Faa Gavino, Gerosa Clara, Fanni Daniela, Nemolato Sonia, Locci Annalisa, Cabras Tiziana, Marinelli Viviana, Puddu Melania, Zaffanello Marco, Monga Guido, Fanos Vassilios
Department of Pathology, Puericultura Institute and Neonatal Section, University of Cagliari, Via Ospedale 54, Cagliari, Italy.
J Matern Fetal Neonatal Med. 2010 Oct;23 Suppl 3:129-33. doi: 10.3109/14767058.2010.510646.
The kidney of low birthweight preterm infants is characterized by a reduced number of mature nephrons at birth. The aim of the present study was to determine whether, in preterms, active glomerulogenesis occurs in the postnatal period and whether it may compensate the reduced number of nephrons developed during the intrauterine life. Kidney samples were obtained at autopsy from 8 human fetuses, 12 premature infants, and 3 term newborns. Glomerulogenesis, as measured by radial glomerular count (RGC), was markedly decreased in all preterm infants as compared with term newborns. A marked interindividual variability was detected in the level of glomerulogenesis, which, in the vast majority of cases, did neither correlate with the gestational age at birth nor with birthweight. Active glomerulogenesis, as demonstrated by the presence of S-shaped bodies in the subcapsular region, was present in all preterm infants in the perinatal period, but it ceased in a preterm surviving for 3 months. Our data show that active glomerulogenesis continues even after birth for a short period, although it is not able to compensate a marked oligonephronia at birth. As a consequence, the incomplete nephrogenesis typical of all extremely low birthweight preterm infants possibly results in a persistent oligonephronia which should likelihood represent a major risk factors of progressive renal disease in adulthood.
低出生体重早产儿的肾脏在出生时具有成熟肾单位数量减少的特征。本研究的目的是确定早产儿出生后是否会发生活跃的肾小球生成，以及它是否可以补偿宫内发育期间形成的肾单位数量减少。从8例人类胎儿、12例早产儿和3例足月儿新生儿的尸检中获取肾脏样本。与足月儿新生儿相比，所有早产儿的肾小球生成（通过径向肾小球计数（RGC）测量）均明显减少。在肾小球生成水平上检测到明显的个体间差异，在绝大多数情况下，其既与出生时的胎龄无关，也与出生体重无关。围产期所有早产儿的肾包膜下区域均存在S形小体，表明存在活跃的肾小球生成，但在存活3个月的早产儿中这种现象停止了。我们的数据表明，活跃的肾小球生成即使在出生后仍会持续较短时间，尽管它无法补偿出生时明显的少肾现象。因此，所有极低出生体重早产儿典型的不完全肾发生可能导致持续性少肾，这很可能是成年期进行性肾病的主要危险因素。
