Commentary: Microalbuminuria: Past, present and glorious future

In 1969, Keen and colleagues demonstrated increased urinary albumin excretion (microalbuminuria) during a 50-g glucose load in people with diabetes, compared with those with borderline diabetes and controls, applying a sensitive radioimmunoassay method.1 The 2-h urinary albumin concentration correlated positively with blood glucose and blood pressure in the diabetic group. This led the authors to suggest: ‘The therapeutic implications of this is that treatment of hypertension associated with diabetes may ameliorate or delay the onset of renal disease’.1 Increased urinary albumin excretion is the net result of glomerular capillary passage and tubular reabsorption. Increased glomerular albumin passage occurs due to functional and structural abnormalities such as: increased glomerular capillary permeability-surface area product (size and charge selectivity); and elevated glomerular hydraulic pressure. Recently, the importance of the glycocalyx for macromolecular transvascular transport has been documented. Poor glycaemic regulation and diabetes reduce the glycocalyx, leading to increased albuminuria. Studies in diabetic animals and man have demonstrated enhanced size and charge selectivity for large macromolecules and raised measured and estimated glomerular capillary hydraulic pressure.2