Background Patients with type 1 diabetes mellitus and microalbuminuriaoften have elevated blood pressure while they are asleep, butit is not known whether the elevation develops concomitantlywith microalbuminuria or precedes it.
Methods We monitored 75 adolescents and young adults who hadhad type 1 diabetes with normal urinary albumin excretion andblood pressure for more than five years. Ambulatory blood-pressuremonitoring was used to assess blood pressure at the initialevaluation and about two years later, at which time all subjectshad normal urinary albumin excretion. Subsequently, subjectswere monitored for the development of microalbuminuria.
Results Microalbuminuria developed in 14 subjects, whereas theother 61 continued to have normal urinary albumin excretion.The mean (±SD) systolic pressure during sleep increasedsignificantly in the subjects who ultimately had microalbuminuria(from 109.9±11.3 to 114.9±11.7 mm Hg, P=0.01)but not in the subjects with normal albumin excretion (from106.0±8.8 to 106.4±14.8 mm Hg). The risk of progressionto microalbuminuria was examined in relation to the ratio ofsystolic pressure during sleep to systolic pressure in the daytime.A ratio of 0.9 or lower, used to define a normal fall in nocturnalpressure, had a negative predictive value of 91 percent forthe development of microalbuminuria. Moreover, the risk of microalbuminuriawas 70 percent lower (95 percent confidence interval, 44 to110 percent) in subjects with a ratio of 0.9 or less than inthose with a ratio higher than 0.9 (P=0.01).
Conclusions In persons with type 1 diabetes, an increase insystolic blood pressure during sleep precedes the developmentof microalbuminuria. In those whose blood pressure during sleepdecreases normally, the progression from normal albumin excretionto microalbuminuria appears to be less likely.
Source Information
From the Pediatric Nephrology Unit, Department of Pediatrics, Hospital General and University of Valencia, Valencia, Spain (E.L., J.T., V.A.); the Hypertension Clinic, Department of Medicine, Hospital Clinico and University of Valencia, Valencia, Spain (J.R.); the Division of Nephrology and Hypertension, Feinberg School of Medicine, Northwestern University, Chicago (A.K., D.B.); and the Department of Medicine, Hospital de Sagunto, Sagunto, Spain (J.M.P.).
Address reprint requests to Dr. Batlle at the Division of Nephrology and Hypertension, Feinberg School of Medicine, Northwestern University, 320 E. Superior St., 10-475 Searle Bldg., Chicago, IL 60611.
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