Circulation, Vol 74, 766-774, Copyright © 1986 by American Heart Association
M Packer, WH Lee and PD Kessler
When renal perfusion pressure is reduced in experimentally induced low-
output states, glomerular filtration rate is preserved by angiotensin
II-mediated efferent arteriolar vasoconstriction, but available evidence in
man suggests that angiotensin II supports renal function only to the extent
that it preserves systemic blood pressure. We performed simultaneous
assessments of cardiac and renal function in 56 patients with severe
chronic heart failure before and after 1 to 3 months of converting-enzyme
inhibition. Among the 29 patients with a pretreatment renal perfusion
pressure under 70 mm Hg, patients with preserved renal function (creatinine
clearance greater than 50 ml/min/1.73 m2) had markedly elevated values for
plasma renin activity (11.8 +/- 3.8 ng/ml/hr) and showed a significant
decline in creatinine clearance after converting-enzyme inhibition (61.1
+/- 3.0 to 45.9 +/- 5.3 ml/min/1.73 m2; p less than .05). In contrast,
although similar with respect to all pretreatment demographic, hemodynamic,
and clinical variables, patients with a creatinine clearance under 50
ml/min/1.73 m2 had low values for plasma renin activity (3.4 +/- 0.8
ng/ml/hr) and, despite similar drug-induced decreases in systemic blood
pressure, showed no change in creatinine clearance after therapy with
captopril or enalapril (32.6 +/- 2.5 to 41.4 +/- 3.8 ml/min/1.73 m2).
Changes in creatinine clearance varied linearly and inversely with
pretreatment values for plasma renin activity (r = - .64, p less than
.001); converting-enzyme inhibition effectively abolished the pretreatment
difference in renal function seen in the high- and low-renin subgroups. In
the 27 patients with a renal perfusion pressure of 70 mm Hg or greater,
creatinine clearance did not vary significantly with plasma renin activity
and was not altered by therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Preservation of glomerular filtration rate in human heart failure by activation of the renin-angiotensin system
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