Medical Nutrition Therapy for Chronic Kidney DiseaseManual of Clinical Nutrition Management G- 13 Copyright © 20 13 Compass Group, Inc.
stage 3 CKD patients; greater than 110 pg/mL in stage 4 CKD patients; or greater than 300 pg/mL in stage 5
CKD patients (3,5,9). Control of serum phosphorus levels is usually not possible by diet alone (5,9). Calcium-
based, or non-calcium-based, non-aluminum-based phosphate binders are given at mealtimes to bind the
phosphate from food. The prescribed amount of phosphate binders should be individualized according to the
amount of phosphate present in a meal. Approximately 60% to 70% of ingested phosphorus is absorbed (10).
However, 100% of additive phosphorus from food enhancers or preservatives is absorbed, and phosphorus is
frequently added to many foods that were once considered to be low-phosphorus foods. One gram of calcium
carbonate (CaCO 3 ) binds roughly 39 mg of phosphorous, and 1 g of calcium acetate binds 40 to 60 mg of
phosphorous. Whereas CaCO 3 contains 40% elemental calcium, calcium acetate is composed of 25%
elemental calcium. Calcium acetate contains 167 mg of elemental calcium in each tablet, and CaCO 3 contains
500 mg. With an increased calcium-phosphorous product, sevelamer hydrochloride, sevelamer carbonate, or
lanthanum carbonate may be more effective and will not contribute to elevated phosphorus and calcium
levels. One 800-mg tablet of sevelamer hydrochloride or sevelamer carbonate replaces a calcium acetate
tablet (11,12). Typical starting doses of lanthanum carbonate are 500 to 1,000 mg with a designated meal. If
calcium and phosphorus levels are at the high end of the normal range, a calcium binder may increase these
levels to exceed the normal range and contribute to soft-tissue calcification. The goal is for the serum
calcium-phosphorus product to be less than 55 mg^2 /dL^2 (5,6,10). Aluminum-containing phosphate binders are
not recommended due to the risk for aluminum toxicity, which can lead to osteodystrophy, anemia, and
encephalopathy (3,9).
Calcium
CKD (stages 1 to 4): The secretion of parathyroid hormone, which affects bone integrity and soft tissue
calcification, is primarily regulated by serum calcium (1). The Chronic Kidney Disease Evidence-Based
Nutrition Practice Guideline recommends that the total elemental calcium intake in adults with CKD (stages 3
and 4, including kidney transplant recipients) not exceed 2,000 mg/day (including dietary calcium, calcium
supplementation, and calcium-based phosphate binders) to decrease the predisposition for mineral and bone
disorders (Grade IV)(1). The use of vitamin D and other supplements that impact the calcium level should also be
considered in the nutrition assessment of calcium needs (1,5,6,9,13). Refer to Section III: Nutrition Management
of Acute Kidney Injury and Chronic Kidney Disease for an expanded discussion on evaluating calcium in CKD
including suggested monitoring parameters and correcting total calcium for low albumin in the assessment of
calcium.
Hemodialysis and peritoneal dialysis: Calcium intake should be less than 2,000 mg/day or individualized
based on calcium, phosphorus, and parathyroid hormone levels and the use of vitamin D supplementation
(2,5,6,9). Intestinal absorption of calcium is impaired in uremia due to the lack of the active form of vitamin D
(3). Also, diets prescribed for patients with CKD tend to be low in calcium because of the restriction of dairy
products (5). Calcium supplementation is not typically recommended due to an association between
increased calcium load and cardiovascular calcification in CKD patients. As in CKD (stages 1 to 4), the general
dietary recommendation for patients who receive RRT depends on serum calcium levels and other factors. If
calcium supplements are needed, they should be taken between meals and not be confused with those
supplements used to bind phosphorus. An activated form of vitamin D can also be used to enhance calcium
absorption. It is important to use an adjusted calcium level in patients with low albumin levels.
Magnesium
The kidney is the organ primarily responsible for the maintenance of serum magnesium. Patients with
uremia should be wary of laxatives, enemas, antacids, or phosphate binders (eg, MagneBindTM, which
combines magnesium and CaCO 3 ) that contain magnesium (3,4). If these products are used, magnesium levels
should be monitored (2). Excess magnesium mainly accumulates in bone tissue, where it is deleterious to
bone metabolism. Symptoms of excess magnesium include muscle weakness, hypotension,
electrocardiographic changes, sedation, and confusion. If the patient’s magnesium levels are too high, the
level of magnesium in the dialysate can be decreased.
Guidelines for Vitamin and Trace Mineral Supplementation in CKD
Vitamins: The diet for CKD contains less than the Dietary Reference Intakes (DRIs) for several water-soluble
vitamins because of the restricted intake of foods high in protein and potassium (5). Other causes of vitamin
deficiencies include impaired food intake as a result of uremia and alterations in the absorption, metabolism,
or activity of some vitamins. The most common vitamin deficiencies in CKD include vitamin D, folic acid,
vitamin B 6 , and vitamin C (5). Studies do not support the routine supplementation of fat-soluble vitamins
other than vitamin D for patients consuming well-balanced, adequate diets (5,9). Patients with CKD have a