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Optimum nutrition for kidney stone disease.

Abstract

We summarize the data regarding the associations of individual dietary components with kidney stones and the effects on 24-hour urinary profiles. The therapeutic recommendations for stone prevention that result from these studies are applied where possible to stones of specific composition. Idiopathic calcium oxalate stone-formers are advised to reduce ingestion of animal protein, oxalate, and sodium while maintaining intake of 800 to 1200 mg of calcium and increasing consumption of citrate and potassium. There are few data regarding dietary therapy of calcium phosphate stones. Whether the inhibitory effect of citrate sufficiently counteracts increasing urine pH to justify more intake of potassium and citrate is not clear. Reduction of sodium intake to decrease urinary calcium excretion would also be expected to decrease calcium phosphate stone recurrence. Conversely, the most important urine variable in the causation of uric acid stones is low urine pH, linked to insulin resistance as a component of obesity and the metabolic syndrome. The mainstay of therapy is weight loss and urinary alkalinization provided by a more vegetarian diet. Reduction in animal protein intake will reduce purine ingestion and uric acid excretion. For cystine stones, restriction of animal protein is associated with reduction in intake of the cystine precursor methionine as well as cystine. Reduction of urine sodium results in less urine cystine. Ingestion of vegetables high in organic anion content, such as citrate and malate, should be associated with higher urine pH and fewer stones because the amino acid cystine is soluble in more alkaline urine. Because of their infectious origin, diet has no definitive role for struvite stones except for avoiding urinary alkalinization, which may worsen their development.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Nephrology Division, Universidade Federal de São Paulo, São Paulo, Brazil.

    Source

    Advances in chronic kidney disease 20:2 2013 Mar pg 165-74

    MeSH

    Beverages
    Calcium, Dietary
    Citric Acid
    Dietary Proteins
    Energy Intake
    Fructose
    Humans
    Kidney Calculi
    Oxalates
    Phytic Acid
    Potassium, Dietary
    Sodium, Dietary

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    23439376

    Citation

    Heilberg, Ita P., and David S. Goldfarb. "Optimum Nutrition for Kidney Stone Disease." Advances in Chronic Kidney Disease, vol. 20, no. 2, 2013, pp. 165-74.
    Heilberg IP, Goldfarb DS. Optimum nutrition for kidney stone disease. Adv Chronic Kidney Dis. 2013;20(2):165-74.
    Heilberg, I. P., & Goldfarb, D. S. (2013). Optimum nutrition for kidney stone disease. Advances in Chronic Kidney Disease, 20(2), pp. 165-74. doi:10.1053/j.ackd.2012.12.001.
    Heilberg IP, Goldfarb DS. Optimum Nutrition for Kidney Stone Disease. Adv Chronic Kidney Dis. 2013;20(2):165-74. PubMed PMID: 23439376.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Optimum nutrition for kidney stone disease. AU - Heilberg,Ita P, AU - Goldfarb,David S, PY - 2012/09/04/received PY - 2012/11/15/revised PY - 2012/12/05/accepted PY - 2013/2/27/entrez PY - 2013/2/27/pubmed PY - 2013/9/26/medline SP - 165 EP - 74 JF - Advances in chronic kidney disease JO - Adv Chronic Kidney Dis VL - 20 IS - 2 N2 - We summarize the data regarding the associations of individual dietary components with kidney stones and the effects on 24-hour urinary profiles. The therapeutic recommendations for stone prevention that result from these studies are applied where possible to stones of specific composition. Idiopathic calcium oxalate stone-formers are advised to reduce ingestion of animal protein, oxalate, and sodium while maintaining intake of 800 to 1200 mg of calcium and increasing consumption of citrate and potassium. There are few data regarding dietary therapy of calcium phosphate stones. Whether the inhibitory effect of citrate sufficiently counteracts increasing urine pH to justify more intake of potassium and citrate is not clear. Reduction of sodium intake to decrease urinary calcium excretion would also be expected to decrease calcium phosphate stone recurrence. Conversely, the most important urine variable in the causation of uric acid stones is low urine pH, linked to insulin resistance as a component of obesity and the metabolic syndrome. The mainstay of therapy is weight loss and urinary alkalinization provided by a more vegetarian diet. Reduction in animal protein intake will reduce purine ingestion and uric acid excretion. For cystine stones, restriction of animal protein is associated with reduction in intake of the cystine precursor methionine as well as cystine. Reduction of urine sodium results in less urine cystine. Ingestion of vegetables high in organic anion content, such as citrate and malate, should be associated with higher urine pH and fewer stones because the amino acid cystine is soluble in more alkaline urine. Because of their infectious origin, diet has no definitive role for struvite stones except for avoiding urinary alkalinization, which may worsen their development. SN - 1548-5609 UR - https://www.unboundmedicine.com/medline/citation/23439376/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S1548-5595(12)00221-2 DB - PRIME DP - Unbound Medicine ER -