title: Relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy.
abstract: We demonstrated previously that the blood pressure of patients with IgA nephropathy becomes salt sensitive as renal damage progresses. We also showed that increased urinary angiotensinogen levels in such patients closely correlate with augmented renal tissue angiotensinogen gene expression and angiotensin II levels. Here, we investigated the relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy. Forty-one patients with IgA nephropathy consumed an ordinary salt diet (12 g/d of NaCl) for 1 week and a low-salt diet (5 g/d of NaCl) for 1 week in random order. The salt-sensitivity index was calculated as the reciprocal of the slope of the pressure-natriuresis curve drawn by linking 2 data points obtained during consumption of each diet. The urinary angiotensinogen:creatinine ratio was significantly higher in patients who consumed the ordinary salt diet compared with the low-salt diet (17.5 μg/g [range: 7.3 to 35.6 μg/g] versus 7.9 μg/g [range: 3.1 to 14.2 μg/g] of creatinine, respectively; P<0.001). The sodium sensitivity index in our patients positively correlated with the glomerulosclerosis score (r=0.43; P=0.008) and changes in logarithmic urinary angiotensinogen:creatinine ratio (r=0.37; P=0.017) but not with changes in urinary protein excretion (r=0.18; P=0.49). In contrast, changes in sodium intake did not alter the urinary angiotensinogen:creatinine ratio in patients with Ménière disease and normal renal function (n=9). These data suggest that the inappropriate augmentation of intrarenal angiotensinogen induced by salt and associated renal damage contribute to the development of salt-sensitive hypertension in patients with IgA nephropathy.
authors.affiliation: Division of Nephrology and Hypertension, Osaka City General Hospital, 2-13-22 Miyakojima-Hondori, Miyakojima-ku, Osaka 534-0021, Japan. ymsry-ko@msic.med.osaka-cu.ac.jp
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Konishi
authors.forename: Akira
authors.initials: A
authors.lastname: Nishiyama
authors.forename: Takashi
authors.initials: T
authors.lastname: Morikawa
authors.forename: Chizuko
authors.initials: C
authors.lastname: Kitabayashi
authors.forename: Mikiko
authors.initials: M
authors.lastname: Shibata
authors.forename: Masahiro
authors.initials: M
authors.lastname: Hamada
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Kishida
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Hitomi
authors.forename: Hideyasu
authors.initials: H
authors.lastname: Kiyomoto
authors.forename: Takenori
authors.initials: T
authors.lastname: Miyashita
authors.forename: Nozomu
authors.initials: N
authors.lastname: Mori
authors.forename: Maki
authors.initials: M
authors.lastname: Urushihara
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kobori
authors.forename: Masahito
authors.initials: M
authors.lastname: Imanishi
mesh_terms: D000328:Adult; D000808:Angiotensinogen / Q000652:urine*; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005922:Glomerulonephritis, IGA / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000502:physiology; D012189:Retrospective Studies; D017673:Sodium Chloride, Dietary / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D017673:Sodium Chloride, Dietary; D000808:Angiotensinogen