Renal Developmental Delay Expressed by Reduced Glomerular Number and Its Association with Growth Retardation in Victims of Sudden Infant Death Syndrome and in “Normal” Infants

2000 ◽  
Vol 3 (5) ◽  
pp. 450-454 ◽  
Author(s):  
Darren J. Beech ◽  
Paul D. Sibbons ◽  
C. Vyvyan Howard ◽  
Dick van Velzen

In victims of sudden infant death syndrome (SIDS), renal development has been reported to be significantly impaired. In the present study, we used stereological techniques to estimate volume of kidney cortex and total number of glomeruli in a group of human infants. Infants were classified according to cause of death—SIDS or non-SIDS. Cases were further subdivided according to birth weight—normal birth weight (NBW) or low birth weight (LBW) (we were unable to identify any non-SIDS LBW infants for our study). No significant differences were found between NBW and LBW infants (irrespective of cause of death) for cortical volume, glomerular density, or total glomerular number ( p > 0.140). Kidney cortical volume, glomerular density, and total glomerular number were not significantly different between SIDS and non-SIDS infants (p > 0.510). Glomerular number was only significantly less in SIDS infants of LBW (p = 0.032) than in controls according to the Wilcoxon rank sum test; using the Kruskal-Wallis for one-way analysis, no significant difference was found (p > 0.010). These results contrast with those from previous studies, as a reduction in glomerular number was not noted in SIDS NBW infants, and the mean value for the control (non-SIDS NBW) group was significantly reduced ( p < 0.01) from those of previous studies. This indicates that glomerular number reduction is seen in SIDS NBW and non-SIDS NBW cases and is therefore directly associated with growth retardation rather than with SIDS.

PEDIATRICS ◽  
1982 ◽  
Vol 69 (3) ◽  
pp. 301-304 ◽  
Author(s):  
Joseph Werthammer ◽  
Elizabeth R. Brown ◽  
Raymond K. Neff ◽  
H. William Taeusch

The association between bronchopulmonary dysplasia and sudden infant death syndrome was studied retrospectively in low-birth-weight infants discharged from the neonatal program at Harvard Medical School. The incidence of sudden infant death syndrome was seven times greater in infants with bronchopulmonary dysplasia when compared with a group of control infants without bronchopulrnonary dysplasia. Confounding factors, including birth weight, sex, multiple birth, socioeconomic status, and apnea were evaluated. The results indicate that there is an association between bronchopulmonary dysplasia and sudden infant death syndrome.


1989 ◽  
Vol 36 (1-2) ◽  
pp. 1-8 ◽  
Author(s):  
Charles B. Nam ◽  
Isaac W. Eberstein ◽  
Larry C. Deeb

1986 ◽  
Vol 108 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Lehman Black ◽  
Richard J. David ◽  
Robert T. Brouillette ◽  
Carl E. Hunt

2004 ◽  
Vol 16 (2) ◽  
pp. 154
Author(s):  
M.R. Park ◽  
S.K. Cho ◽  
J.Y. Park ◽  
K.M. Kim ◽  
Y.J. Choi ◽  
...  

In this study, we investigated the relationship between the sex of cloned pigs and sudden infant death syndrome (SIDS). Three cell lines (2 male and 1 female) were obtained from F1 fetuses derived from 3 different dams (Yorkshire) inseminated by the same sire (Landrace); one female fibroblast cell line was obtained from a Duroc-strain fetus acquired from a slaughterhouse, the age of the fetus unknown. The fetal fibroblast cells were cultured in DMEM supplemented with 10% fetal bovine serum under 5% CO2 in air at 37°C. For NT, we used the 4 cell lines described above. All 37 cloned piglets derived from 10 pregnant recipients were alive at term and began breathing readily. Of those piglets born, 18/22 males and 5/15 females died within 2 months of age. A total of 350 paraffin blocks from 18 deceased cloned male piglets and 90 paraffin blocks from six age-matched normal control piglets were prepared from the midbrain, medulla oblongata, liver, lung, kidney, spleen, small and large intestine, thymus, uterus, placenta, ovary, testis, skin, and skeletal muscle. We found that the birth weights of male clones were 57% lower than those of control age- and sex-matched piglets. Piglets with low birth weight (&lt;900g) had more than twice the risk of SIDS relative to those piglets weighing more than 1000g. The low birth weights of the cloned male piglets (0.84±0.05kg) were not merely an artifact, as the average birth weights of cloned female piglets (1.47±0.09kg) were not lower than weights of piglets produced by AI-derived control female piglets (1.36±0.12kg). An initial examination of brain samples from 18 cloned male piglets that died soon after birth identified seven piglets with meningitis characterized by severe neutrophilic inflammation in the temporal brain lobes (38.8%, 7/18). We verified meningitis when more than 1000 neutrophils were counted per cubic millimeter of tissue. Next, we found hepatopneumonic congestion (16.6%, 3/18). The deceased male clones with meningitis showed extensive neuronal cell death and blood-brain barrier damage, whereas cloned piglets with congestion had fewer and larger alveolar air sacs. Extensive alveolar cell death, especially of pneumocytes and the bronchial epithelium, was confirmed by TUNEL assay. Lung and liver congestion may be caused by a slowly flowing blood stream from heart, resulting in CO2 and O2 exchange problems. Although the gross anatomy of the cloned male piglets was normal, they were associated with other severe handicaps, the commonest being leg abnormality which occurred in 33% (6/18) of dead male cloned piglets followed by Leydig cell hypoplasia and short face. Even though 4 of 41 AI-derived control piglets died within 1 week after birth, we could not find any anomalies in them. Thus, the present study suggests that our data might reflect sex difference but not cell type difference, and that death of the cloned male piglets might be caused by risk factors of sudden infant death syndrome such as low birth weight and multiple organ failure in conjunction with hepatopneumonic congestion and cerebromeningitis.


PEDIATRICS ◽  
1993 ◽  
Vol 91 (1) ◽  
pp. 106-112
Author(s):  
Joel E. Haas ◽  
James A. Taylor ◽  
Abraham B. Bergman ◽  
Gerald van Belle ◽  
Judy L. Felgenhauer ◽  
...  

The risk of sudden infant death syndrome (SIDS) is said to be enhanced by factors such as prematurity, low birth weight, and perinatal distress. The significance of risk factors for SIDS research was questioned because the majority of SIDS victims seem to lack them. Therefore, postmortem records of 1144 infants who died suddenly and unexpectedly in King County, Washington, over a 25-year period were studied. Deaths were classified as "explained" if a cause was apparent, "classic" SIDS if the history and autopsy were unrevealing or, where the diagnosis of SIDS was doubtful, as "probable" or "possible" SIDS. The infants' birth certificates were compared with those of 3647 infants born during a similar period. Seventy-nine deaths (7%) were explained. The 1065 previously certified as SIDS were reclassified classic SIDS (82%), probable SIDS (13%), and possible SIDS (5%). Low birth weight, small size for gestational age, prematurity, and low 5-minute Apgar scores each form a "continuum"; the possible-SIDS group had the highest proportion of such infants, followed by the probable- and classic-SIDS groups, which exhibit extensive overlap with the control population. A 5-minute Apgar score of less than 7 and delayed postnatal growth rate are not risk factors for classic SIDS. Risk factors are more prevalent in SIDS infants where the diagnosis may be doubtful. The great majority of SIDS victims possess fewer risk factors. To avoid the bias of confounding variables, SIDS research should focus on as "pure" a SIDS population as is possible.


PEDIATRICS ◽  
1994 ◽  
Vol 93 (5) ◽  
pp. 774-777
Author(s):  
Peter H. Gray ◽  
Yvonne Rogers

Objective. To compare the incidence of sudden infant death syndrome (SIDS) and apparent life-threatening event (ALTE) in infants with bronchopulmonary dysplasia (BPD) and birth weight-matched control infants in view of the changing pattern of chronic lung disease of prematurity. Methods. The study population consisted of 78 preterm infants of 26 to 33 weeks gestation who were diagnosed as having BPD and discharged. The 78 control infants were matched with the study infants for birth weight categories. Infants unable to maintain adequate oxygenation without supplemental oxygen when they were feeding well and thriving were discharged on home oxygen. All infants were at least 8 months of age at follow-up and information concerning the occurrence of any ALTE was obtained by direct parent interview. Results. No infant died during the period of follow-up. Seven (8.9%) of the study group compared with eight (10.5%) of the control infants had an ALTE. Three infants (one study, two control infants) were hospitalized for further investigation. No infant discharged on the home oxygen program had an ALTE. Conclusions. The data from this study suggest that preterm infants with BPD are not at increased risk from SIDS compared with preterm infants without this condition. This may be related to close monitoring of the infants' oxygenation status and the provision of home oxygen when appropriate, which should eliminate episodes of unrecognized and untreated hypoxemia. Home monitoring for infants with BPD may not be warranted.


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