Renal development and neonatal adaptation.

The structural and functional development of the kidney is responsible for a significant impact on postnatal adaptation to extrauterine life. Prenatal or neonatal impairment of nephrogenesis may carry long term, lifelong consequences in terms of reduced nephron endowment, chronic kidney disease, and cardiovascular risks at adulthood. Intrauterine growth restriction, preterm birth, congenital renal, and urinary tract anomalies are for long widely incriminated. Neonatal administration of nephrotoxic drugs has been associated with short-term acute kidney injury and longer chronic kidney disease. This review attempts at offering a comprehensive understanding of the renal development, the neonatal renal transition to extrauterine life and subsequent maturation phase during early infancy. It also focuses on developmental and maturational changes that impact lifelong renal function and adult health.

Developmental origins of chronic renal disease: an integrative hypothesis.

Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the "early programming" of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a "factor of vulnerability" when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways.

[Kawasaki disease in a young infant: difficulties for diagnosis and early complications]. / Syndrome de Kawasaki chez 1 nourrisson: difficultés diagnostiques et complications liées à l'âge.

UNLABELLED: We report 1 case of Kawasaki disease in young infant, featuring atypical presentation and severe outcome. CASE REPORT: A 3-month-old patient was admitted with initial cervical lymphadenitis, and lasting fever. He subsequently developed the classical manifestations of Kawasaki disease. Treatment with intravenous gamma globulins was successful only after a second perfusion. The early echocardiography revealed a coronary vasculitis, which progressed rapidly and was followed by complications as right coronary thrombosis, several aneurysms, and some others as exsudative enteropathy, aseptic meningitis and hepatitis. CONCLUSION: Patients less than 6 months with Kawasaki disease are at increased risk of atypical presentation, severe prognosis and are often predicted to be non-responsive to the first administration of IVIG.