The impaired control of plasma renin activity in hypertensive patients with end-stage renal disease due to chronic glomerulonephritis.
In twelve hypertensive patients with end-stage renal disease (ESRD) due to chronic glomerulonephritis (CGN), the mechanisms of renin and aldosterone regulation were studied by exogenously infused angiotensin II, captopril, and upright posture. The results were compared to those obtained in ten patients with unilateral renovascular hypertension (RVH), eleven patients with essential hypertension (EH), and in eleven normal subjects (NS). Exogenously infused angiotensin II (5.0 ng/kg/min) failed to decrease the plasma renin activity (PRA) in the ESRD group but significantly decreased the PRA in the RVH, EH, and NS groups. The plasma aldosterone concentration (PAC) in the ESRD group and in the other control groups significantly increased after the addition of exogenous angiotensin II. An oral dose of 50 mg of captopril failed to increase the PRA in the ESRD group. However, it significantly raised the PRA in the RVH, EH, and NS groups. The plasma aldosterone concentration was significantly reduced by captopril in the ESRD group, and similar results were obtained in the other three groups. The ratio between the PRA before and after being in an upright posture for 4 hours in the ESRD group was lower than that in the three other groups. Meanwhile, there was no difference in the PAC ratio between the ESRD group and the control groups. Thus, we conclude that, in hypertensive patients with ESRD due to CGN, PRA regulation is different from that in the other three groups, although there were no differences in the regulation of the PAC among the four groups, suggesting that renin production in the ESRD group is somewhat autonomous.
Second Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
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G
Yasuda
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Nagasawa
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Umemura
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Shionoiri
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M
Ishii
D000328:Adult; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril; D005260:Female; D005921:Glomerulonephritis / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D006977:Hypertension, Renal / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology; D006978:Hypertension, Renovascular / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011187:Posture / Q000502:physiology; D012083:Renin / Q000097:blood*; D012084:Renin-Angiotensin System / Q000502:physiology*
D000804:Angiotensin II; D000450:Aldosterone; D002216:Captopril; D012083:Renin