52 In living subjects, kidney mass is obtainable by weighing the donor kidney prior to transplantation and has proven to have clinical relevance (vide infra). Kidney Volume Kidney volume can be readily measured by ultrasound. Spencer et al. found relatively lower kidney volumes in LBW Australian Aboriginal children aged 5–18 when adjusted for body size.60 In contrast, Rakow et al. did not find a significant difference between kidney volumes of individuals who had been term AGA, term SGA, or preterm, when adjusting for body surface Inhibitors,research,lifescience,medical area (BSA), gender, and age.61 Kidney

size is dependent on AUY-922 chemical structure nephron number and the degree of nephron hypertrophy and is strongly correlated

with current body size.15 In fetuses and at birth, kidney volume is proportional to nephron number; however, subsequently, normal kidney growth (impacted Inhibitors,research,lifescience,medical by BSA, age, and gender), glomerulomegaly (hypertrophy due to low nephron number, obesity, etc.), and nephron loss through injury are likely to affect kidney volume disproportionately, Inhibitors,research,lifescience,medical making a direct relationship less clear.60 Among young adults born prematurely (either AGA or SGA) compared with term age-matched controls, prematurity was associated with smaller kidneys at age 20 years, whereas IUGR had only a small, non-significant effect.62 Kidney volume may

therefore not be ideally reliable as a surrogate for nephron endowment. CLINICAL CONSEQUENCES OF IMPAIRED DEVELOPMENTAL PROGRAMMING IN THE KIDNEY Nephron Number, Size, and Blood Pressure In adult animals, surgical removal of one kidney under varying circumstances and in different Inhibitors,research,lifescience,medical species does not always result in spontaneous hypertension Inhibitors,research,lifescience,medical and renal disease.63 In contrast, however, uni-nephrectomy on postnatal day 1 in rats, or fetal uni-nephrectomy in sheep, i.e. loss of nephrons at a time when nephrogenesis is still on-going, does lead to adult hypertension prior to any evidence of renal injury.64–66 These data support the possibility that intrauterine or also congenital reduction in nephron number may elicit different compensatory responses compared to later nephron loss, augmenting the risk of hypertension. Consistent with this view, kidneys from rats that underwent uni-nephrectomy at day 3 of age had similar total number but a greater proportion of immature glomeruli in adulthood, compared with those who underwent nephrectomy at day 120 of age.67 In addition, mean glomerular volume in neonatally nephrectomized rats was increased by 59% compared with 20% in adult nephrectomized rats, suggesting a greater degree of compensatory hypertrophy and hyperfunction in response to neonatal nephrectomy.