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Objective: To improve compliance with the completion of speakers' evaluation forms in a pediatric hospital continuing medical education program. Design: Preintervention and postintervention analysis. Setting: Pediatric hospital in Cincinnati, Ohio. Participants: Attendees at pediatric grand rounds programs. Main Outcome Measure: Analysis of speaker evaluation forms for each of 20 pediatric grand rounds programs were used as the basis for speakers' awards. Results: Spontaneous written comments were found on a mean of 7.3 evaluations per preintervention program and 13.5 evaluations per postintervention program (P [is less than] .01). The distribution of objective scores in 3 items examined was wider postintervention than preintervention (P [is less than] .01). Conclusion: When participants in continuing medical education programs know that their evaluations of an activity are used as the basis for an educational award, they may be more reflective in completing such evaluations. Arch Pediatr Adolesc Med. 2000; 154:81-82

Researchers studied the association between excessive calcium in urine, or hypercalciuria, high levels of calcium deposited in the kidney, and Bartter syndrome, a proliferation of the normal cells in a section of the kidney. The study was intended to define the extent of the renal (kidney) tubular abnormality in six children and to identify a mechanism for their hypercalciuria. The effect of therapy with the anti-inflammatory drug indomethacin on their condition was also reviewed. The data suggest that an excess of a byproduct of vitamin D metabolism is associated with the development of hypercalciuria in some children with Bartter syndrome. There is also evidence linking prostaglandin, which modulates many biochemical processes, and calcium metabolism with this condition. In other studies, reduction of elevated prostaglandin (PG) levels with aspirin or indomethacin corrected hypercalciuria. For reasons that are not clear, an increase in PGE2 (urinary PG) accompanies tubular disorders associated with Bartter syndrome. The degree of hypercalciuria in Bartter syndrome may be a function of such factors as the degree of increased PG activity, age at onset of the disorder, and end-organ sensitivity to vitamin D metabolites.

Activation of C4 releases into the fluid phase a fragment of the alpha chain, C4a. Unlike the analogous fragments of C3 and C2, there is no evidence for an anaphylatoxic effect of C4a. There is actually some in vitroevidence that it could have a modulating effect on inflammation by inhibiting monocyte chemotaxis. We induced an immune complex glomerulonephritis in wild-type (WT) and C4 knock out (C4KO) mice. Although the glomerular component of the disease did not differ in the two groups of animals, there were marked differences in the accompanying tubulo-interstitial injury. Compared to WT animals, the C4KO mice had significantly more infiltrating interstitial cells (1910 vs 2720/mm2), foci of tubular atrophy (6.3 vs 14.8/section), and interstitial space (22 vs 30% of cortex). C4 is expressed constitutively by renal tubular epithelial cells. These data support a role for such local C4 in modulating interstitial inflammation, consistent with in vitroexperiments.

The complement system has long been recognized as having a role in immune glomerular disease. This review provides an update on this association, some strategies for the clinical testing of complement in disease, and a brief commentary on current research directions. Evidence of complement activation in glomerulonephritis comes from characteristic patterns of a decrease in the serum concentrations of specific components, some of which are virtually diagnostic of certain nephritides. These patterns are often accompanied by the presence of complement components in the glomeruli and the detection of complement breakdown products in the circulation. In certain diseases, circulating complement-activating substances can be detected. Although there are over 20 complement proteins, clinical analysis is most often directed at C3 and C4, with occasional measurement of B and C5. Recently, a variety of mechanisms for complement-induced injury has been recognized. These mechanisms go far beyond simple passive lysis of erythrocytes, the earliest functional effect of complement studied. The role of such mechanisms in renal disease is just beginning to be studied. Local synthesis of complement components in the kidney may play a role both in host defense and in the promotion of interstitial inflammation and scarring. Such mechanisms will likely be defined more precisely with the availability of animals with specific complement deficiencies. Ultimately, an understanding of the role of complement in renal disease may permit specific targeted inhibition of one or more complement functions as a form of therapy.

C57/B6 mice received intraperitoneal horse spleen apoferritin (4 mg) with lipopolysaccharide (0.05 mg); control mice received 0.15 M NaCl. Control and treated animals were killed weekly for 6 wk; blood and urine specimens were obtained, and tissue samples were secured. Treated animals showed evidence of significant chronic disease, with proteinuria, hematuria, and uremia. A mild glomerulonephritis was present at 2 wk, with significant proliferative glomerulonephritis at 4 wk, progressing to chronic disease with tubulointerstitial changes at 6 wk. Changes at each time period were uniform between animals. C3 mRNA was first detected by in situ hybridization at 3 wk. Message was restricted to proximal tubular and periglomerular epithelial cells. Presence of C3 message preceded the development of interstitial inflammation and fibrosis by 1–2 wk, and its location and intensity paralleled the evolving interstitial disease. Although extensive mesangial C3 protein deposits appeared early, there was never C3 message in glomeruli or infiltrating cells. Before C3 message became apparent, two cytokines known to up-regulate C3 transcription in vitro, IL-1 and IL-6, were detected by immunohistochemistry. The temporal sequence in this model is consistent with our hypothesis that local synthesis and activation of C3 in tubular epithelium is important to the interstitial component of chronic glomerulonephritis. The process is independent of the deposition of circulating complement in the glomerulus, but may be triggered by glomerular cytokines.

The calciotropic activity of urine from a subject with neonatal Bartter syndrome (NBS) has been partially purified using ion-exchange and gel chromatographic techniques. A bioassay using bone disk from rat calvaria was used to estimate calciotropic activity, which in the urine of the subject with NBS appears to be due to basic fibroblast growth factor (bFGF) bound to a glycosaminoglycan susceptible to heparitinase digestion. The calciotropic activity is eluted from DEAE-Sephacel and Sepharose CL-6B in a narrow band in association with metachromatic material and is destroyed by heparitinase and blocked by an antibody to bFGF. After treatment of purified preparations with heparitinase, a component that is inactive alone but develops calciotropic activity in association with heparin can be isolated by affinity chromatography on heparin-Sepharose columns. This component is recovered from the column at NaCl concentrations expected to elute bFGF and is inactivated by antibodies to bFGF. No calciotropic activity can be shown in glycosaminoglycan-containing fractions from urine from a normal boy or a normal man, but such fractions exhibit calciotropic activity if bFGF is added to the assay system. When bFGF is added to urine from either normal subject followed by ion-exchange chromatography on DEAE-Sephacel, calciotropic activity is eluted at NaCl concentrations closely similar to those found to elute calciotropic activity from the urine of the NBS subject. It appears that the abnormal findings in NBS urine are due to excess bFGF, although they could be due to some abnormality of the glycosaminoglycan component.

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)

Ten patients with Henoch-Schöenlein purpura (HSP) were selected for study because their early renal biopsies showed focal and segmental hypercellularity, with IgA present only in deposits at the periphery of the lobules. Mesangial deposits of IgA were absent. All had laboratory evidence of nephrotic syndrome and/or renal compromise. The glomerular hypercellularity was largely the result of the infiltration of monocytes whose cytoplasm often contained tubular lysosomes and wrapping lysosomal membranes, evidence of monocyte activation. Mean levels of C3 were normal but those of C4 and properdin significantly depressed. This complement profile, as well as a glomerular monocytic infiltrate, are also seen in essential cryoglobulinemia in the adult. Of follow-up biopsies in six patients, the glomeruli were normal in three, with no IgA deposition. In the other three, mesangial deposits of IgA typical of HSP were present. The initial focal-segmental glomerulitis of these patients appeared to be the benign first phase of a disease which had the potential to culminate in mesangial IgA deposition. Patients like the three who escaped mesangial IgA would be among those responsible for the observed dissociation between severity of the initial illness and ultimate prognosis.

We and others have shown an association between autoimmune disorders and the major histocompatibility complex extended haplotype HLA-A1,-B8,-SCO1,-DR3. The primary gene or genes within this haplotype conferring such susceptibility, however, have not been defined. In this study, we tested the hypothesis that linkage disequilibrium in this haplotype extends through the DP locus, and that DP type may be linked to membranoproliferative glomerulonephritis (MPGN) and systemic lupus erythematosus (SLE). DP and DQ typing was performed by restriction fragment length polymorphism analysis for 43 chromosomes (19 healthy controls, 9 SLE, 15 MPGN) bearing the-A1,-B8,-SCO1,-DR3 extended haplotype. Although all were DQw2, a variety of DP types were identified (DPw1, 0.26; DPw2, 0.09; DPw3, 0.14; DPw4, 0.44). Although DPw1 was represented on extended haplotypes with greater frequency than on 113 non-A1,-B8,-SCO1,-DR3 haplotypes (0.26 vs. 0.03;P<0.001), there were no significant differences between healthy individuals with this haplotype and those with autoimmune disease. We conclude that the strong linkage disequilibrium of this haplotype breaks down between the DQ and DP loci. Loci important to disease susceptibility, therefore, are more likely to occur telomeric to DP.

The relations among dietary and calcium kinetic factors and 24‐h urinary mineral excretion were evaluated in a group of 89 healthy girls (51 white and 38 black) aged 4.9‐16.7 years. Nutrient intakes were calculated for each participant using a weighed intake of all food and beverage on the day of the 24‐h urine collection study and two subsequent 24‐h food records. A significant relation was noted between urinary calcium and sodium excretion (r= 0.55; p< 0.0001). No significant relations were found between urinary calcium and (a) calcium intake (r= 0.08), (b) protein intake (r= 0.14), or (c) phosphorus intake (r= 0.11). Urinary calcium was not significantly related to fractional calcium absorption (r= 0.03) or net calcium absorption (r= 0.11), but was significantly associated with the bone calcium deposition rate (r= 0.24; p< 0.03). Using a multiple regression model, both urinary sodium and the bone calcium deposition rate were independent predictors of urinary calcium excretion in this population (r= 0.57; p= 0.0001). A substantial number of the children in this population had urinary calcium excretion >4 mg/kg/day (12%). The incidence of hypercalciuria differed between the racial groups and was markedly higher in the white than in the black children (17.6 vs. 5.3%). Over a range of usual calcium intakes, during the rapid‐bone‐growth period in childhood and early adolescence, urinary calcium appears relatively unaffected by calcium intake and is most strongly associated with urinary sodium levels.

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.

The human insulin-like growth factor type 2 receptor gene (IGF2R) is biallelically expressed in a variety of fetal and adult tissues. In contrast, the imprinted mouseIgf2rgene is expressed exclusively from the maternally inherited chromosome. The mouse gene contains two CpG islands that are methylated in a parent-specific manner. Methylation of the CpG island in the promoter region occurs on the repressed paternal gene copy. Methylation of the CpG island in intron 2 is specific for the active maternal allele and may represent the primary imprint. Here, we have analyzed the humanIGF2Rgene to investigate whether these motifs and their parent-of-origin-specific epigenetic modification have been conserved. As in the mouse, the humanIGF2Rgene was found to contain two CpG islands, one encompassing the transcription start site (CpG 1) and the other in the second intron (CpG 2). CpG 2 is hypermethylated on the maternalIGF2Rallele. In contrast to the situation in the mouse, however, the human CpG 1 is completely unmethylated on both parental chromosomes. The human and mouse intronic CpG islands lack significant sequence homology, which suggests that DNA conformation plays a role in allele-specific methylation.

An increased frequency of specific major histocompatibility complex (MHC) class I, II and III antigens in children with steroid-responsive nephrotic syndrome (SRNS) has been reported. This frequency distortion, in some cases, is thought to affect the outcome of the disorder. We studied the phenotypic frequency of HLA antigens-A,-B, and-DR, as well as complement proteins Bf and C4 in an unrelated population of 25 SRNS children. Complete MHC haplotypes were also derived for four families in which 8 individuals developed SRNS. HLA-DR8, with a relative risk of 4.8, showed the strongest association with SRNS. Nonetheless, the 95% confidence intervals of this and the relative risks for all other antigens fell below 1.0. No common haplotype was found in SRNS patients in whom complete family studies were available, and disease and inheritance of the MHC were discordant in two of these families. In this study of well-characterized SRNS patients we were unable to discover a clear association between this disorder and the MHC.

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 used C3-deficient (C3D) guinea pigs to evaluate the role of C3 in an active model of experimental nephritis. Normal strain 2 (C3N, n= 13) and C3D (n= 6) guinea pigs were immunized with cationized bovine γ-globulin (CBGG). Fourteen days later (Day 0), daily intravenous injections of CBGG were given for 3 to 7 days and the animals were sacrificed on Day 10 or 21. Immunofluorescence (IF) microscopy of renal tissue revealed two patterns of glomerular IgG deposition: granular loop (11/13 C3N, 3/6 C3D), and predominantly mesangial (2/13 C3N, 3/6 C3D). Codeposited C3 was seen in all C3N and in no C3D animals. Electron microscopy showed subepithelial deposits in all. A significant correlation (P< 0.005) was seen between an animal's IF pattern and its level of serum antibodies to CBGG; those with lower antibody levels exhibited the mesangial pattern. C3D animals had lower mean antibody levels than C3N (P< 0.01), but both IF patterns were represented. Urine protein concentration, which was increased relative to controls, did not differ between C3N and C3D groups, but was significantly greater in those with loop IF. Serum albumin was significantly reduced in animals with loop IF. C3N animals showed a significant reduction in mean serum C3. In this model, immune deposit location and degree of proteinuria are independent of C3 deposition and dependent upon the level of antibody response to CBGG. Induction of antibody to CBGG is impaired in the absence of C3.

Forty-eight of the 50 state health departments in the United States responded to a questionnaire about giardiasis in their jurisdictions. The agencies had reports of 34348 cases during 1991 and studied 80 outbreaks in the same period. Nineteen of these outbreaks were attributed to consumption of contaminated drinking water; only two outbreaks were reported among individuals identified as campers or backpackers. Only two departments considered water-associated giardiasis to be a problem for backpackers in their jurisdiction, and neither had any data to support this concern. The surveillance data of health departments indicate that giardiasis is a common communicable disease in the United States. They do not, however, provide any evidence that wilderness water is an important cause of the disease in this country.

Renal insufficiency may evolve over several years following an initial insult. Current models are inadequate, however, for predicting the rate of this progression, especially if they employ creatinine-based methods of measuring the glomerular filtration rate. Recombinant human erythropoietin has proven to be of great benefit in the treatment of renal anemia and may reduce pretransplant sensitization. Recombinant human growth hormone therapy can accelerate the growth of children with renal insufficiency, but the long-term effects of this therapy are still unclear. Cardiovascular disease is a major source of morbidity in adult survivors of renal transplantation. The complex lipid disorders of renal disease and corticosteroid therapy probably play a role in the development of coronary disease.

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.

The major histocompatibility complex (MHC)-linked complotype region includes alleles for B, C2, and C4 loci. These loci are closely linked to each other and to HLA-DR on chromosome 6. The duplicated C4 loci,, C4A and B, are especially polymorphic. In seven patients with renal insufficiency, we observed a C4 variant with electrophoretic mobility between C4B2 and C4B3. Four of these patients were detected during a study of MHC markers in mernbranoproliferative glomerulonephritis. Complete complotype and HLA data from families of five of the seven patients demonstrated that the variant was not inherited. The pattern was revealed by immunofixation electrophoresis and also by C4-specific hemolytic overlay. In serial plasma specimens taken from one patient, the C4 variant appeared only after the patient became uremic. However, the variant could not be produced in normal plasma after incubation with C4-depleted uremic plasma. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions of immunoprecipitated C4 from these patients showed C4A and C4B a chains of normal molecular mass; incompletely processed forms of C4 were not observed. We believe that this variant is probably acquired in the presence of uremia and may represent the C4B2.9 allele found by Wank and co-workers in many patients with glomerulonephritis. Family studies are mandatory to distinguish genetic variants from acquired alterations in the C4 phenotype.

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.

ABSTRACT: Metabolic investigations, including the use of stable isotopes of calcium, were used to study calcium kinetics in three children with the hyperprostaglandin E syndrome. The studies were performed both during indomethacin treatment and in the absence of therapy. Off therapy, each child had hypercalciuria (mean urinary calcium excretion 0.478 mM/kg/d), hyperprostaglandinuria, and elevated serum calcitriol concentration. All had diminished bone density and were euparathyroid. Indomethacin treatment was associated with a marked reduction in serum calcitriol concentration, as well as decreased prostaglandin E excretion. Mean urinary calcium excretion fell to 0.135 mM/kg/d. The stable isotope studies defined two components to the hypercalciuria of this disease: an indomethacin-sensitive dietary contribution and a relatively indomethacin-resistant bone resorptive element. Bone densitometry confirmed the presence of the resorptive element by demonstrating skeletal demineralization.

The blood-borne hepatitis viruses, hepatitis B virus (HBV) and hepatitis C virus (HCV), have similar epidemiological features. The association of chronic HBV infection and glomerulonephritis is well established, particularly in children. Recent reports have shown an association between HCV infection and glomerulonephritis in adults. In order to assess the role of these hepatotropic viruses in membranoproliferative glomerulonephritis (MPGN) we screened 34 children with idiopathic MPGN for the presence of HBV and HCV infection using highly sensitive polymerase chain reaction techniques for the detection of HBV DNA and HCV RNA. Also, enzyme-linked immunosorbent assays were used to detect the presence of antibody to hepatitis B surface antigen and antibody to HCV. No evidence of HBV or HCV infection was demonstrated in any of the patients. We conclude that HBV and HCV are not significant causes of idiopathic MPGN in children in the United States.

Acute hyperammonemia is an emergent cause of central nervous system dysfunction for which renal replacement therapy is advocated. We report the successful use of continuous venovenous hemodiafiltration in this metabolic emergency, and report the calculated ammonia clearances for both continuous venovenous hemofiltration and hemodiafiltration.

Comments on the procedures and operations of the Army logistics in the United States. Relevance of eliminating work order logistics file data from Standard Army Maintenance System; Effects of the elimination of requisition order number on requisition processing costs; Impact of Single Stock Fund on retail stock fund.

In Reply.—The patient report by Cachero et al illustrates two interesting points about the development of end-stage renal disease in IgA nephropathy. First, it points out the important negative prognostic significance of hypertension and heavy proteinuria. As Cachero et al mention, this observation has been made in other series of patients. Although recurrent gross hematuria is often regarded as the hallmark of IgA nephropathy, the disease may occur in the total absence of hematuria.This patient report also demonstrates that end-stage renal disease can evolve in IgA nephropathy in the absence of crescents. Patients such as the five we described, with crescenteric nephritis and rapid deterioration, are probably not typical. The child described by Cachero et al, in whom there was about a five-year course before end-stage renal disease occurred, probably represents a more usual situation. This is the type of natural history described by Droz,1 in whose

The (MHC) includes the alleles for HLA-A, B, DR; the complement components C2, Bf, and C4; and glyoxylase I (GLO I). C4 synthesis is controlled by two loci (A and B) and unexpressed (“null”) alleles are fairly common (C4AQO, C4BQO).Study of 26 patients affected by MPGN I or III and their families allowed unambiguous determination of 52 “disease associated” MHC haplotypes. The extended haplotype HLA-A1, B8, DR3, SC01 (BfS, C2C, C4AQO, C4B1), GLO I 2 comprised 8 (15%) of these haplotypes, and was present in 31% of patients. This pattern, however, was found in only 1/102 normal (i.e. not occurring in MPGN patients) haplotypes (p <.001). Family members who did not share haplotypes with the patients did not differ from the normal population in haplotype frequencies. The presence of C4AQO on this haplotype accounts for our earlier finding of a high frequency of C4 nulls in MPGN.The identical extended haplotype has been reported by others to occur with increased frequency in insulin dependent diabetes mellitus. Without data on the GLO I variant, it has also been reported in SLE. Although A1B8DR3SC01 is a common Caucasian haplotype (8% of our normal haplotypes), the disease associated haplotype always bears the GLO I 2 variant. These data suggest that a “disease susceptibility” gene(s) may be located between the DR/complotype loci and GLO I, and may be more closely linked to them than to HLA A and B.

In Reply.—The case reported by Itami et al is consistent with our belief that MPT does not improve the course of rapidly progressive IgA nephropathy. As we stated in our article, such therapy was attempted in three of the five patients with no discernible benefit. The rationale for using the therapy in these patients had been our apparent success in using MPT for the treatment of some patients with idiopathic RPGN.1 In retrospect, it is obvious to us that this approach is of no use in rapidly progressive IgA nephropathy or in any other crescentic immune complex glomerulonephritis. Whether such therapy can actually hasten the deterioration in renal function is not clear. With a creatinine clearance of 27.5 mL/min/1.73 m2 and a biopsy specimen showing globally sclerotic glomeruli, it would seem that the renal function of the patient of Itami et al was destined to deteriorate whether or not

Sir.—The article "A Benefit-Cost Analysis of Mumps Vaccine" by Koplan and Preblud (Journal 1982;136:362-364) on mumps immunization requires some elaboration.It should be stressed that their careful benefit-cost analysis was based on the use of mumps vaccine in combination with measles and rubella vaccines during the course of a routine health visit at 1 year of age. While this is in keeping with current recommendations, it does not address another aspect of the mumps vaccine program: recall of unimmunized children beyond infancy. We believe that Koplan and Preblud's analysis can be expanded to demonstrate the folly of such programs.Specifically, the state of New York now mandates exclusion from school of any child who does not have evidence of immunization against a number of diseases, including mumps. School nurses review the immunization records of all pupils and contact physician offices or parents to clarify immunization status. Parents of children who