Management of Acute Kidney Injury and Chronic Kidney DiseaseManual of Clinical Nutrition Management III- 113 Copyright © 2013 Compass Group, Inc.
renal failure, it is usually caused by oliguria (24-hour urine output <500 mL); excessive potassium intake;
acidosis; the catabolic stress of infection, surgery, or trauma; inadequate dialysis or renal replacement
therapy; or hypoaldosteronism. Excessive potassium intake is frequently related to the use of potassium-
containing salt substitutes and dietary noncompliance. Hypokalemia, which is a potassium level less than 3.5
mEq/L, is caused by decreased dietary intake; vomiting; diarrhea; potassium-depleting diuretics; excessive
use of sodium polystyrene sulfonate (Kayexalate), a potassium binder; or a low-potassium dialysate.
Sodium: The evaluation of serum sodium levels must always include the patient’s hydration status.
Hypernatremia can be caused by excessive water loss through diarrhea and vomiting (dehydration) and
aggressive diuretic therapy without sodium restriction. Signs of hypernatremia include flushed skin, dry
tongue and mucous membranes, and thirst. Hyponatremia can be caused by fluid overload and sodium
depletion from sodium restriction along with sodium-losing nephropathy. Symptoms of hyponatremia
include abdominal cramps, hypotension, and headaches.
Calcium: In CKD, calcium absorption decreases secondary to the abnormal metabolism of vitamin D.
Hyperphosphatemia also leads to decreased serum calcium levels, which contribute to secondary
hyperparathyroidism and renal osteodystrophy (14). Derangements in mineral and bone metabolism common
to CKD are associated with increased morbidity and mortality (14). This finding prompted the development of
Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease by the Kidney
Disease Outcomes Quality Initiative (K/DOQI) (14). These guidelines provide recommendations for the
evaluation of phosphorus, calcium, and plasma intact parathyroid hormone and management and treatment
with vitamin D, phosphate binders, and the dialysate bath (14). Serum levels of phosphorus, ionized calcium
or a corrected total calcium, and plasma parathyroid hormone should be monitored, and the appropriate
guideline recommendations should be implemented when necessary (14). The goal of therapy is to achieve a
normal range of serum calcium, with the optimum level of 8.4 to 9.5 mg/dL (5,14). The presence of calcium in
the dialysate helps to normalize serum calcium levels in patients who receive hemodialysis, along with the
use of an activated source of vitamin D (calcitriol), an oral calcium supplement, a vitamin D analog
(doxercalciferol or paricalcitol), and a phosphorus binder. The most accurate method for assessing calcium
abnormalities is to measure the ionized calcium directly (2). It is an accepted practice that total calcium levels
need to be adjusted for the level of albumin to better reflect the ionized calcium (14). The corrected total
calcium is considered when the albumin level—not the serum calcium—is low (14). Currently two formulas
are suggested by K/DOQI guidelines for use (14). The first formula presented used a preferable study design in
the validation and most closely approximates corrected total calcium in patients with CKD (14):
Corrected calcium (mg/dL) = Total Calcium (mg/dL) + 0.0704 x [34 – Serum albumin (g/L)] (2,14)
uses g/L vs. g/dL
However, for the routine clinical interpretation of serum calcium needed for appropriate care of patients
with kidney disease, a simple formula for adjutsting total serum calcium concentrations for changes in serum
albumin concentration can by used by clinicians. This formula yields similar results to the formula described
above (2,14).
Corrected total calcium: Total calcium (mg/dL) + 0.8 x [4.0 – Serum albumin (g/dL)] (2,14).
The most accurate method for assessing calcium abnormalities is to measure the ionized calcium directly.
The second equation often overestimates the correted calcium concentration in critically ill patients receiving
specialized nutrition support (2,15).
Phosphorus: Low levels of serum phosphate may lead to phosphorus depletion and osteomalacia. The goal
of therapy is to maintain the phosphorus level between 2.7 to 5.0 mg/dL in patients who have stages I-IV CKD
and between 3.5 to 5.5 mg/dL in patients who receive renal replacement therapy (5,6). Refer to the Clinical
Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease by the Kidney Disease
Outcomes Quality Initiative (14).
Calcium-phosphorus product: The calcium-phosphorus product, which is the result of multiplying the
serum values of calcium and phosphorus, should be less than 55 mg^2 /dL^2 to prevent soft-tissue calcification
(16). Research regarding the calcium-phosphorus product is limited. Therefore, a target phosphorus level of
less than 5.0 mg/dL is suggested for patients who have CKD.
Creatinine: Creatinine is a product of muscle metabolism that is used to assess renal function. A serum
creatinine level that is double the normal level of 0.5 to 1.5 mg/dL suggests a greater than 50% nephron loss,