Renal effects of mild hypertension and therapy have not been established. Since urinary albumin and N-acetyl-β-ᴅ-glucosaminidase excretions reflect renal effects of hypertension, they were related to blood pressure, other cardiovascular risk factors, cardiac target organ effects, and response to therapy in mild hypertension (diastolic blood pressure 85–99 mm Hg). Participants were from two clinics of the Treatment of Mild Hypertension Study (TOMHS), a multicenter randomized, doubleblind, controlled trial. Participants received nutritional-hygienic therapy and one of five active drugs or placebo. Urinary albumin and N-acetyl-β-ᴅ-glucosaminidase excretions were assessed prospectively using office “spot” collections from one clinic (n = 213) and retrospectively using overnight collections from the other clinic (n = 210). Relationships were determined between protein excretions and blood pressure, age, gender, race, blood glucose, cholesterol concentrations, and indices of body mass and left ventricular mass and function at baseline. Treatment effects were assessed after 3 to 12 months. Spot and overnight albumin excretions related positively to baseline systolic blood pressure by univariate analyses. Spot albumin excretion related positively to systolic blood pressure, age, creatinine clearance, and left ventricular function while overnight albumin excretion related positively to left ventricular mass and female gender by multiple regression analyses. Spot, but not overnight, albumin excretion declined significantly with active drug therapy. N-acetyl-β-ᴅ-glucosaminidase excretion did not relate to blood pressure or decline with therapy. The combined results suggest albumin excretion correlates with blood pressure, decreases with antihypertensive drug therapy, and is associated with greater left ventricular function and mass, as well as glomerular filtration rate, even at mild levels of hypertension. Am J Hypertens 1994;7:965–974.
|Original language||English (US)|
|Number of pages||10|
|Journal||American journal of hypertension|
|State||Published - Nov 1994|
Bibliographical noteFunding Information:
This work was supported by grants from the National Heart, Lung, and Blood Institute, Bethesda, MD; Biomedical Research Support Grant (University of Minnesota); and Merck Sharp and Dohme Research Laboratories, Boehringer Ingelheim Pharmaceuticals, Inc., Pfizer Inc., and Wyeth Laboratories.
- Left ventricular hypertrophy