[Nephropathy associated with arterial hypertension: genes and Barker's hypothesis].
For about three decades glomerular diseases have been the most intensively investigated research area in nephrology. The increasing proportion of patients with end-stage renal disease (ESRD) secondary to hypertension has now revived interest in hypertension. Prospective studies have firmly established that high blood pressure is associated with an increased risk of renal failure independent of other risk factors. Hypertension-related renal injury might be interpreted in a general context taking into account genes, intrauterine growth and environmental factors. Disturbed intrauterine growth (due to malnutrition or other factors) has a negative influence on the development of the cardiovascular system and favours the occurrence of hypertension, insulin resistance, hypercholesterolaemia and hyperuricaemia in adult life (Barker's hypothesis). Altered intrauterine growth has also been associated with a reduced number of nephrons at birth. Damage attributable to glomerular hyperperfusion in kidneys with a reduced number of nephrons is aggravated by vascular lesions in middle and small arterial vessels (secondary to hypertension, hyperlipidaemia and environmental risk factors such as smoking). The observation that subjects homozygous for the D allele of the ACE gene are predisposed to both cardiovascular complications and nephrosclerosis, suggests that genetic factors may interact with altered intrauterine growth in determining the risk of cardiovascular and renal diseases.
Zoccali
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Divisione di Nefrologia, Azienda Ospedaliera di Reggio Calabria e Centro di Fisiologia Clinica CNR, Reggio Calabria.
D000483:Alleles; D000818:Animals; D002319:Cardiovascular System / Q000196:embryology; D002879:Chromosomes, Human, Pair 10 / Q000235:genetics; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications*; D020022:Genetic Predisposition to Disease; D006801:Humans; D006937:Hypercholesterolemia / Q000209:etiology; D006973:Hypertension / Q000150:complications* / Q000196:embryology / Q000235:genetics; D007333:Insulin Resistance; D007676:Kidney Failure, Chronic / Q000209:etiology; D007678:Kidney Glomerulus / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D023421:Models, Animal; D008954:Models, Biological; D009399:Nephrons / Q000196:embryology; D009400:Nephrosclerosis / Q000196:embryology / Q000209:etiology* / Q000235:genetics; D009748:Nutrition Disorders; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011247:Pregnancy; D011248:Pregnancy Complications; D051381:Rats; D011922:Rats, Mutant Strains; D012084:Renin-Angiotensin System / Q000235:genetics / Q000502:physiology; D012307:Risk Factors; D014527:Uric Acid / Q000097:blood
D014527:Uric Acid; D007703:Peptidyl-Dipeptidase A