Nephrolithiasis.

Authors

Editors

In: Feingold KR¹, Anawalt B², Boyce A³, Chrousos G⁴, Dungan K⁵, Grossman A⁶, Hershman JM⁷, Kaltsas G⁸, Koch C⁹, Kopp P¹⁰, Korbonits M¹¹, McLachlan R¹², Morley JE¹³, New M¹⁴, Perreault L¹⁵, Purnell J¹⁶, Rebar R¹⁷, Singer F¹⁸, Trence DL¹⁹, Vinik A²⁰, Wilson DP²¹, editors.

Source

Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-.
2016 Dec 11.

Author information

1: Professor of Medicine, University of California, San Francisco, CA
2: Chief of Medicine at the University of Washington Medical Center and Professor and Vice Chair of the Department of Medicine, University of Washington
3: Pediatric Endocrinologist and Associate Research Physician in the Skeletal Diseases and Mineral Homeostasis Section, National Institute of Dental and Craniofacial Research, National Institutes of Health
4: Professor of Pediatrics and Endocrinology, Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, "Aghia Sophia" Children's Hospital, Athens, Greece
5: Associate Professor of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Ohio State University
6: Professor of Endocrinology and Director of the Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, UK
7: Distinguished Professor of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA; Associate Chief, Endocrinology and Diabetes Division and Director, Endocrine Clinic, West Los Angeles VA Medical Center, Los Angeles, CA
8: Professor of General Medicine-Endocrinology, First Department of Propaedeutic Internal Medicine, Laiko University Hospital, Athens, Greece
9: Head of the Medicover MVZ Oldenburg; affiliated with the Carl von Ossietzky University and the Technical University of Dresden
10: Professor of Medicine and Chief of the Division of Endocrinology, Diabetology and Metabolism, University of Lausanne, Switzerland
11: Professor of Endocrinology and Metabolism, Centre Lead for Endocrinology and Deputy Institute Director, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, England
12: Director of Clinical Research, Hudson Institute of Medical Research; Consultant Endocrinologist, Monash Medical Centre, Melbourne, Australia
13: Dammert Professor of Gerontology and Director, Division of Geriatric Medicine and Director of the Division of Endocrinology, Saint Louis University Medical Center
14: Professor of Pediatrics, Professor of Genetics and Genomic Sciences, and Chief of the Adrenal Steroid Disorders Program, Icahn School of Medicine, Mount Sinai School of Medicine, New York, NY
15: Associate Professor of Medicine and Epidemiology, University of Colorado Anschutz Medical Campus
16: Professor of Medicine, Knight Cardiovascular Institute and the Division of Endocrinology, and Associate Director, Bob and Charlee Moore Institute for Nutrition and Wellness, Oregon Health and Science University, Portland, OR
17: Professor and Chair, Department of Obstetrics and Gynecology, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI
18: Director of the Endocrine/Bone Disease Program, John Wayne Cancer Institute at Saint John’s Health Center, Santa Monica, CA; Clinical Professor of Medicine, UCLA School of Medicine, Los Angeles, CA
19: Director of the Diabetes Care Center and Associate Professor of Medicine, University of Washington Medical Center, Seattle, WA
20: Murray Waitzer Endowed Chair for Diabetes Research, Professor of Medicine/Pathology/Neurobiology, Director of Research and Neuroendocrine Unit Division of Endocrine and Metabolic Disorders, Eastern Virginia Medical School, Norfolk, VA
21: Endowed Chair, Cardiovascular Health and Risk Prevention, Pediatric Endocrinology and Diabetes, Cook Children's Medical Center, Fort Worth, TX
22: Professor of Medicine, The University of Chicago, Chicago, 5841 S. Maryland Ave. Mail Code 2037, Chicago, IL 60637

Excerpt

The majority (65 to 75%) of stones are composed of either pure or mostly of calcium salts, including those of calcium oxalate, mixed calcium oxalate with uric acid, and calcium phosphate (brushite). Uric acid, cystine, and magnesium ammonium phosphate (struvite) compose the remainder of the stones. In the United States the lifetime risk for stone formation is 12% in men and 5% in women. Recurrence rates of new stone formation are high. If untreated, stones will recur at the rate of 50% in 5 to 10 years. An episode of renal colic has a sudden onset, with fluctuation and intensification over 15 to 45 minutes. Stones may obstruct the urinary tract and impair renal function. There is increased risk of infection with chronic obstruction. Bleeding may be chronic and accompany obstruction. The size, number, and metabolic composition of new stones strongly influence the natural history and complication rates. Composition of the stone reflects metabolic abnormalities in the urine. High urine calcium leads to calcium oxalate or calcium phosphate stones, high urine uric acid or low urine uric acid solubility (low pH) lead to uric acid stones; hyperoxaluria results in calcium oxalate stones; cystinuria is complicated by cysteine stones; and urinary tract infection with gram negative bacteria that produce urease and promote the infection and magnesium ammonium phosphate stones (struvite). The acute passage of a kidney stone is the 9^th most common reason for visits to an emergency room. In the differential diagnosis of acute abdominal/flank pain, renal ultrasound is almost as good as abdominal CT for diagnosis. Diagnosis includes inspection of a first morning urine for crystals, chemical analysis of a stone if available, and fasting serum chemistries and 24 hour urine collection for chemical analyses of calcium, creatinine, phosphorus, oxalate, citrate, pH, volume, sodium and potassium, bicarbonate, ammonium. Supersaturation calculations of calcium oxalate, calcium phosphate, uric acid and other ions with the use of software is helpful. Fasting serum calcium, phosphorus, magnesium, creatinine and uric acid are also indicated. Treatment depends upon the biochemical blood and urine tests which will identify the composition of the stone. Hypercalciuria with normal serum calcium is most likely due to idiopathic hypercalciuria (IH). Lowering high urine calcium is best accomplished by daily thiazide therapy. Calcium oxalate or calcium phosphate kidney stone recurrence is reduced by 80 to 90%. Hyperoxaluria depends on whether oxalate overproduction or over-absorption is present. Low urine volume and low urine citrate should be corrected. Uric acid stones can be reduced by decreasing purine precursor intake, or correcting a very acidic urine which reduces uric acid solubility. Infection stones, often staghorn, requires careful surgical removal of all of the stone material. Cystine stone of infancy and childhood requires aggressive control of the high urine cysteine by specific agents. For complete coverage of all related areas of Endocrinology, please see our FREE on line web-book, www.endotext.org.