Changes in insulin sensitivity, renal function, and markers of endothelial dysfunction in hypertension—the impact of microalbuminuria: a 13-year follow-up study

Microalbuminuria (MA) clusters with the metabolic syndrome and insulin resistance and may reflect endothelial dysfunction. Microalbuminuria may also represent renal dysfunction. The aim of the present follow-up study was to assess changes over 13 years in insulin sensitivity, markers of endothelial dysfunction, and renal function in hypertensive subjects with and without MA in 1992-1993, matched for age, sex, and body mass index. Fourteen subjects with and 17 without MA at baseline (1992-1993) participated. At follow-up (2005-2006), MA status was unchanged in 75% of the subjects. The groups had comparable age, blood pressure, body mass index, markers of endothelial dysfunction, and metabolic traits, assessed by oral glucose tolerance test and hyperglycemic clamp. Estimated glomerular filtration rate decreased significantly in the MA group (P = .049) and tended to be lower in the MA than the non-MA group in 2005-2006 (79.9 ± 24.5 vs 90.8 ± 13.3 mL min-1 (1.73 m2)−1, P = .2). Urinary albumin excretion in 1992-1993 predicted estimated glomerular filtration rate in 2005-2006 in adjusted analysis (β = −0.47, P = .006). Estimated glomerular filtration rate less than 60 mL min−1 (1.73 m2)−1 was more frequent in the MA than non-MA group at follow-up (P = .03). In conclusion, long-standing MA was not associated with progression of metabolic disturbances or markers of endothelial dysfunction in hypertensive individuals. A decline in renal function predicted by urinary albumin excretion was suggested. Microalbuminuria may not be a metabolic trait, but a marker mainly of renal endothelial dysfunction.