By Deepa H. Chand, MD, MHSA Children with kidney disease are more prone to develop growth failure, especially if diagnosed with progressive renal failure under the age of 10 years. Growth failure can be defined as lack of linear growth as measured by height velocity, failure to gain weight, or both. There are treatments available and should be individualized to each child. Failure to thrive, as shown by a lack of weight gain, may be the initial sign that a child has kidney failure. First, the need for intervention, specifically dialysis or transplantation needs to be determined. Even despite appropriate intervention, the pediatric patient may still have persistent growth failure due to several other contributing factors. Specifically, the patient may have a disturbance in the biochemical pathway that regulates growth hormone (the body’s hormone which is responsible for growth), which would then present as a functional growth hormone deficiency. This typically occurs when the child’s kidney function has decreased to 30 percent or less of normal. However, there are other variables that can factor into growth failure such as nutritional deficiencies, metabolic acidosis (an offset in the body’s acid-base balance), anemia and renal osteodystrophy (bone disease related to renal failure). The confounding factors need to be corrected prior to supplementation with a growth hormone; otherwise the patient may not have maximum benefit from the growth hormone therapy. The nutritional needs of a child with renal failure are very different from those of healthy children. Due to chemical imbalances, the child’s taste buds may be altered causing a decrease in oral intake. Many children require additional nutrition in the form of a nasogastric or gastrostomy tube which is placed into the stomach to allow for food to be given directly into the stomach. While the patient is receiving tubule nutrition, a speech therapist may be able to assist with oral stimulation and oral intake. The caloric needs of a child with renal failure are generally much higher than a healthy child. Prior to any other intervention, caloric intake needs to be optimized. Protein intake needs are also increased in kidney failure patients, especially for those receiving peritoneal dialysis or who may have increased protein losses through dialysis. Appropriate vitamin and mineral supplementation need to be provided as well. In addition to optimizing nutritional needs, metabolic acidosis needs to be corrected. Children with renal failure often have an altered acid-base balance which can interfere with growth. Even if growth hormone therapy is given, acidosis can cause resistance to the medication, making it ineffective. Often times, metabolic acidosis can be corrected with dialysis; however, in the patient who does not yet require dialysis or the post transplant patient, correction of the acidosis may be achieved by giving the patient an oral form of bicarbonate either as a liquid or a pill. Anemia in renal failure is due to lack of production of erythropoietin (Epo), which is a major component of red blood cells. Ninety percent of the body’s Epo is produced in the kidneys, so when the kidneys fail, there is not enough production of Epo. Without adequate Epo, red blood cells cannot be formed, which causes a lower level of oxygen delivered throughout the body. This can lead to symptoms such as fatigue, decreased tolerance to exercise, decreased cognitive functioning and poor growth, among other symptoms. Epo can be given either through dialysis or by giving an injection of a synthetic form of the substance. Along with Epo deficiency, patients with kidney failure, especially those receiving hemodialysis, are also prone to iron deficiency, which can worsen anemia. The iron deficiency needs to be corrected by providing iron in either an intravenous or oral form. The current recommendations are to keep the patient’s hemoglobin between 11-12 gm/dl which corresponds to a hematocrit between 33-36 percent. Renal osteodystrophy, otherwise known as renal rickets, arises when the patient’s renal function declines to less than 40 percent of normal. At that point, the kidneys are not able to remove phosphorus, causing an increase in blood phosphorus levels which leads to a decrease in blood calcium levels. The low blood calcium triggers the parathyroid gland to secrete excess parathyroid hormone, which in turn increases bone resorption leading to rickets. Resorption is when material is broken down and absorbed by the body. Fortunately, this can be treated by providing supplemental calcitriol, which is an active form of Vitamin D. Calcitriol feeds back to the parathyroid gland thereby inhibiting the oversecretion of parathyroid hormone, preventing bony abnormalities. In addition to therapy with calcitriol, the patient should also receive phosphate binders so that the blood level of phosphorus remains in the normal range. By preventing the bony deformities of renal osteodystrophy, the patient is given the opportunity for optimum growth. If bony abnormalities are present, the patient may benefit from physical and occupational therapy in order to strengthen the bones and improve conditions for growth. Once all other factors have been optimized, consideration must be given to recombinant growth hormone to enhance linear growth. In renal failure, the body’s receptors to a growth hormone are altered; thereby making a person’s own growth hormone ineffective. Giving the recombinant form overcomes this functional deficiency and allows the growth hormone to work as it should. Prior to starting a growth hormone, the growth failure must be documented on the child’s age appropriate growth curve. Additionally, wrist x-rays need to be performed in order to document the patient’s bone age. The bone age is then correlated to the chronological age of the patient to make sure that the bones are not advanced for any reason, in which case growth hormone therapy may be detrimental. Furthermore, if the patient’s growth plates are fused, indicating that growth is complete, there will be no benefit from growth hormone therapy. Recombinant growth hormone is given by subcutaneous injection (similar to an insulin shot) typically every night. There is a long acting form of growth hormone which is also given by subcutaneous injection; however, it is only given once every other week. The patient’s physician and family should make the decision regarding which formulation is best for each patient. After therapy has been initiated, it is very important to track growth velocity and periodic bone age films. The decision to stop therapy should be made by the physician, patient and patient’s family as deemed appropriate. In children with chronic renal failure, many factors contribute to growth failure and must be considered, monitored and treated to optimize the pediatric renal patient’s growth and development. Dr. Chand is a pediatric nephrologist and medical director of the pediatric dialysis program at The Children’s Hospital, Cleveland Clinic, Cleveland, Ohio. This article originally appeared in the September 2003 issue of aakpRENALIFE, Vol. 19, No. 2. |