Nutrition Interventions for Children with Special Health Care Needs

Section 3 - Condition-Specific Nutrition Interventions
Even with adequate nutrition, a child with CKD will not grow unless metabolic
acidosis is corrected and bone disease is treated. Metabolic acidosis (diagnosed by a
low serum bicarbonate level) is a major factor in failure to thrive and contributes to
bone demineralization; it is generally corrected by giving sodium bicarbonate.
The biggest factor in bone demineralization is 1,25(OH)2 vitamin D deficiency.
Vitamin D is activated in the kidney. As kidney function decreases with CKD,
activation of 25 (OH) vitamin D to1,25 (OH)2 vitamin D is decreased. This results
in decreased intestinal absorption of calcium and subsequent hypocalcemia.
Hypocalcemia stimulates the production of parathyroid hormone (PTH), which results
in release of calcium from the bone. Deficiency of 25(OH) D is also common in
children with CKD and should be corrected prior to treatment with activated Vitamin
D. In the early stages of CKD, correction of 25(OH) Vitamin D levels may result in a
normal PTH level.
Another factor in bone disease is retention of phosphorus in the blood. This also
stimulates production of parathyroid hormone, further increasing mineral loss from
the bone. Bone disease is prevented and treated by giving vitamin D2 or 3 if 25 (OH)
Vitamin D level is low, as well as 1,25 (OH)2 vitamin D (calcitriol, paricalcitol) based
on PTH levels. It is also necessary to limit phosphorus in the diet and give phosphate
binders with meals. Calcium carbonate, calcium acetate and sevelamer are the
most commonly used phosphate binders. The calcium based binders also serve to
supplement calcium. With vigilant attention to treatment, bone development can be
fairly normal (1).
Anemia is a major problem for all patients with significant CKD. The main cause
of anemia is decreased production of the hormone erythropoietin by the kidneys.
Erythropoietin stimulates the bone marrow to produce red blood cells. Anemia is
treated by giving erythropoiesis-stimulating agents (ESA’s), such as epoetin alpha or
darbepoetin, subcutaneously or parenterally up to 2 to 3 times per week. In order for
ESA’s to work to produce red blood cells, adequate amounts of iron must be given.
Iron stores are quickly depleted when ESA’s are started, and hematocrit is rapidly
increased (5). It is often necessary to give IV iron to patients on ESA’s to keep up
with the demand for production of red blood cells (1).
Despite early medical intervention and adequate nutrition support, children with
CKD often continue to exhibit slow growth and rarely achieve catch-up linear growth
without the use of recombinant growth hormone therapy (1,4,5,9). Long-term
growth hormone treatment of growth retarded children with CKD results in significant
improvement in linear growth with few side effects. Many children with CKD treated
with growth hormone from a young age are able to reach their genetic potential.
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