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EDITORIAL
Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 1

Striking balance between protein requirement and dietary phosphorus restrictions


Editor, JRNM; Department of Nephrology, SGPGIMS, Lucknow, Uttar Pradesh, India

Date of Web Publication15-Nov-2019

Correspondence Address:
Dr. Anita Saxena
Editor, JRNM; Department of Nephrology, SGPGIMS, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_51_19

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How to cite this article:
Saxena A. Striking balance between protein requirement and dietary phosphorus restrictions. J Renal Nutr Metab 2019;5:1

How to cite this URL:
Saxena A. Striking balance between protein requirement and dietary phosphorus restrictions. J Renal Nutr Metab [serial online] 2019 [cited 2019 Dec 11];5:1. Available from: http://www.jrnm.in/text.asp?2019/5/1/1/271046





Editorial from 2018 (Issue 4)

This Editorial is in the reference to the special issue of SRNMCON 2018 published recently (Volume 4 - Issue 4). In that special issue, two articles on “protein intake and phosphate restriction in chronic kidney disease – can we separate the wheat from chaff?” and “dietary management of hyperphosphatemia in CKD” emphasizes on the importance of providing appropriate protein while maintaining phosphorus content of diet within recommended limits and also on the importance of addressing phosphorus-to-protein ratio in foods during dietary counseling of patients with CKD.

Dietary phosphorus intake is credited in part to natural abundance of phosphorus in foods and also to the use of phosphate-containing food additives. The net phosphorus load from food intake is a function of phosphorus content of the ingested food and bioavailability of phosphorus from different sources of diet, food preparation techniques, and Vitamin D status. In health, the phosphorus ingested is utilized in metabolism for the maintenance of homeostasis.[1] However, when renal excretion is impaired, phosphorus retention occurs even from normal dietary phosphorus intake. In chronic kidney disease (CKD), hyperphosphatemia causes secondary hyperparathyroidism and elevated blood levels of fibroblast growth factor receptor 23 and parathyroid hormone (PTH) by lowering the levels of ionized calcium, interfering with the production of 1,25(OH)2D3, and directly affecting PTH secretion. It has been shown that serum phosphate levels above 3.5 mg/dL are significantly associated with mortality (Kestenbaum's study) and that the risk of mortality increases progressively with every 0.5 mg/dL increase in the phosphate serum levels. In CKD, hyperphosphatemia is considered a risk factor for the progression of coronary artery calcification/disease. The RIND study evaluated progression of coronary artery calcification in incident hemodialysis patients and demonstrated that vascular calcification processes start manifesting in CKD patients before the dialysis stage, which may be closely linked to early and invisible derangements in calcium and phosphate homeostasis.[2] Striking balance between optimal protein requirement while maintaining dietary phosphorus intake within recommended target (800–1000 mg/day) is an important issue in CKD. The naturally existing organic phosphorus is only partially (<60%) absorbed in the gastrointestinal tract; however, this absorption varies with source of phosphorus. Phosphorus absorption is low (<40%) from plant-based protein as the human body does not produce enzyme phytase. Phosphorus absorption is higher from foods of animal origin and foods enhanced with inorganic phosphorus-containing preservatives (>80%). The KDIGO guidelines 2009 recommend maintaining phosphate serum levels within normal range in CKD patients in Stages 3–5. In predialysis, dietary phosphorus burden is limited in patients on low protein diet, i.e., 0.6 g/kg/day, while patients in dialysis requiring higher protein intake of 1.2 g/kg/day, are exposed to a higher dietary phosphorus intake.[3]



 
  References Top

1.
Ketteler M. Phosphate metabolism in CKD stages 3-5: Dietary and pharmacological control. Int J Nephrol 2011;2011:970245.  Back to cited text no. 1
    
2.
Block GA, Spiegel DM, Ehrlich J, Mehta R, Lindbergh J, Dreisbach A, et al. Effects of sevelamer and calcium on coronary artery calcification in patients new to hemodialysis. Kidney Int 2005;68:1815-24.  Back to cited text no. 2
    
3.
Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl 2009;188:S1-130.  Back to cited text no. 3
    




 

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