title: Renal abnormalities in normotensive insulin-dependent diabetic offspring of hypertensive parents.
abstract: To assess the effects of genetic predisposition of essential hypertension on early renal function in recent insulin-dependent diabetics, we studied inulin, para-aminohippuric, sodium, and lithium clearances in 69 unselected diabetics with (n = 20) and without (n = 49) a family history of essential hypertension. Despite similar metabolic control, glomerular filtration rate and mean arterial pressure were significantly higher in diabetics with than in those without a family history of hypertension. However, no difference was found between the two groups regarding renal vascular resistance, sodium excretion, or fractional proximal and distal sodium reabsorption. Renal responses to acute captopril (75 mg) administration were evaluated in 27 patients (six with family history of hypertension). Captopril decreased filtration fraction and mean arterial pressure similarly in both groups, whereas glomerular filtration rate and renal vascular resistance decreased more dramatically in diabetics with family history of hypertension. These findings indirectly suggest an abnormal response to angiotensin of vascular tone in recent diabetics with familial predisposition to hypertension. Renal response to acute nicardipine (2.5 mg i.v.) administration was analyzed in 24 patients (five with family history of hypertension). In both groups, nicardipine similarly decreased mean arterial pressure and renal vascular resistance and induced a marked natriuretic effect due to a predominant reduction in proximal reabsorption of sodium. However, the increase in sodium excretion was twofold to threefold more pronounced in diabetics with a family history of hypertension. Whether these early renal abnormalities may contribute to the risk of diabetic nephropathy, as suggested by retrospective studies, remains to be determined.
authors.affiliation: Department of Nephrology, Hôpital Necker, Paris, France.
authors.forename: T P
authors.initials: TP
authors.lastname: Hannedouche
authors.forename: L P
authors.initials: LP
authors.lastname: Marques
authors.forename: S
authors.initials: S
authors.lastname: Natov
authors.forename: A G
authors.initials: AG
authors.lastname: Delgado
authors.forename: C
authors.initials: C
authors.lastname: Boitard
authors.forename: B
authors.initials: B
authors.lastname: Lacour
authors.forename: J P
authors.initials: JP
authors.lastname: Grünfeld
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology*; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics* / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000235:genetics* / Q000503:physiopathology*; D005190:Family; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000503:physiopathology*; D008297:Male; D012039:Regional Blood Flow; D012964:Sodium / Q000378:metabolism*; D014655:Vascular Resistance
chemical_list: D012964:Sodium