Until now oligonephropathy to indicate "too few nephrons" has been associated with intrauterine growth restriction and experimentally induced abnormalities of renal development. The purpose of this study was to determine whether there is evidence of abnormal postnatal glomerulogenesis in extremely low birth weight preterm infants. Renal autopsy tissue was studied by computer-assisted morphometry from 56 extremely premature infants (birth weight < or = 1000 g) and 10 fullterm infants as controls. Preterm infants were divided into two groups (short survival < or = 40 days vs. long survival > or = 40 days). Each group was subdivided into those with renal failure (RF) and those with normal renal function. Forty-two of 56 preterm infants (75%) were adequate for gestational age. Glomerulogenesis as measured by radial glomerular counts (RGC) was markedly decreased in all preterm infants as compared to term controls and correlated significantly with gestational age (r = 0.87; P < 0.001). Active glomerulogenesis with "basophilic S-shaped bodies" was absent in longer surviving preterm and all term infants. RGC of preterm infants surviving > or =40 days with RF were significantly less than RGC of those with long survival and no RF (P < 0.001). Only this latter group demonstrated increased glomerular size as measured by mesangial tuft area and Bowman's capsule area compared to all other groups (P < 0.001). The kidney continues to form postnatally in preterm neonates, but glomerulogenesis ceases after 40 days. Moreover, it is further inhibited by RF. Compensatory mechanisms in longer surviving preterm infants include glomerular hypertrophy and mesangial proliferation that could lead to hyperfiltration.

Children born with very low birth weight have a decreased nephron number. Low nephron mass is associated with adult hypertension, proteinuria, and diabetes mellitus. The histomorphometry and radial glomerular count (RGC) of a total nephrectomy from a child with renal disease associated with extreme prematurity was compared with the kidney from a full-term age-matched child of normal gestation with chronic renal failure due to focal and segmental glomerulosclerosis (FSGS) and to a child without renal disease. Bowman's space area, mesangium and mesangial tuft area were determined in 50 glomeruli of each specimen by computer-assisted morphometry. RGC was 4 in the ex-preterm child, 8 in the patient with FSGS, and 9 in normal control. The patient with FSGS had larger glomerular area expressed as square micrometers (mum(2)) of Bowman's capsule, the mesangium and the mesangial tuft area measurements than the normal control and the child born preterm who subsequently developed renal failure had significantly larger Bowman's capsule and mesangium than the two controls. This case report begins to identify important pathologic findings of decreased nephron numbers and glomerulomegaly associated with preterm birth.