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      Medical Management of Urinary Stone Disease

      Nephron Clinical Practice

      S. Karger AG

      Diet, Kidney stones

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          A variety of dietary and metabolic factors may contribute or cause stone formation in idiopathic calcium oxalate nephrolithiasis. Dietary factors include a high intake of animal proteins, oxalate and sodium, and a low intake of fluids and potassium-containing citrus products. Some of the metabolic causes of stones are hypercalciuria, hypocitraturia, gouty diathesis, hyperoxaluria, and hyperuricosuria. Dietary modification, to be applied in all patients with stones includes a high fluid intake, restriction of oxalate and sodium, and balanced diet with animal proteins complemented by adequate intake of fruits and vegetables. When dietary modification is ineffective in controlling stone formation or in the presence of severe metabolic derangements, a pharmacologic intervention may be necessary. In a simple approach, thiazide or indapamide with potassium citrate is recommended for patients with hypercalciuria, and potassium citrate alone for the remaining normocalciuric subjects.

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          Most cited references 10

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          Effect of low-carbohydrate high-protein diets on acid-base balance, stone-forming propensity, and calcium metabolism.

          Low-carbohydrate high-protein (LCHP) diets are used commonly for weight reduction. This study explores the relationship between such diets and acid-base balance, kidney-stone risk, and calcium and bone metabolism. Ten healthy subjects participated in a metabolic study. Subjects initially consumed their usual non-weight-reducing diet, then a severely carbohydrate-restricted induction diet for 2 weeks, followed by a moderately carbohydrate-restricted maintenance diet for 4 weeks. Urine pH decreased from 6.09 (Usual) to 5.56 (Induction; P < 0.01) to 5.67 (Maintenance;P < 0.05). Net acid excretion increased by 56 mEq/d (Induction; P < 0.001) and 51 mEq/d (Maintenance; P < 0.001) from a baseline of 61 mEq/d. Urinary citrate levels decreased from 763 mg/d (3.98 mmol/d) to 449 mg/d (2.34 mmol/d; P < 0.01) to 581 mg/d (3.03 mmol/d; P < 0.05). Urinary saturation of undissociated uric acid increased more than twofold. Urinary calcium levels increased from 160 mg/d (3.99 mmol/d) to 258 mg/d (6.44 mmol/d; P < 0.001) to 248 mg/d (6.19 mmol/d; P < 0.01). This increase in urinary calcium levels was not compensated by a commensurate increase in fractional intestinal calcium absorption. Therefore, estimated calcium balance decreased by 130 mg/d (3.24 mmol/d; P < 0.001) and 90 mg/d (2.25 mmol/d; P < 0.05). Urinary deoxypyridinoline and N-telopeptide levels trended upward, whereas serum osteocalcin concentrations decreased significantly (P < 0.01). Consumption of an LCHP diet for 6 weeks delivers a marked acid load to the kidney, increases the risk for stone formation, decreases estimated calcium balance, and may increase the risk for bone loss. Copyright 2002 by the National Kidney Foundation, Inc.
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            Pathophysiologic basis for normouricosuric uric acid nephrolithiasis.

            Low urinary pH is the commonest and by far the most important factor in uric acid nephrolithiasis but the reason(s) for this defect is (are) unknown. Patients with uric acid nephrolithaisis have normal acid-base parameters according conventional clinical tests. We studied steady-state plasma and urinary parameters of acid-base balance in subjects with normouricosuric pure uric acid stones. We also tested the ability of these subjects to excrete ammonium in response to an acute acid load. We compared these parameters in patients with pure uric acid stones to patients with mixed uric acid/calcium oxalate stones, pure calcium stones, and normal volunteers. Pure uric acid stone formers have a much higher incidence of either diabetes or glucose intolerance. After equilibration to a control diet, patients with uric acid stones have lower urinary pH and they excrete less of their acid as ammonium. This is compensated by higher titratable acidity and hypocitraturia. Despite their low baseline urinary pH, uric acid stone formers further acidify their urine after an acid load because of a severely impaired ammonia excretory response. Their characteristics are significantly different from normal volunteers and pure calcium stone formers. Patients with mixed uric acid/calcium stones exhibit intermediate characteristics. We propose that certain patients with normouricosuric uric acid nephrolithiasis have a renal acidification disease. The primary defect lies in renal ammonium excretion, which may be linked to the insulin-resistant state. Although net acid excretion is maintained at the expense of increased titratable acidity and to some degree hypocitraturia, the compromise is acid urine pH and may result in uric acid nephrolithiasis.
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              Randomized trial of allopurinol in the prevention of calcium oxalate calculi.

              In a double-blind study, we examined the efficacy of allopurinol in the prevention of recurrent calcium oxalate calculi of the kidney. Sixty patients with hyperuricosuria and normocalciuria who had a history of calculi were randomly assigned to receive either allopurinol (100 mg three times daily) or a placebo. After the study, the placebo group had 63.4 percent fewer calculi (P less than 0.001), whereas the allopurinol group had 81.2 percent fewer calculi (P less than 0.001). During the study period, the mean rate of calculous events was 0.26 per patient per year in the placebo group and 0.12 in the allopurinol group. When the treatment groups were compared by actuarial analysis, the allopurinol group was found to have a significantly longer time before recurrence of calculi (P less than 0.02). We conclude that allopurinol is effective in the prevention of calcium oxalate stones in patients with hyperuricosuria. The large reduction in the frequency of calculi in the placebo group underscores the positive treatment bias that regularly occurs in trials of prophylaxis against renal calculi when historical controls are used.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                October 2004
                17 November 2004
                : 98
                : 2
                : c49-c53
                Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Tex., USA
                80252 Nephron Clin Pract 2004;98:c49–c53
                © 2004 S. Karger AG, Basel

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                Tables: 1, References: 18, Pages: 1
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                Cardiovascular Medicine, Nephrology

                Kidney stones, Diet


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