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      Nutritional therapy, phosphate control and renal protection.

      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Nephron. Clinical practice
      Publisher: S. Karger AG

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          Abstract

          Dietary management of chronic kidney disease (CKD) focusses on limiting the intake of substances that might accumulate to toxic levels (such as potassium, phosphorus or salt) and, although still a matter of debate for some, restricting dietary protein to retard kidney damage. Recent evidence brings the opportunity to revisit the role of a healthy diet on disease progression and on some of the cardiometabolic complications of moderate/advanced CKD, such as inflammation or oxidative stress control. This review provides a brief overview of dietary strategies that delay CKD progression and CKD complications, and discusses currently limited data addressing the development of malnutrition and protein-energy wasting before dialysis initiation.

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          Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline.

          Paul E. Stevens (2013)
          The Kidney Disease: Improving Global Outcomes (KDIGO) organization developed clinical practice guidelines in 2012 to provide guidance on the evaluation, management, and treatment of chronic kidney disease (CKD) in adults and children who are not receiving renal replacement therapy. The KDIGO CKD Guideline Development Work Group defined the scope of the guideline, gathered evidence, determined topics for systematic review, and graded the quality of evidence that had been summarized by an evidence review team. Searches of the English-language literature were conducted through November 2012. Final modification of the guidelines was informed by the KDIGO Board of Directors and a public review process involving registered stakeholders. The full guideline included 110 recommendations. This synopsis focuses on 10 key recommendations pertinent to definition, classification, monitoring, and management of CKD in adults.
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            Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease.

            Sharon Moe, Miriam P Zidehsarai, Mary Chambers … (2011)
            Patients with advanced chronic kidney disease (CKD) are in positive phosphorus balance, but phosphorus levels are maintained in the normal range through phosphaturia induced by increases in fibroblast growth factor-23 (FGF23) and parathyroid hormone (PTH). This provides the rationale for recommendations to restrict dietary phosphate intake to 800 mg/d. However, the protein source of the phosphate may also be important. We conducted a crossover trial in nine patients with a mean estimated GFR of 32 ml/min to directly compare vegetarian and meat diets with equivalent nutrients prepared by clinical research staff. During the last 24 hours of each 7-day diet period, subjects were hospitalized in a research center and urine and blood were frequently monitored. The results indicated that 1 week of a vegetarian diet led to lower serum phosphorus levels and decreased FGF23 levels. The inpatient stay demonstrated similar diurnal variation for blood phosphorus, calcium, PTH, and urine fractional excretion of phosphorus but significant differences between the vegetarian and meat diets. Finally, the 24-hour fractional excretion of phosphorus was highly correlated to a 2-hour fasting urine collection for the vegetarian diet but not the meat diet. In summary, this study demonstrates that the source of protein has a significant effect on phosphorus homeostasis in patients with CKD. Therefore, dietary counseling of patients with CKD must include information on not only the amount of phosphate but also the source of protein from which the phosphate derives.
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              Timing of onset of CKD-related metabolic complications.

              Bruno Fouqueray, Cédric Gauci, Jean-Philippe Haymann … (2008)
              Chronic kidney disease (CKD) guidelines recommend evaluating patients with GFR <60 ml/min per 1.73 m(2) for complications, but little evidence supports the use of a single GFR threshold for all metabolic disorders. We used data from the NephroTest cohort, including 1038 adult patients who had stages 2 through 5 CKD and were not on dialysis, to study the occurrence of metabolic complications. GFR was measured using renal clearance of (51)Cr-EDTA (mGFR) and estimated using two equations derived from the Modification of Diet in Renal Disease study. As mGFR decreased from 60 to 90 to <20 ml/min per 1.73 m(2), the prevalence of hyperparathyroidism increased from 17 to 85%, anemia from 8 to 41%, hyperphosphatemia from 1 to 30%, metabolic acidosis from 2 to 39%, and hyperkalemia from 2 to 42%. Factors most strongly associated with metabolic complications, independent of mGFR, were younger age for acidosis and hyperphosphatemia, presence of diabetes for acidosis, diabetic kidney disease for anemia, and both male gender and the use of inhibitors of the renin-angiotensin system for hyperkalemia. mGFR thresholds for detecting complications with 90% sensitivity were 50, 44, 40, 39, and 37 ml/min per 1.73 m(2) for hyperparathyroidism, anemia, acidosis, hyperkalemia, and hyperphosphatemia, respectively. Analysis using estimated GFR produced similar results. In summary, this study describes the onset of CKD-related complications at different levels of GFR; anemia and hyperparathyroidism occur earlier than acidosis, hyperkalemia, and hyperphosphatemia.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nephron Clin Pract
                Title: Nephron. Clinical practice
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2110
                ISSN (Print): 1660-2110
                Publication date (Electronic): 2014
                Volume: 126
                Issue: 1
                Affiliations
                [1 ] Division of Nephrology and Center for Molecular Medicine, Karolinska Institute, Stockholm, Sweden.
                Article
                Publisher Item ID: 000357679
                DOI: 10.1159/000357679
                PubMed ID: 24434650
                SO-VID: 15f1d1a2-a963-4096-a015-7b6bfacf5674
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