Cardio-renal consequences of low birth weight and preterm birth

In this comprehensive review of cardio-renal syndrome in preterm, low birth weight infants, we present contemporary evidence for alterations in nephrogenesis and vasculogenesis among this vulnerable population. There is substantial evidence that the nephron endowment, the number of nephrons that an individual is allotted for a lifetime, is determined by the length of gestation, the intra-uterine environment and the brief, but significant, postnatal course. Since nephrogenesis is complete by 36 weeks' gestation in utero, preterm birth during active nephrogenesis predisposes to an abrupt cessation in development leading to a reduced nephron endowment. In addition, other organ systems are simultaneously developing by “branching morphogenesis” including the lungs, vascular tree and endocrine organs such as the pancreas. Importantly, elastin, the scleroprotein that imparts elasticity to the vascular tree, is laid down during angiogenesis in utero and its production after birth is negligible. Instead, elastin is replaced by collagen and fibrosis with aging imparting stiffness to the macro-vessels. Moreover, the micro-vessels (capillaries) are similarly affected with a decreased density, termed rarefaction, in vital organ tissues leading to retinopathy and insulin resistance. This developmental synergism predisposes to concordant abnormalities in endovascular function, nephropenia, hyperfiltration, vascular stiffness and simultaneous cardio-renal disease throughout a lifespan. The longevity of preterm-born adults has been substantially abbreviated by these structural and functional alterations in organ systems. It is essential to recognize early indicators of cardio-renal syndrome and to provide early life-style and pharmacological interventions directed towards preserving vascular and renal function throughout a lifetime with the goal to promote longevity and quality of life.