ELEVATED AMBULATORY BLOOD-PRESSURE IN MICROALBUMINURIC IDDM PATIENTS IS INVERSELY ASSOCIATED WITH RENAL PLASMA-FLOW - A COMPENSATORY MECHANISM

Citation
Pl. Poulsen et al., ELEVATED AMBULATORY BLOOD-PRESSURE IN MICROALBUMINURIC IDDM PATIENTS IS INVERSELY ASSOCIATED WITH RENAL PLASMA-FLOW - A COMPENSATORY MECHANISM, Diabetes care, 20(3), 1997, pp. 429-432
Citations number
25
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
01495992
Volume
20
Issue
3
Year of publication
1997
Pages
429 - 432
Database
ISI
SICI code
0149-5992(1997)20:3<429:EABIMI>2.0.ZU;2-3
Abstract
OBJECTIVE - To evaluate the relationship between renal function, ambul atory blood pressure (AMBP), and glycemic control in microalbuminuric IDDM patients compared with normoalbuminuric patients. RESEARCH DESIGN AND METHODS - Nineteen male patients (age 33 +/- 6 years) with slight microalbuminuria (UAE 20-70 mu g/min) were compared with 19 normoalbu minuric (UAE < 15 mu g/min) age-matched (33 +/- 6 years) male patients . Through constant infusion technique, I-125-iothalamate marked the gl omerular filtration rate (GFR), and I-131-hippuran marked effective re nal plasma flow (RPF). AMBP was measured by oscillometric technique (S pacelabs 90202). RESULTS - The microalbuminuric group had higher dayti me systolic AMBP (132 +/- 11 vs. 125 +/- 7 mmHg, P < 0.05) and a poore r glycemic control (HbA(1c) 9.5 +/- 1.5 vs. 8.2 +/- 1.3%, P < 0.01). G FR (135 +/- 22 and 135 +/- 17 ml/min) and RPF (598 +/- 112 and 542 +/- 98 ml/min) were similar in the two groups. In the microalbuminuric gr oup, daytime systolic AMBP was inversely correlated to both RPF (r = - 0.77, P < 0.005) and GFR (r = -0.53, P = 0.02). HbA(1c) and GFR correl ated positively in the microalbuminuric group (r = 0.47, P < 0.04). In contrast, the normoalbuminuric patients exhibited no such association s CONCLUSIONS - IDDM patients with moderate microalbuminuria have elev ated AMBP and a strong negative association between AMBP and RPF. This leaves several possibilities of interpretation. Primary blood pressur e increase (of unknown origin) may induce morphological changes leadin g to reduction in renal function. Alternatively, blood pressure increa se early in the course of incipient nephropathy may represent a compen satory mechanism, initially aiming at preservation of renal function, but later becoming maladaptive.