Nephron number in patients with primary hypertension.

By N. Hollenberg. Current Hypertension Reports, 2003

650 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/82c1f38c7461a5d17885ed06a2169535c6a9f4a2

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Citations in the corpus

The Vascular Endothelium and Human Diseases (2013, background): “Renal dysfunction per se may be an underlying abnormality conducive to hypertension because hypertension “goes with the kidney” in cross-transplantation experiments, and a congenital reduction in the number of nephrons likely represents an important cause of glomerular endothelial dysfunction and hy”
The Developmental Origins of Adult Disease (2004, background): “Those being treated for hypertension had fewer but larger glomeruli [27].”
Fetal Origins of Adult Disease (2011, unknown): “Infants born SGA are at ncreased risk for developing obesity, T2DM, CAD, ypertension, kidney disease, premature pubarche, and polycystic ovarian syndrome, dyslipidemia, short stature, and osteoporosis.(1-4,13,32,37,45,46,49,50) Many of these phenotypic changes are known to be secondary to or associa”
The developmental origins of chronic adult disease (2004, background): “Those being treated for hypertension had fewer but larger glomeruli (27).”
Adult Consequences of Fetal Growth Restriction (2006, background): “Those being treated for hypertension had fewer, but larger, glomeruli.(39) Evidence to support the development of self-perpetuating cycles comes from a study of elderly people in Helsinki among whom the effect of birthweight on blood pressure was confined to those being treated for hypertension.”
Developmental plasticity and human health (2004, background): “The resulting increased functional demand on each individual nephron, for example by increased blood flow through each nephron, may lead to acceleration of the nephron death that accompanies normal ageing, with a consequent rise in blood pressur”