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      Medical Prevention of Renal Stone Disease


      S. Karger AG

      Kidney stones, Hypercalciuria, Treatment, renal stone disease

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          Medical treatment designed to prevent stone formation is important in idiopathic calcium oxalate nephrolithiasis, because of the high rate of stone recurrence. Several randomized trials have established the values of conservative and drug treatments. A high fluid intake alone has been reported to inhibit the recurrence of stone formation in single stone formers. In patients with recurrent disease, a significant reduction in stone formation rate from pretreatment was found in the placebo group maintained on a conservative program, underscoring the importance of increased fluid intake and dietary modification. In patients with active recurrent stone disease, treatment with drugs along with a conservative program is necessary. Allopurinol, thiazide, potassium citrate and potassium-magnesium citrate have been shown to inhibit stone formation compared with placebo. It has not been clearly established that a selective treatment is more effective than a more randomly chosen drug treatment. Another advantage of medical approach is its ability to correct nonrenal complications of stone disease, such as bone loss that sometimes accompanies stone disease.

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          Effect of Medical Management and Residual Fragments on Recurrent Stone Formation Following Shock Wave Lithotripsy

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            Recurrent nephrolithiasis: Natural history and effect of phosphate therapy

            In a double-blind controlled clinical study, 71 patients with recurrent calcium oxalate stones were divided into three treatment groups: those who received potassium acid phosphate, those who received an inert placebo, and those who received a low calcium diet only. Follow-up periods averaged 2.9 years. Although the mean urinary calcium level of the patients who received phosphate was reduced 33 per cent, their renal stone disease did not diminish. Mean urinary phosphorus increased 88 per cent with phosphate treatment but did not correlate with the decrease in urinary calcium, or with treatment success. The data did not suggest that phosphorus and its metabolites retard calcium oxalate crystallization in urine. No evidence appeared for an association of hypercalciuria with severe stone disease, or with a specific clinical or chemical response to phosphate therapy. Patients whose urinary calcium level fell more than 25 percent when dietary calcium was reduced may have excessive gastrointestinal calcium absorption, which appears to be associated with improved chemical response to phosphate therapy.

              Author and article information

              S. Karger AG
              December 1998
              24 December 1998
              : 81
              : Suppl 1
              : 60-65
              Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Tex., USA
              46300 Nephron 1999;81(suppl 1):60–65
              © 1998 S. Karger AG, Basel

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              Page count
              Tables: 1, References: 20, Pages: 6
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              Cardiovascular Medicine, Nephrology

              Hypercalciuria, Kidney stones, Treatment, renal stone disease


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