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Year : 2018  |  Volume : 4  |  Issue : 4  |  Page : 95-97

Protein intake and phosphate restriction in chronic kidney disease – Can we separate the wheat from chaff?

Consultant Nephrologist, Meenakshi Mission Hospital and Research Centre, Madurai, Tamil Nadu, India

Date of Web Publication19-Sep-2019

Correspondence Address:
Dr. K Sampathkumar
Meenakshi Mission Hospital and Research Centre, Madurai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_41_19

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Chronic kidney disease (CKD) has evolved into a major noncommunicable disease in India due to both increased incidence and diagnosis. It is believed to affect <10% of adult population who are at excess risk of cardiovascular (CV) and renal morbidity and mortality. The incidence of end-stage renal disease is about 152 per million which is driven by diabetes, hypertension, and chronic glomerulonephritis. In later stages of CKD, phosphate (P) retention is the rule with its myriad pathological links to vascular calcification and CV mortality. This article focuses on protein intake and P restriction in CKD.

Keywords: Chronic kidney disease, diet, fibroblast growth factor 23 (FGF23), phosphate

How to cite this article:
Sampathkumar K. Protein intake and phosphate restriction in chronic kidney disease – Can we separate the wheat from chaff?. J Renal Nutr Metab 2018;4:95-7

How to cite this URL:
Sampathkumar K. Protein intake and phosphate restriction in chronic kidney disease – Can we separate the wheat from chaff?. J Renal Nutr Metab [serial online] 2018 [cited 2020 Aug 13];4:95-7. Available from: http://www.jrnm.in/text.asp?2018/4/4/95/267205

  Introduction Top

Chronic kidney disease (CKD) has evolved into a major noncommunicable disease in India due to both increased incidence and diagnosis. It is believed to affect <10% of adult population who are at excess risk of cardiovascular (CV) and renal morbidity and mortality. The incidence of end-stage renal disease is about 152 per million, which is driven by diabetes, hypertension, and chronic glomerulonephritis. As renal function takes on a downward spiral, multiple abnormalities accrue in the bone mineral axis which are broadly designated as CKD mineral and bone disorder. It was originally believed that phosphate (P) retention with depression of serum calcium levels leads to hypersecretion of parathyroid hormone, setting the stage for renal osteodystrophy. This paradigm stands changed, as it is now known that bone starts releasing fibroblast growth factor-23 at much higher levels of glomerular filtration rate (GFR) to facilitatePexcretion from the proximal nephron. In late stages of CKD, Pretention is the rule with its myriad pathological links to vascular calcification and CV mortality. Hence, dietary phosphorus restriction is an important anchor in the conservative management of CKD.

Serum levels of phosphorus are not raised in the CKD 2 and 3 stages (2.5–4.5 mg/dl) but show upward trend in Stage 4 and 5 CKD onward. It is a misconception that hyperphosphatemia is less of an issue in Indian population given their predominant agro-based food habits. However, publications show that up to 60% of Stage 4 and 75% of Stage 5 CKD patients are hyperphosphatemic.[1] Dietary phosphorus reduction goes a long way in reducing the whole body burden in advanced stages of CKD.

  Dietary Sources Of Phosphorus Top

The usual daily intake of phosphorus varies significantly across nations and societies. For the typical Indian diet, young- and middle-aged men consume about 800 mg/day (D), while comparably aged women consume about 1000 mg/D. These are only guesstimates of dietary phosphorus intake since what is absorbed may be different depending on the source. Indian diet, including rice and wheat-based rotis, is high in phosphorus content. A cup of rice has about 160 mg of phosphorus, which becomes challenging for Indian patients with advanced CKD. Three major sources ofPare natural phosphorus contained in raw food as cellular and protein content, phosphorus additives in processing, and phosphorus in dietary supplements. Recommended dietary reference intake (DRI) ofPis 700 mg/D in healthy adults. According to the Kidney Disease Outcomes Quality Initiative recommendations, Pintake should not exceed DRI in patients with early stages of CKD (Stages 2 and 3) and to 80% of DRI in CKD Stages 4 and 5. This applies to those with normal serumPlevels also. The dietary source ofPcan be either plant or animal based [Figure 1]. OrganicPis bound to proteins, andPis released after hydrolysis in the gut. Plant sources ofPare bound to phytates. Since humans lack the enzyme phytase in their intestines, bioavailability ofPis less when compared to animal source. Hence, when the bulk of proteins in CKD is available from plant source, the threat of hyperphosphatemia is less as shown in studies comparing both sources of protein in CKD.[2] Less than 50% ofPis absorbed from the plant source. On the other hand, food processing industry has turned to inorganicPfor storage and taste-enhancing capabilities. InorganicPis not bound to proteins and is more readily absorbed with up to 90% absorption. Although it is a worrying phenomenon in the west, its threat is real in the urban Indian population too.
Figure 1: Phosphorus pyramid, a visual tool for planning low phosphorus diet

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It has recently been recognized that absorption of P from the gastrointestinal tract is not downregulated in CKD.[3] This is counterintuitive given the expected feedback inhibition ofPabsorption. This maladaptive response maintains higher levels ofPabsorption, thereby contributing to thePburden. Moreover, in response to a low-P diet, as often is prescribed to such patients, gutPabsorption may be enhanced, much the same way as the distal nephron increases the sodium absorption in the face of diuretic therapy. This undermines the benefits of dietaryPrestriction.

  Phosphate: Protein Ratio Top

The intricate relationship between P and protein is highlighted in [Table 1], which shows a higher P:protein ratio in the lactoovovegetarian source than animal source.[4] However, the bioavailability in the plant source is restricted due to the reasons described above.
Table 1: Relationship between phosphorus and protein in common food items[4]

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Italian investigators have developed a phosphorus pyramid for quick visual education.[5] The pyramid consists of six levels, in which foods are arranged on the basis of their phosphorus content, phosphorus to protein ratio, and phosphorus bioavailability. Each has a colored edge (from green to red) that corresponds to recommended intake frequency, ranging from “unrestricted” to “avoid as much as possible.”

  When Should Serum Phosphate Be Measured? Top

Hitherto, serumPlevels were measured in fasting samples only in major studies. A small but insightful study showed that serumPlevels are lowest at 8 AM and shows two circadian peaks at 4 PM and 4 AM.[3] In CKD patients whosePintake was restricted, the 4 PM peak was absent. Hence, an early evening sample can be used as a measure ofPreduction.

  Drugs Top

When dietary restriction fails to reduce the elevated phosphorus levels in CKD, recourse must be taken to drugs to reducePabsorption from the gut. There are calcium-based and noncalcium-containingPbinders. The former includes calcium carbonate and acetate. The binding power of acetate moiety is better although the calcium absorption is higher with a potential for vascular deposition. Pill burden is a signifi cant dampener to its compliance. Patients skipping regular doses is a common scenario. Sevelamer carbonate and lanthanum carbonate have shown excellent P-binding properties with reduced vascular calcium deposition. In a 3-year prospective study of predialysis patients with hyperphosphatemia and vascular calcification, it was shown that sevelamer delivered beneficial results.[6] A significant reduction in all-cause mortality, dialysis initiation, and composite end-point risk was achieved by combining phosphorus-restricted diet and sevelamer in nondialysis CKD patients with absent or moderate but not accelerated coronary artery calcification progression. Pill burden and cost considerations weigh in for Indian patients. Niacin is a low-cost alternative, and pill burden is as low as single tablet of 500 mg/D.[7]

  Phosphate Control in Maintained Hemodialysis Top

Phosphorus is relatively well dialyzed through most currently used hemodialyzers. Its molecular weight is 134 (creatinine molecular weight = 113), and hence, it is classified as small solute in the same frame as urea and creatinine. However, it differs in one important aspect that it is predominantly an intracellular solute.

At stable serum phosphorus concentration, the clearance by high flux dialyzer approximates creatinine clearance which is approximately 230 ml/min at a blood pump speed of 300 ml/min. At aPlevel of 6 mg/dl, this clearance should provide a total phosphorus removal of about 3312 mg/240 min session. However, in reality, thePremoval is three-fold less and amounts to 800–1000 mg/D. Prolonged daily nocturnal dialysis achieves the bestPclearance, and it cannot be matched by short daily dialysis schedules which are popular.[8]

  Protein Intake and Phosphate Intake of Chronic Kidney Disease Patients – Meenakshi Mission Hospital Data Top

In our center, a food diary-based estimate of mean dailyPintake in 50 patients with Stage 4 CKD with a mean eGFR of 21 ml/min showed that it was 614 ± 73 mg against a mean protein intake of 51 g/D (0.8 g/kg/D of protein intake). In comparison, when we queried the dietary intake of 56 maintained hemodialysis patients, the mean dailyPintake was 632 ± 131 mg with protein intake of 54 ± 7 g/D. This translates into 0.89 g/kg/D of protein intake. Somewhat surprisingly, the protein and phosphorus intake of dialysis patients was trending better than in advanced Stage 4 CKD, which possibly points toward a better appetite after uremic retention products are removed.

In the absence of a trial looking at clinically relevant endpoints such a CV events and mortality in those randomized to high versus low serumPlevels, recourse should be taken to expert recommendations only. Such a trial has just been convened in the US (Hilo trial). We will await the results of the trial with interest [Figure 2].
Figure 2: Phosphorus control

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  Conclusion Top

When confronted with the clinical conundrum of balancing adequate protein intake withPrestriction, combining aPbinder with minimum pill burden should be the way forward.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Ghosh B, Brojen T, Banerjee S, Singh N, Singh S, Sharma OP, et al. The high prevalence of chronic kidney disease-mineral bone disorders: A hospital-based cross-sectional study. Indian J Nephrol 2012;22:285-91.  Back to cited text no. 1
[PUBMED]  [Full text]  
Moe SM, Zidehsarai MP, Chambers MA, Jackman LA, Radcliffe JS, Trevino LL, et al. Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease. Clin J Am Soc Nephrol 2011;6:257-64.  Back to cited text no. 2
Ix JH, Anderson CA, Smits G, Persky MS, Block GA. Effect of dietary phosphate intake on the circadian rhythm of serum phosphate concentrations in chronic kidney disease: A crossover study. Am J Clin Nutr 2014;100:1392-7.  Back to cited text no. 3
Uribarri J. Phosphorus homeostasis in normal health and in chronic kidney disease patients with special emphasis on dietary phosphorus intake. Semin Dial 2007;20:295-301.  Back to cited text no. 4
D'Alessandro C, Piccoli GB, Cupisti A. The “phosphorus pyramid”: A visual tool for dietary phosphate management in dialysis and CKD patients. BMC Nephrol 2015;16:9.  Back to cited text no. 5
Russo D, Bellasi A, Pota A, Russo L, Di Iorio B. Effects of phosphorus-restricted diet and phosphate-binding therapy on outcomes in patients with chronic kidney disease. J Nephrol 2015;28:73-80.  Back to cited text no. 6
Sampathkumar K. Niacin for phosphate control: A case of David versus Goliath. Indian J Nephrol 2016;26:237-8.  Back to cited text no. 7
[PUBMED]  [Full text]  
Elias RM, Alvares VR, Moysés RM. Phosphate removal during conventional hemodialysis: A decades-old misconception. Kidney Blood Press Res 2018;43:110-4.  Back to cited text no. 8


  [Figure 1], [Figure 2]

  [Table 1]


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