Mj. Deazevedo et al., LACK OF EFFECT OF CAPTOPRIL ON GLOMERULAR HYPERFILTRATION IN NORMOALBUMINURIC NORMOTENSIVE INSULIN-DEPENDENT DIABETIC-PATIENTS, Hormone and Metabolic Research, 29(10), 1997, pp. 516-519
The aim of the present study was to evaluate the effects of captopril
on the glomerular filtration rate (GFR) and urinary albumin excretion
rate (UAER) of normoalbuminuric normotensive insulin-dependent diabete
s mellitus (IDDM) patients with and without glomerular hyperfiltration
. Eleven normoalbuminuric (UAER < 30 mu g/min) patients (age: 34.3 +/-
4.6 years; diabetes duration: 9.5 +/- 6.4 years) participated in the
study. Six patients were considered to be hyperfiltering (GFR greater
than or equal to 134 ml/min/1.73 m(2)). GFR (Cr-51-EDTA single injecti
on technique), extracellular volume (ECV; distribution volume of Cr-51
-EDTA), UAER (RIA) and metabolic and biochemical parameters were measu
red at baseline, after 6 weeks on captopril (25 mg p.o. twice daily) a
nd after 6 weeks off captopril. plasma renin activity (PRA; RIA), plas
ma aldosterone (RIA) and blood volume (Cr-51 red cell labeled) were me
asured at baseline and after 6 weeks on captopril. The baseline clinic
al and laboratory characteristics of hyperfiltering and normofiltering
IDDM patients were similar. GFR did not change during the study (144.
1 +/- 28.8; 139.7 +/- 21.8; 132.8 +/- 29.9 ml/min/1.73 m(2)) either in
patients with hyperfiltration (164.6 +/- 20.7; 153.8 +/- 18.3; 148.6
+/- 31.0 ml/min/1.73 m(2); n = 6) or without hyperfiltration (119.6 +/
- 11.1; 123.2 +/- 11.9; 113.8 +/- 14.4 ml/min/1.73 m(2); n = 5). Also,
ECV (22.2 +/- 3.6; 21.5 +/- 4.3; 21.5 +/- 3.5 L/1.73 m(2)), UAER (3.9
[0.4-22.1]; 4.0 [0.2-11.4]; 3.7 [2.0 - 26.2] mu g/min), systolic (112
+/- 13; 105 +/- 10; 111 +/- 11 mmHg) and diastolic (76 +/- 12; 72 +/-
9; 73 +/- 12 mmHg) blood pressure did not change. No difference in bl
ood volume (60.8 +/- 10.4; 62.3 +/- 8.4 ml/kg) or plasma aldosterone (
10.4 +/- 4.9; 7.7 +/- 3.8 ng/dl) was observed between baseline values
and values after captopril use. PRA increased (2.4 [0.4-22.1]; 12.9 [2
.2-41.1]ng/ml/h) at the end of 6 weeks on captopril (P=0.002). Fasting
plasma glucose, glycated hemoglobin, fructosamine, plasma cholesterol
and potassium, 24 h urinary urea and sodium were similar during the s
tudy. These results were unchanged when patients with and without hype
rfiltration were analyzed as separate groups. From baseline to the end
of 6 weeks on captopril there was no correlation between change in GF
R and change in glycated hemoglobin (r = 0.02, P = 0.96), systolic (r
= 0.23; P = 0.49) and diastolic (r = - 0.32, P = 0.32) blood pressure,
urinary urea (r = 0.21; P = 0.53) and UAER (r = - 0.16; P = 1.00). In
conclusion, captopril has no effect on the GFR and UAER of normoalbum
inuric normotensive IDDM patients irrespective of the presence of glom
erular hyperfiltration.