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In the past 20 years, with the use of dialysis and kidney transplantation, there has been great improvement in the care of patients with chronic kidney failure. Improvements in the care still need to be made and the best course of treatment is not certain. There are problems, unique to children, who have chronic kidney failure. Growth in children is impaired because of chronic kidney failure. This problem is compounded because children with chronic kidney failure do not eat as much. An aggressive approach must be taken for the child to receive nutrients, including dietary supplements given through tubes in the stomach or nose, until the child is old enough to undergo kidney transplantation. The youngest age that a child can receive a kidney transplant without increased risks of rejection has not been determined. Some institutions have had good success rates in very young children. However, data compiled by the North American Pediatric Renal Transplant Cooperative Study on over 1,200 kidney transplants in children from various institutions in North America, show that graft rejection is greater in infants younger than two years old. With new biological products now available through recombinant DNA technology, treatment of children with kidney disease has improved. The administration of erythropoietin, a hormone that causes maturation of red blood cells and corrects anemia, improves appetite. Preliminary studies show that the administration of human growth hormone results in increased growth of children with chronic kidney disease. Other studies show that children who are on dialysis for long periods of time do not have a better rate of survival of the kidney transplant than children who have not been on dialysis for long periods of time. This differs from the case with adults, where those on dialysis for long periods of time have better survival rates of kidney grafts compared with those not on dialysis. Thus, with new options available, the best approach for treatment of children with kidney failure must be further analyzed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Various conditions associated with failure to thrive have been associated with chronic depletion of salt in the body. Babies born with certain structural kidney diseases are unable to retain adequate amounts of salt in their bodies. Children with chronic diseases, such as congenital heart disease or lung dysplasia (abnormal development), often need long-term treatment with strong diuretics (drugs that promote the formation and excretion of urine from the body). Depletion of body sodium (salt) is often considered a result of growth failure, rather than a cause. A case is presented of a boy with long-term salt-depletion who was followed from infancy. The salt depletion was a result of removal of the colon. The child was born without ganglia (nerve cells) in the entire large intestine, which required removal of the colon, and the ileal portion of the small intestine was used as an artificial anus. The patient had further surgery at one year of age and decreased blood sodium level was observed. He was seen again at age seven for slowed development (height and weight below the 5th percentile). When he was seen again at age nine with the same complaint, sodium chloride supplementation with increasing dosages were administered; with this supplementation, he reported feeling better. At age nine his height was -4.8 standard deviation score for height (SDS). Between ages seven and nine his growth velocity averaged -1.4 SDS/year; over the next two and one half years his growth velocity increased to +0.2 and +2.1. A significant correlation was noted between actual growth per month and salt intake during that period. It is suspected that salt depletion may be an associated factor in growth impairment of chronically ill children. (Consumer Summary produced by Reliance Medical Information, Inc.)

Renal and liver transplantation are now recognized as therapeutic modalities for children with kidney and liver failure. This article reviews the general indications for transplantation, recipient selection, descriptions of the procedures, and the expected outcome of these two procedures in the pediatric setting.

Although appropriate nutrition may not reverse the progression of renal disease or restore growth and body composition to normal, inattention to dietary factors is associated with more severe growth failure, more significant alterations in body composition, and more rapid deterioration in the patient’s sense of well-being. This article identifies the nutritional problems associated with chronic renal insufficiency and suggests tentative approaches to treatment.

The effects of feeding a sodium-deficient (NaD) diet were examined in young, growing rats. All animals were fed the same diet and drank distilled water. In the control group the water contained 37 mM sodium chloride. After 2-3 wk body composition measurements were performed and epitrochlearis muscle protein synthesis and degradation rates determined. The experimental group gained only 45 of the wt and 70 of the length seen in the control group. The difference in wt gain could not be accounted for by differences in extracellular volume which averaged only 4 of body wt. Although total food intake was equivalent in both groups, urinary ammonia plus urea nitrogen excretion was higher in the experimental animals. Protein synthesis, measured as the incorporation of 14C-phenylalanine into muscle protein was significantly lower in NaD rats (56.58 versus68.79) and (65.26 versus 83.88 nmol phenylalanine/h/g wet wt (both p< 0.01) when incubated with or without the addition of insulin (1 mU/ mL). Net protein degradation rates were unchanged. Gastrocnemius muscle RNA concentrations were also lower in NaD rats (1.09 versus 1.52 mg/g wet wt, p< 0.001). There were no changes noted in the concentration of protein within either gastrocnemius or epitrochlearis muscles. These results suggest that in rats, the growth failure seen in sodium deficiency: 1) affects both length and wt gain; 2) is not associated with decreased nutrient intake; 3) is due to decreased rates of muscle protein synthesis without affecting net protein degradation rates; and 4) is associated with diminished muscle tissue RNA concentrations.

Nτ-Methylhistidine (MH) and creatinine levels were determined in amniotic fluid and maternal serum from 81 women undergoing midtrimester amniocentesis for reasons other than the diagnosis of neuromuscular disease. Samples were also examined in three pregnancies with male fetuses who were subsequently found to have Duchenne muscular dystrophy (DMD). Between 16 and 20 weeks' gestation, amniotic fluid and maternal serum MH levels averaged 3.22 and 1.94 μmoles/L, respectively. No significant differences were found between the control and affected fetuses for MH and creatinine levels or for MH/creatinine ratios from amniotic fluid or maternal serum. Determination of amniotic fluid MH level thus has no apparent value in the prenatal diagnosis of DMD.

In situations where complete urine collections are difficult to obtain, single-injection methods have been recommended for the assessment of glomerular filtration rates (GFRs) without recourse to urine collections.1-6 These methods have generally used millicurie doses of isotope or smaller doses and scanning equipment. This report describes the effectiveness of technetium Tc 99m pentetate at a dose of 1 to 2 μCi/kg for the assessment of GFR.Methods.—The technetium Tc 99m pentetate was prepared from a commercial kit, diluted to 1 to 2 μCi/kg in approximately 3 mL of physiologic saline, and placed in a plastic syringe. After weighing the syringe on an analytical balance, 0.1 mL was injected into a 100-mL volumetric flask for use as a counting standard, and the syringe was reweighed. The remaining solution was injected into the subject's vein through a butterfly needle, the butterfly was flushed with 10 mL of saline, the time