BLOOD-PRESSURE CONTROL, PROTEINURIA, AND THE PROGRESSION OF RENAL-DISEASE - THE MODIFICATION OF DIET IN RENAL-DISEASE STUDY

Citation
Jc. Peterson et al., BLOOD-PRESSURE CONTROL, PROTEINURIA, AND THE PROGRESSION OF RENAL-DISEASE - THE MODIFICATION OF DIET IN RENAL-DISEASE STUDY, Annals of internal medicine, 123(10), 1995, pp. 754
Citations number
32
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
00034819
Volume
123
Issue
10
Year of publication
1995
Database
ISI
SICI code
0003-4819(1995)123:10<754:BCPATP>2.0.ZU;2-H
Abstract
Objective: To examine the relations among proteinuria, prescribed and achieved blood pressure, and decline in glomerular filtration rate in the Modification of Diet in Renal Disease Study. Design: 2 randomized trials in patients with chronic renal diseases of diverse cause. Setti ng 15 outpatient nephrology practices at university hospitals. Patient s: 840 patients, of whom 585 were in study A (glomerular filtration ra te, 25 to 55 mL/min 1.73 m(2)) and 255 were in study B (glomerular fil tration rate, 13 to 24 mL/min . 1.73 m(2)). Diabetic patients who requ ired insulin were excluded. Interventions : Patients were randomly ass igned to a usual blood pressure goal (target mean arterial pressure, l ess than or equal to 107 mm Hg for patients less than or equal to 60 y ears of age and less than or equal to 113 mm Hg for patients less than or equal to 61 years of age) or a low blood pressure goal (target mea n arterial pressure, less than or equal to 92 mm Hg for patients less than or equal to 60 years of age and less than or equal to 98 mm Hg fo r patients less than or equal to 61 years of age). Main Outcome Measur es: Rate of decline in glomerular filtration rate and change in protei nuria during follow-up. Results: The low brood pressure goal had a gre ater beneficial effect in persons with higher baseline proteinuria in both study A (P = 0.02) and study B (P = 0.01). Glomerular filtration rate declined faster in patients with higher achieved blood pressure d uring follow-up in both study A (r = -0.20; P < 0.001) and study B (r = -0.34; Pt 0.001), and these correlations were stronger in persons wi th higher baseline proteinuria (P < 0.001 in study A; P < 0.01 in stud y B). In study A, the association between decline in glomerular filtra tion rate and achieved follow-up blood pressure was nonlinear (P = 0.0 11) and was stronger at higher mean arterial pressure. in both studies , the low blood pressure goal significantly reduced proteinuria during the first 4 months after randomization. This, in turn, correlated wit h a slower subsequent decline in glomerular filtration rate. Conclusio ns: Our study supports the concept that proteinuria is an independent risk factor for the progression of renal disease. For patients with pr oteinuria of more than 1 g/d, we suggest a target blood pressure of le ss then 92 mm Hg (125/75 mm Hg). For patients with proteinuria of 0.25 to 1.0 g/d, a target mean arterial pressure of less than 98 mm Hg (ab out 130/80 mm Hg) may be advisable. The extent to which lowering blood pressure reduces proteinuria may be a measure of the effectiveness of this therapy in slowing the progression of renal disease.