Albumin Excretion Rate and Cardiovascular Risk

Could the Association Be Explained by Early Microvascular Dysfunction?

  1. W. David Strain1,
  2. Nish Chaturvedi1,
  3. Christopher J. Bulpitt2,
  4. Chakravarthi Rajkumar2 and
  5. Angela C. Shore3
  1. 1International Centre for Circulatory Health, Faculty of Medicine, Imperial College London at St Mary’s, London, U.K.
  2. 2Care of the Elderly, Faculty of Medicine, Imperial College London at the Hammersmith Hospital, London, U.K.
  3. 3Clinical Microvascular Research, Institute of Biomedical and Clinical Science, Peninsula Medical School, Exeter, U.K.
  1. Address correspondence and reprint requests to Professor Angela Shore, Clinical Microvascular Research, Institute of Biomedical and Clinical Science, Peninsula Medical School, Barrack Rd., Exeter EX2 5AX, U.K. E-mail: angela.shore{at}


Elevated albumin excretion rate (AER) independently predicts total and cardiovascular mortality in a variety of conditions, although the exact mechanisms are unknown. Laser Doppler fluximetry was used to study associations with risk factors and renal damage (AER calculated from a timed overnight urine collection) in 188 people without diabetes and 117 individuals with diabetes. Skin flow (flux) in response to arterial occlusion (ischemia) was measured. Three distinct patterns of postischemic peak flow were observed: 1) gradual rise to peak (normal), 2) nondominant early peak, and 3) dominant early peak. Those with a dominant early peak were more likely to have diabetes (P = 0.01), hypertension (P = 0.001), and obesity (P < 0.001) and had a higher AER (12.6 μg/min [95% CI 7.8–20.2] vs. 7.2 [5.5–9.5] nondominant early peak group and 3.7 [3.2–4.1] normal group; P < 0.001 for trend). This could not be accounted for by conventional cardiovascular risk factors (P < 0.001 after adjustment). A rapid peak flow response after ischemia is associated with an elevated AER and increased cardiovascular risk. This may represent shared mechanistic pathways and causative or con-sequential changes in the microvasculature and supports the hypothesis that microvascular dysfunction may contribute to large vessel pathophysiology.


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    • Accepted February 21, 2005.
    • Received August 27, 2004.
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