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The development of effective treatments for children with end‐stage renal disease has been realized over the past three decades. Progress in dialysis and transplantation has resulted in a sophisticated management approach to this problem. Supportive care of the child with chronic renal insufficiency includes attention to nutritional status, prevention and control of bone disease, maximization of growth potential, treatment of anemic, as well as surgical correction of anatomic malformations of the urinary tract. Successful control of these aspects will result in improved rehabilitation and physical and psychological outcomes in the child with end‐stage renal disease. Medication compliance remains a serious problem in these children.

• Five children had rapidly progressive glomerulonephritis, determined by biopsy specimen and terminating in end-stage renal disease. All had mesangial deposition of IgA and C3 in the pattern typically seen with IgA nephropathy (Berger's disease). These children ranged in age from 7 to 13 years; four were boys. Severe hypertension was present in all, and three had a nephrotic syndrome. Other than hypertension and findings related to renal insufficiency or nephrotic syndrome, no clinical or laboratory finding was a consistent marker distinguishing these patients from those with uncomplicated IgA nephropathy, and no therapy proved useful in halting the rapid decline in renal function. The disease has not recurred in the kidney transplant of any of the five children.(AJDC 1988;142:789-793)

An evaluation of the alternative pathway of complement was undertaken in patients with otitis media with effusion (OME). Middle ear fluid (MEF) and serum specimens were obtained from 34 patients at the time of elective myringotomy for OME. Bacterial, viral, and mycoplasma cultures were made for all specimens of the fluids. Immunochemical determinations by radial immunodiffusion were performed for C3, C5, factor B, properdin, factor H, factor I, and albumin. Each patient's recent clinical course and past history were reviewed. The results of all viral and mycoplasma cultures were negative. Three of 55 bacterial cultures were positive for type B Haemophilus Influenzae. All components of the alternative pathway measured were found to be present in varying amounts in MEF. When the levels of the complement components were compared to the clinical factors studied, there were no observable differences. These data suggest that components of the alternative pathway Of complement are present in OME and are not useful in predicting the clinical course or outcome of this disorder.

C4 and factor B typing were performed in 37 pediatric patients with primary IgA nephropathy. Null alleles for C4B occurred with a frequency of 26% in patients, as compared to 15% in healthy controls (NS). The phenotype of C4B deficiency (homozygous C4B null), however, was found in 16% of patients and 4% of controls (P<0.05). Comparison of observed C4B phenotypes with those predicted from the Hardy-Weinberg equilibrium also confirmed an excess of C4B deficiency (P<0.0005). In contrast, there was no evidence of distortion in the frequencies of the C4A null allele or phenotype, or of the factor B alleles. The data suggest that C4B deficiency may be one of multiple interacting factors contributing to the development of this glomerulopathy.

We evaluated urinary calcium excretion in 21 premature infants fed either a formula containing high concentrations of calcium (Ca) and phosphorus (P) or human milk fortified with a commercially available human milk fortifier. Dual-tracer stable-isotope Ca absorption studies were performed on all infants. Urinary Ca excretion was not significantly related to Ca or P intake or true Ca absorption. The recovery of the orally administered tracer in the urine was used to evaluate the source of calciuria in study subjects. In almost all subjects, tissue-derived (Fbu), rather than diet-derived (Vou), Ca was the principal source of urinary Ca. Hypercalciuric subjects demonstrated greater Vbuand Vouthan nonhypercalciuric subjects. Our data demonstrate that moderate hypercalciuria is common in premature infants whose diets are high in mineral content and that hypercalciuria is not related to inadequate mineral intake or Ca absorption but is related, instead, to losses of both tissue and dietary Ca.