Birth weight, malnutrition and kidney-associated outcomes—a global concern

Abstract

An adverse intrauterine environment is associated with an increased risk of elevated blood pressure and kidney disease in later life. Many studies have focused on low birth weight, prematurity and growth restriction as surrogate markers of an adverse intrauterine environment; however, high birth weight, exposure to maternal diabetes and rapid growth during early childhood are also emerging as developmental risk factors for chronic diseases. Altered programming of nephron number is an important link between exposure to developmental stressors and subsequent risk of hypertension and kidney disease. Maternal, fetal, and childhood nutrition are crucial contributors to these programming effects. Resource-poor countries experience the sequential burdens of fetal and childhood undernutrition and subsequent overnutrition, which synergistically act to augment the effects of developmental programming; this observation might explain in part the disproportionate burden of chronic disease in these regions. Numerous nutritional interventions have been effective in reducing the short-term risk of low birth weight and prematurity. Understanding the potential long-term benefits of such interventions is crucial to inform policy decisions to interrupt the developmental programming cycle and stem the growing epidemics of hypertension and kidney disease worldwide.

New insights on glomerular hyperfiltration: a Japanese autopsy study

“…We previously reported a direct correlation between total nephron number and birth weight in white and African Americans (14). The Dutch Winter Famine (29) and the Leningrad Siege (30), periods of starvation, poverty, and stress, have been linked with adverse health outcomes in adulthood (31)(32)(33). It is therefore possible that the Japanese subjects investigated in the present study were born with low birth weight and low nephron endowment.…”

An approach to the young hypertensive patient

“…[14,15] Lowbirthweight and/or smallforgestationalage infants have a lower nephron number at birth (the socalled 'nephron endowment'), which induces physiological changes that lead to hypertension and chronic kidney disease later in life. [13] Hyperuricaemia as a cause for hypertension in adolescents is an intriguing concept. Experimental data indicate that hyperuricaemia invokes renal changes that drive hypertension.…”

“…[11] Hypertensive children and adolescents go on to become hypertensive adults -a phenomenon known as 'BP tracking' . [12] Novel mechanisms implicated in the pathogenesis include low birth weight (the BarkerBrenner hypothesis) [13] and hyperuricaemia. [14,15] Lowbirthweight and/or smallforgestationalage infants have a lower nephron number at birth (the socalled 'nephron endowment'), which induces physiological changes that lead to hypertension and chronic kidney disease later in life.…”

The Neglected Significance of Glomerular Density as a 5-year Progression Indicator for IgA Nephropathy△

“…This can be explained by the fact that low GD and glomerulosclerosis could be separate processes, even though glomerular sclerosis plays an important part in leading to low glomerular density. 13 Lower GD can also be caused by low birth weight, [14][15] hypertensive nephrosclerosis, 16 higher body surface, and older age.…”