Correspondence
The Pathogenesis and Treatment of Kidney Stones
N Engl J Med 1993; 328:444-445February 11, 1993
- Article
To the Editor:
The article by Coe et al. on the treatment of renal stones (Oct. 15 issue)1 provides an excellent summary, clearly defining a thorough approach to treating patients with this disorder. The ease and economy with which their care may be managed contrasts with what I observe in the world around me. Many patients are never evaluated or treated medically, but merely offered lithotripsy. Though I frequently consult with local practitioners about stone disease, I have yet to meet a patient who has had both lithotripsy and an evaluation for the cause of the disease. Could the continuing exorbitant charges for lithotripsy be contributing to this result? If so, one must look to the medical profession to police itself.
1 ReferencesDonald J. Sherrard, M.D.
Veterans Affairs Medical Center, Seattle, WA 981081
Coe FL ,Parks JH ,Asplin JR . The pathogenesis and treatment of kidney stones. N Engl J Med 1992;327:1141-1152
Full Text | Web of Science | Medline
To the Editor:
The recent review of the pathogenesis and treatment of kidney stones by Coe et al. was thorough, but we were disappointed by their omission of Corynebacterium urealyticum (formerly corynebacterium group D2) as a possible cause of struvite stones. C. urealyticum, a slow-growing, gram-positive bacillus with a strong urease activity and high resistance to most antimicrobial agents, can infect the lower and upper urinary tract1. It has been isolated from about 21 percent of urine samples that are alkaline and contain struvite stones,1 and it has been implicated in the development of urolithiasis2. Recently, we reported that C. urealyticum was involved in cases of pyelic struvite stones (encrusted pyelitis) in kidney-transplant recipients3. The presence of urolithiasis, especially in a renal-transplant recipient, with an alkaline urinary pH, magnesium ammonium phosphate stones, and a negative routine urine culture strongly suggests the presence of C. urealyticum.
3 ReferencesJose M. Aguado, M.D.
Jose M. Morales, M.D.
Hospital 12 de Octubre, 28041 Madrid, Spain1
Soriano F ,Aguado JM ,Ponte C ,Fernandez-Roblas R ,Rodriguez-Tudela JL . Urinary tract infection caused by Corynebacterium group D2: report of 82 cases and review. Rev Infect Dis 1990;12:1019-1034
CrossRef | Medline2
Nadal D ,Schwobel M ,von Graevenitz A . Corynebacterium group D2 and urolithiasis in a boy with megacalycosis. Infection 1988;16:245-247
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Morales JM ,Aguado JM ,Diaz-Gonzalez R , et al. Alkaline-encrusted pyelitis/cystitis and urinary tract infection due to Corynebacterium urealyticum: a new severe complication after renal transplantation. Transplant Proc 1992;24:81-82
Web of Science | Medline
To the Editor:
The excellent review by Coe et al. on kidney stones did not discuss the usefulness of high fluid intake, widely prescribed to treat renal colic and to prevent recurrence. If it is useful, what type of fluid is recommended?
For the short-term management of renal colic, do the authors prefer a nonsteroidal antiinflammatory drug (in spite of the renal side effects) or an opiate drug (in spite of the potential for increasing antidiuretic hormone secretion)?
For imaging in a patient with renal colic of new onset, do the authors advocate ultrasonography with a plain film of the abdomen, or intravenous pyelography?
Mayer Brezis, M.D.
Hadassah University Hospital-Mt. Scopus, 91 240 Jerusalem, IsraelTo the Editor:
In their review of the pathogenesis and treatment of kidney stones, Coe et al. do not mention salt intake. About three fourths of all kidney stones are made of calcium oxalate, and as the authors point out, hypercalciuria is strongly associated with this type of stone. However, they fail to point out that salt intake is a major determinant of urinary calcium excretion,1 not only in normal subjects2 and patients with hypercalciuria3 with and without hyperparathyroidism,4 but also in patients with osteoporosis5 and at any level of calcium intake6. Even within the range of day-to-day variation in sodium intake in Western societies -- i.e., from approximately 50 to 200 mmol per day -- urinary calcium excretion will vary by 40 to 80 mg per day (1 to 2 mmol per day)7. Coe et al., by ignoring the importance of salt intake in their diagnostic criteria, will make a misdiagnosis in many patients with so-called idiopathic hypercalciuria. The authors have also overlooked a very important cause contributing to hypercalciuria. . . .
7 ReferencesFrancesco P. Cappuccio, M.B., B.S., M.D.
Graham A. MacGregor, M.A., F.R.C.P.
St. George's Hospital Medical School, London SW17 0RE, United Kingdom1
Hodgkinson A ,Pyrah LN . The urinary excretion of calcium and inorganic phosphate in 344 patients with calcium stone of renal origin. Br J Surg 1958;46:10-18
CrossRef | Web of Science | Medline2
Kleeman CR ,Bohannan J ,Bernstein D ,Ling S ,Maxwell MH . Effect of variations in sodium intake on calcium excretion in normal humans. Proc Soc Exp Biol Med 1964;115:29-32
Web of Science | Medline3
Muldowney FP ,Freaney R ,Moloney MF . Importance of dietary sodium in the hypercalciuria syndrome. Kidney Int 1982;22:292-296
CrossRef | Web of Science | Medline4
Muldowney FP ,Freaney R ,Muldowney WP ,Murray F . Hypercalciuria in parathyroid disorders: effect of dietary sodium control. Am J Kidney Dis 1991;17:323-329
Web of Science | Medline5
McParland BE ,Goulding A ,Campbell AJ . Dietary salt affects biochemical markers of resorption and formation of bone in elderly women. BMJ 1989;299:834-835
CrossRef | Web of Science | Medline6
McCarron DA ,Rankin LI ,Bennett WM ,Krutzik S ,McClung MR ,Luft FL . Urinary calcium excretion at extremes of sodium intake in normal man. Am J Nephrol 1981;1:84-90
CrossRef | Web of Science | Medline7
Cappuccio FP ,MacGregor GA . Preventing osteoporosis. BMJ 1991;303:921-921
CrossRef | Web of Science
Author/Editor Response
The authors reply:
To the Editor: Dr. Sherrard raises a possibly disturbing matter about which we have no objective information, but we would agree that the medical profession should assume the responsibility for ensuring that, when possible, preventive measures are taken. At least two treatments for stones have proved effective. Recently, Gleeson et al. listed 39 organisms that can produce struvite stones,1 most of which we could not mention in our review; we regret that the organism described by Drs. Aguado and Morales could not be singled out. Dr. Brezis mentions high fluid intake, as we did, but however appealing as a preventive measure and apparently valuable, the use of water has yet to achieve the status of a proved remedy, and to rely on it seems wrong. For colic itself, vomiting often makes the use of oral fluids impractical. We prefer opiates or their analogues to manage pain, and we use intravenous urography to localize obstructing stones. Like Drs. Cappuccio and MacGregor, we believe that high salt intake increases urinary calcium excretion, but in clinical practice the interpretation of urinary calcium levels in terms of urinary sodium levels would require some kind of nomogram, which may not be available or fully practical.
1 ReferencesFredric L. Coe, M.D.
Joan H. Parks, M.B.A.
John R. Asplin, M.D.
University of Chicago, Chicago, IL 60637- Citing Articles (1)
Citing Articles
1
H. Kesteloot , I. Tzoulaki, I. J. Brown, Q. Chan, A. Wijeyesekera, H. Ueshima, L. Zhao, A. R. Dyer, R. J. Unwin, J. Stamler, P. Elliott. (2011) Relation of Urinary Calcium and Magnesium Excretion to Blood Pressure: The International Study of Macro- and Micro-Nutrients and Blood Pressure and the International Cooperative Study on Salt, Other Factors, and Blood Pressure. American Journal of Epidemiology 174:1, 44-51
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