of an increase in fluid intake, historical data strongly suggest that hydration is effective in preventing stone formation. While strict guidelines are not available, a doubling of the urinary output or a 24-hour urinary output of greater than 2 liters is generally recommended to reduce new stone formation. In actual practice, however, the beneficial effects of hydration may be seen with much less increase in urinary volume.

Specific Treatments

Calcium Oxalate Stones.

Calcium oxalate stones may be either "idiopathic" or the result of a specific metabolic abnormality, such as hyperparathyroidism, sarcoidosis, renal tubular acidosis or primary hyperoxaluria, which together account for less than 10 percent of all calcium oxalate renal stones. Treatment of stones caused by specific diseases rests upon the correction of the underlying disease condition, for example, parathyroidectomy for patients with primary hyperparathyroidism.

For patients with idiopathic calcium oxalate stone disease, treatment is directed toward mechanisms that will reduce abnormal urinary metabolite excretion. Stone disease in these individuals is the result of increased urinary calcium, oxalate, or uric acid excretion, or decreased urinary citrate excretion, or abnormal urinary pH. Contrary to earlier beliefs, it is becoming clear that most patients have more than one abnormality of urinary metabolite excretion. Hypercalciuria, an increase in urinary calcium excretion, is the commonest abnormality seen in these patients. Hypercalciuria is almost invariably the result of increased intestinal calcium absorption. Abnormalities of vitamin D metabolism, renal handling of calcium, and bone turnover may also be found in hypercalciuric patients. Hypercalciuria can be familial.

This condition is generally treated by both counseling against certain dietary excesses, and by drug administration. Patients are advised against a calcium intake of more than 1 g per day, and a high sodium intake. The most commonly used drug treatment consists of thiazide diuretics, which reduce renal calcium excretion. High salt intake lessens the effectiveness of thiazides and generally increases calcium excretion. Other drug treatments not yet evaluated in double-blind and prospective studies are cellulose phosphate, which binds calcium in the gut, and orthophosphate, which may reduce intestinal calcium absorption and urinary calcium phosphate crystal formation.

A second abnormality associated with calcium oxalate stone is increased urinary uric acid excretion. It is not clear why this might predispose to formation of calcium oxalate stones, but one mechanism may be the deposition of calcium oxalate crystals upon uric acid crystals. Hyperuricosuria may either be isolated or associated with hypercalciuria. Treatment is with allopurinol, an agent that reduces uric acid excretion, and with restriction of excess purine and animal protein intake.

A third metabolic abnormality, detected with increasing frequency in recent years, is hypocitraturia, a decrease in urinary citrate excretion. Citrate binds calcium thereby decreasing the calcium oxalate concentration in the urine. This condition is best treated with citrate supplementation.

Although urinary oxalate concentration does influence calcium oxalate supersaturation more than a proportional increase in urine calcium would, urinary oxalate levels are only slightly elevated in most patients with idiopathic calcium nephrolithiasis. The clinical significance of this mild hyperoxaluria is unclear, as is the effectiveness of available treatment, which consists of counseling to reduce excessive dietary oxalate intake. Since oxalic acid is a metabolic byproduct of vitamin C, there has been concern about excess intake of vitamin C, above 0.5 or 1.0 g per day; but evidence that this promotes stone formation is very limited.

The efficacy of thiazide therapy for preventing stones by lowering urine calcium excretion, and of allopurinol therapy for preventing calcium oxalate stones due to hyperuricosuria has been demonstrated in a limited number of randomized controlled trials. Specific drug therapy appears to reduce stone recurrence rates by half. Even though hydration and dietary restrictions are widely accepted by experts in the field, their efficacy and that of citrate and phosphates have not been tested by randomized controlled trials. A difficulty in evaluating studies that do not contain randomized concurrent controls is that the natural history of idiopathic calcium oxalate stone disease has not been well documented. Limited evidence to date suggests that approximately 60 percent of patients presenting to their physician with symptomatic stones for the first time will not form another stone for 10 years (the so-called "stone clinic effect"). In the absence of randomized controlled trials, claims of success in stone treatment must be evaluated cautiously. On the other hand, the majority of clinical studies of treatments of stone disease, which have not employed the randomized, double-blind design, should be carefully considered, especially those showing a treatment effect greater than the 60 percent stone clinic effect. Better definition of the side effects of medical treatment is needed.

Uric Acid Stones.

Uric acid stones are formed in patients with a persistently acid urine and/or massively increased urinary uric acid excretion (greater than 1,000 mg per day). Initial treatment is alkalinization of the urine with agents such as bicarbonate or citrate. Patients with recalcitrant uric acid stones may be treated with allopurinol, in addition. Reduction of dietary purine intake is also widely recommended.

Infection Stones.

These stones are formed in the presence of infection by urea-splitting organisms. The most effective treatment must include complete removal of the stone(s) and appropriate antibacterial therapy. In patients who are not candidates for surgical treatment, randomized controlled trials have shown that chronic antimicrobial therapy together with urease inhibitors such as acetohydroxamic acid are effective, but limited in usefulness by side effects.

Cystine Stones.

These stones occur in patients with the inherited transport disorder, cystinuria. Medical treatment lies in reducing urinary cystine concentration by hydration, by increasing cystine solubility using alkalinization, and by lowering urine cystine concentration with agents such as d-penicillamine or thiola.  

What Is the Role of Lithotripsy, and Can It Replace Medical Prevention?

Extracorporeal shock wave lithotripsy (ESWL) has become widely used for the treatment of renal stone disease and is based on the use of shock waves to break up kidney stones so that they can be passed through the ureter.

Lithotripsy has proven to be effective for removal of renal stones less than 2 cm in diameter, which constitute the majority of the cases. The morbidity of ESWL is less than that of percutaneous nephrolithotomy. For kidneys containing only single stones, treatment success defined as kidneys that are made stone free or left with only asymptomatic residual fragments, compares well with percutaneous nephrolithotomy, except if lower-pole stones greater than 1 cm are present, as they are in 20 percent of these patients. Stone-free rates for kidneys with multiple stones are lower than for kidneys with only one stone.

For patients with stones larger than 2 cm--infected or not-- combined techniques of ESWL and percutaneous nephrolithotomy tend to produce better results. Initial percutaneous nephrolithotomy followed by ESWL and a "second look" percutaneous nephrolithotomy give the best results. In treatment of infected stones, removal of all stone fragments and appropriate antimicrobial therapy are essential to prevent stone recurrence. For the small group of patients with large infected staghorn calculi, complex anatomy, or obstruction, open surgery may be the recommended course. The complexity of treating large stones--greater than 2 cm, infected or not--requires that such patients be managed in settings where ESWL, percutaneous nephrolithotomy, and conventional surgery are all available.

In regard to the use of ESWL for treatment of patients with small (less than 5 mm) stones that are incidentally discovered and cause no symptoms, treatment is not universally recommended, but additional data are needed in this area. Current practice relies upon the evaluation of individual patients.

With regard to ureteral stones, spontaneous passage is ideal. If spontaneous passage seems unlikely, or unduly delayed, ESWL is best for stones in the upper two-thirds of the ureter, whereas endoscopic techniques remain best for lower ureteral stones. Uretero-pelvic junction obstruction or other obstructions, or stones in calyceal diverticulae, may be best managed by endourological methods. Cystine stones are best treated by percutaneous nephrolithotomy.

Since ESWL is relatively new, the long-term effects of this therapy are unknown. Concerns relative to the effects on kidney function, adjacent tissues and organs, increased new stone growth, and subsequent diseases, such as hypertension, will require long-term evaluation. Caution in regard to levels of energy used is necessary, and guidelines need to be established and implemented for single treatments, frequency of treatments, as well as for cumulative doses. ESWL treatment should be used with caution in children.

Lithotripsy cannot replace medical prevention. Rather, surgical and medical therapy are complementary approaches. Medical therapy prevents recurrence, is efficacious (see question one), avoids renal colic, reduces the need for surgery, may correct extra-renal manifestations of systemic disease, and is cost-effective. It is particularly important for patients with stones, whether treated with lithotripsy or not, to receive continuity of medical therapy and monitoring at regular intervals to prevent or delay recurrence.  

What Are Clinical and Laboratory Approaches for the Evaluation of Patients With Stones?

Clinical and laboratory evaluation of the patient should allow insight into the type, extent, and intensity of nephrolithiasis.

The approach to the evaluation of patients with stones depends upon the initial presentation; only a basic evaluation is undertaken for the initial stone former. Multiple stones or recurrent disease require more complex evaluation.

In all patients, every effort should be made to collect and analyze all stone material. Although conventional analysis has relied upon polarization microscopy, evaluation by x-ray crystallography and, if necessary, infrared analysis promise to provide greater analytical precision in the future.

The basic evaluation begins with a history and identification of any possible medical or environmental risk factors for stone disease. History may disclose evidence of familial stone disease and allow some estimation of prior stone frequency. History and physical examination may reveal evidence of malignancy, skeletal disease, inflammatory bowel disease, intestinal bypass, urinary tract infection, and will allow identification of environmental factors known to modulate the expression and severity of stone disease. Such factors include fluid intake or restriction, urine volume, climate, geographic variables, occupation, immobilization, diet, and medication. The basic laboratory examination includes urinalysis; urine culture if clinically indicated; and blood chemical profile including calcium, phosphorus, uric acid, electrolytes and creatinine. A urine aliquot should be obtained for qualitative cystine screening when stone composition is unknown. Overtly hypercalcemic patients should undergo parathyroid hormone assay. KUB and intravenous urography should be performed in every patient, unless contraindicated. This will identify urinary tract obstruction and allow definition of existing stones as well as collecting system anatomy. Renal tomograms are ideal for visualizing stones, when practical and indicated.

Metabolically active stone formers are defined as those who have formed or who have passed a second or multiple stones within a 1-year follow-up period, or have growing stones. These patients and all children with renal calculi deserve further scrutiny. Their further laboratory evaluation should include a 24-hour urine collection for analysis of volume, calcium, sodium, uric acid, oxalate, citrate, pH, and creatinine. Twenty-four hour urinary creatinine excretion is measured to assess adequacy of the urine collection. Follow-up 24-hour urine collection is required to monitor patient compliance and effectiveness of treatment.

Specialized testing is not recommended for most patients. Occasionally, provocative acid-loading tests, oral calcium deprivation and loading studies, determination of urinary inhibitor concentration, calculation of urinary saturation indices may be indicated. N-terminal PTH assay or immunoradiometric parathyroid hormone evaluation may be indicated in patients with high-normal or marginally elevated serum calcium levels.  

What Are the Directions for Future Research?

The NIH Consensus Development Conference on the Prevention and Treatment of Kidney Stones has provided an overview of the current state of knowledge on the etiology, pathophysiology, and medical and surgical management of nephrolithiasis. Numerous unresolved issues were discussed, demonstrating the need for additional basic and clinical research. Some of the questions posed have been the subject of previous studies, but fundamental issues remain unresolved. The solution to these questions will require collaborative endeavors between basic scientists and clinicians.

Randomized controlled clinical trials are necessary to assess methods of medical and surgical treatment that have not been so evaluated. Long-term follow-up studies are needed to assess the safety and efficacy of both medical and surgical therapy of nephrolithiasis.

Basic Research

  1. What are the mechanisms and sites of initial crystal formation and retention? Can the role of the renal cell in these processes be defined?
  2. What are the mechanisms of action of inhibitors and promoters on crystal formation and growth, and on stone nucleation and maturation?
  3. What are the biochemical characteristics, genetic modes of regulation, and mechanism of action of macromolecular inhibitors and promoters of crystal formation? Are abnormal molecules produced in patients with genetic disorders?
  4. Can appropriate animal models be developed for studies on ESWL effects and the pathogenesis of human nephrolithiasis?
  5. Is there a genetic basis for idiopathic nephrolithiasis? Using genetic probes, can individuals at risk be identified? For defined genetic disorders (e.g., cystinuria, renal tubular acidosis), will gene therapy have practical application?
  6. Are the enzymes involved in 1,25(OH)2D3 synthesis, and the receptors for parathyroid hormone and 1,25(OH)2D3 action useful sites of attack for new therapeutic agents? Will their molecular characterization be helpful in designing new inhibitors?
  7. What are the biochemical and molecular biological characteristics of ion transporters relevant to the pathogenesis of nephrolithiasis? Can their activity be regulated?
  8. What are the fundamental mechanisms of oxalate synthesis, absorption and transport?
  9. Are there in vitro or animal model studies with ESWL that would be useful in characterizing the potential risks for cellular and tissue damage in man?
  10. Are there improvements possible in the physics and technology of ESWL that can reduce tissue injury?

Clinical Research

  1. What are the fundamental mechanisms of idiopathic hypercalciuria? Is renal tubular dysfunction involved in the pathogenesis of stones? Can individuals at risk for nephrolithiasis be identified? Why does stone disease predominate in men?
  2. What is the optimal duration of drug therapy in recurrent calcium stone formers? Are patients at decreased risk for recurrent stone episodes after several years of therapy? Are there new agents that could increase calcium reabsorption in the kidney without producing the known side effects of thiazides?
  3. Is there subclinical bone disease in patients with idiopathic hypercalciuria? Does thiazide therapy alter bone mineral content?
  4. What are the biological effects of ESWL on the kidney and surrounding tissues such as the liver or pancreas? Are those patients who have received ESWL treatments at greater or lesser risk for recurrent stone disease years after treatment? Are there altered effects on membrane physiology (e.g., renal tubule or epithelium)? Is hypertension a complication of ESWL, and if so, how do we prevent it? Are there other effects on the kidney and what are the best renal function tests to assess this issue? Should an asymptomatic stone be treated with ESWL?
  5. Can better chemolytic agents for stone fragment removal be developed?
  6. What is the potential role of vitamin D antagonists in treating calcium stone disease?
  7. Can new drugs be developed to alter oxalate synthesis or metabolism? What are the effects on stone formation of reduction of urine oxalate?
  8. Can safer inhibitors of urease be developed?

Nephrolithiasis is a chronic illness that requires an integrated combination of medical and surgical care; the first is concerned mainly with prevention of recurrent stones, the latter mainly with the removal of existing stones.

A small fraction of patients have calcium oxalate stones due to specific disorders such as primary hyperparathyroidism, renal tubular acidosis, and primary or acquired forms of hyperoxaluria. Treatment of patients with these disorders or of patients who have uric acid or cystine stones is not controversial and is effective in preventing recurrence.

The majority of patients, 80 percent, form calcium oxalate stones not due to specific diseases but to idiopathic hypercalciuria, hyperuricosuria, mild hyperoxaluria, or hypocitraturia. Thiazides and allopurinol, as treatments of idiopathic hypercalciuria and hyperuricosuria, respectively, have been effective in controlled trials. Although hydration, dietary counseling to reduce oxalate or calcium intake, and oral citrate have not yet been tested adequately, virtually all physicians recommend hydration to patients who form stones.

New techniques and instruments, percutaneous nephrolithotomy, and extracorporeal shock wave lithotripsy (ESWL) have greatly improved removal of stones. ESWL seems an excellent treatment for small, uninfected stones, less than 2 cm in diameter. Larger stones or infected stones are best treated in clinical settings that offer both ESWL and a comprehensive array of percutaneous and open surgical procedures. Potential long-term adverse consequences of ESWL are not yet defined.

All patients who form stones should be evaluated to detect treatable causes and to prevent recurrence. Complete clinical history, physical examination, urinalysis, analysis of all available stone material, intravenous program (IVP), urine culture, a routine cystine screening, and a multitest blood profile comprise the minimum evaluation appropriate for patients with only a single stone. Patients who have formed multiple stones should also have assessed their 24-hour urine excretions of calcium, oxalate, uric acid, sodium, citrate and creatinine, and urine pH. The outcome of treatment should be evaluated clinically and by appropriate follow-up measurements.  

Consensus Development Panel

Fredric L. Coe, M.D.
Panel and Conference Chairperson
Professor of Medicine and Physiology
Director, Program in Nephrology
Department of Medicine
University of Chicago School of Medicine
Chicago, Illinois
William H. Boyce, M.D.
Professor of Surgery
Section of Urology
Wake Forest University
Bowman Gray School of Medicine
Winston-Salem, North Carolina
Gary D. Friedman, M.D., M.S.
Assistant Director for Epidemiology and Biostatistics
Division of Research
Kaiser Permanente Medical Care Program
Oakland, California
Donovan L. Gay
Board Member
National Kidney Foundation
Senior Administrative Hearing Examiner
Bureau of Motor Vehicle Services
Washington, D.C.
Richard C. Inskip, M.D.
Past President
American Academy of Family Physicians
Clinical Associate Professor
Department of Family and Community Medicine
University of Nevada School of Medicine
Reno, Nevada
Franklyn G. Knox, M.D., Ph.D.
Director for Education
Mayo Foundation
Professor of Physiology and Medicine
Mayo Medical School
Rochester, Minnesota
Neil S. Mandel, Ph.D.
Professor of Medicine, Biochemistry, and Orthopedic Surgery
National Veterans Administration Crystal Identification Center
Medical College of Wisconsin
Zablocki Veterans Administration Medical Center
Milwaukee, Wisconsin
David R. McNutt, M.D., M.P.H.
Employee Health Service
Cook County Hospital
Chicago, Illinois
Mani Menon, M.D.
Professor of Surgery and Physiology
Division of Urologic and Transplantation Surgery
University of Massachusetts Medical Center
Worcester, Massachusetts
Richard P. O'Connor, Jr., M.D.
Assistant Clinical Professor of Medicine
College of Human Medicine
Michigan State University
Staff Nephrologist
Saint Mary's Hospital
Grand Rapids, Michigan
Carol K. Redmond, Sc.D.
Professor and Chairman
Department of Biostatistics
University of Pittsburgh Graduate School of Public Health
Pittsburgh, Pennsylvania
Louis M. Sherwood, M.D.
Senior Vice President of Medical and Scientific Affairs
Merck, Sharp & Dohme International
Rahway, New Jersey
Professor of Medicine and Biochemistry
Albert Einstein College of Medicine
Bronx, New York
Ian J. Spence, M.D.
Clinical Associate Professor
Division of Urology
Department of Surgery
Georgetown University
Washington, D.C.


Arthur E. Broadus, M.D., Ph.D.
"Primary Hyperparathyroidism"
Professor of Medicine
Section Chief
Endocrinology and Metabolism
Yale University School of Medicine
New Haven, Connecticut
Vardaman M. Buckalew, Jr., M.D.
"Renal Tubular Acidosis"
Professor of Medicine
Chief of Nephrology
Wake Forest University
Bowman Gray School of Medicine
Winston-Salem, North Carolina
Christian Chaussy, M.D.
"Role of Lithotripsy"
Krankenhaus Harlaching
George W. Drach, M.D.
"Surgical Overview of Nephrolithiasis"
Medical Director
University Physicians, Inc.
Professor and Chief of Urology
University of Arizona Health Sciences Center
Tuscon, Arizona
Bruce Ettinger, M.D.
Clinical Professor of Medicine and Radiology
University of California at San Francisco Staff
Department of Endocrinology, Metabolism, and
Internal Medicine
Kaiser Permanente Medical Center
San Francisco, California
Murray J. Favus, M.D.
"Familial Forms of Hypercalciuria"
Associate Professor of Medicine University of
Chicago, Illinois
Birdwell Finlayson, M.D., Ph.D.
"Overview of the Surgical Treatment of Urolithiasis with Special Reference to Lithotripsy"
Graduate Research Professor Division of Urology
Department of Surgery
University of Florida College of Medicine
Gainesville, Florida
Donald P. Griffith, M.D.
"Infection Stones"
Professor of Urology
Baylor College of Medicine
Houston, Texas
Emil Thomas Kaiser, Ph.D.
"Protein Inhibitors of Crystal Growth"
Professor of Chemistry
The Rockefeller University
New York, New York
Jacob Lemann, Jr., M.D.
"Idiopathic Hypercalciuria"
Professor of Medicine
Nephrology Division
Medical College of Wisconsin
Froedtert Memorial Lutheran Hospital
Milwaukee, Wisconsin
James E. Lingeman, M.D.
"The Role of Lithotripsy and Its Side Effects"
Director of Research
Methodist Hospital Institute for Kidney Stone
Indianapolis, Indiana
Charles Y.C. Pak, M.D.
"The Role of Medical Prevention"
Professor of Internal Medicine
Department of Internal Medicine
University of Texas
Southwestern Medical Center
Dallas, Texas
Glenn M. Preminger, M.D.
"The Metabolic Evaluation of Patients with Recurrent Nephrolithiasis: A Review of Comprehensive and Simplified Approaches"
Assistant Professor of Urology and Internal Medicine
Division of Urology
Department of Surgery
University of Texas
Southwestern Medical Center
Dallas, Texas
Joseph W. Segura, M.D.
"The Role of Percutaneous Surgery in Renal and Ureteral Stone Removal"
Carl Rosen Professor of Urology
Mayo Medical School
Mayo Clinic
Rochester, Minnesota
Lynwood H. Smith, M.D.
"The Medical Aspects of Urolithiasis: An Overview"
Professor of Medicine
Mayo Medical School
Consultant in Internal Medicine, Nephrology, and Urology
Mayo Clinic
Rochester, Minnesota
Hibbard E. Williams, M.D.
"Oxalate Synthesis and Transport and the Hyperoxaluric Syndromes"
University of California at Davis School of Medicine
Davis, California
David M. Wilson, M.D., F.A.C.P.
"Clinical and Laboratory Approaches for Evaluation of Nephrolithiasis"
Department of Internal Medicine
Department of Laboratory Medicine and Pathology
Mayo Clinic
Mayo Foundation
Rochester, Minnesota
Edmund R. Yendt, M.D., F.R.C.P.(C)
"Clinical and Laboratory Approaches for Evaluation of Nephrolithiasis"
Department of Medicine
Division of Endocrinology
Queen's University
Kingston, Ontario

Planning Committee

MaryAnn Lange, M.D.
Planning Committee Chairperson
Assistant to the Director
Division of Kidney, Urologic, and Hematologic Diseases
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Michael Bernstein
Director of Communications
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Fredric L. Coe, M.D.
Panel and Conference Chairperson
Professor of Medicine and Physiology
Director, Program in Nephrology
Department of Medicine
University of Chicago School of Medicine
Chicago, Illinois
Jerry M. Elliott
Program Analyst
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
James N. Fordham, M.A.
Writer and Editor
Office of Health Research Reports
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Jay Y. Gillenwater, M.D.
Professor of Urology
Department of Urology
University of Virginia Medical School
Charlottesville, Virginia
William H. Hall
Writer and Editor
Office of Health Research Reports
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
John L. Meyer, Ph.D.
Health Science Administrator
Executive Secretary
Pathology A Study Section
Division of Research Grants
National Institutes of Health
Bethesda, Maryland
Gary E. Striker, M.D.
Kidney Division
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
John D. Young, M.D.
Professor and Head
Division of Urology
Acting Chairman
Department of Surgery
University of Maryland Hospital
Baltimore, Maryland

Conference Sponsors

National Institute of Diabetes and Digestive and Kidney Diseases
Phillip Gorden, M.D.
NIH Office of Medical Applications of Research
William T. Friedewald, M.D.
Acting Director

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