Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-6-6
pubmed:abstractText
It has been proposed that "nephron underdosing," i.e., a low number of nephrons at the time of birth, is linked to essential hypertension and a greater propensity to develop progressive loss of renal function after renal injury. This hypothesis was confirmed recently by examining the number of glomeruli in patients with essential hypertension. The mechanisms through which a low number of nephrons causes hypertension have not been clarified, but it is likely that functional changes in postglomerular segments of the nephron, e.g., handling of sodium, play an important role. Neonatal uninephrectomy increases BP, renders BP salt sensitive, and renders the kidney more susceptible to damage. Apart from genetic factors, fetal/maternal malnutrition during pregnancy seems to play an important role in the pathogenesis of nephron underdosing. Furthermore, intrauterine programming during organogenesis, e.g., by hyperglycemia, seems to be important: In animal experiments, offspring of either hyperglycemic or diabetic mothers have fewer nephrons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
16 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S27-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Nephron number and renal risk in hypertension and diabetes.
pubmed:affiliation
Department of Pathology, Ruprecht-Karl University, Heidelberg, Germany.
pubmed:publicationType
Journal Article, Review