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26
Klinisk Kjemi i Norden 2, 2002
Excretion of small amounts of albumin in the
urine is normal. Microalbuminuria is defined as
persistently increased albumin excretion (20 –
200 mg/min) undetectable by conventional test
strips of about 0.2 – 0.3 g/l sensitivity (1). For
over two decades microalbuminuria has been
known to predict the onset of clinical proteinuria
and chronic renal failure in both type 1 and type 2
diabetes. Recently, it has been found to be an
independent risk factor for cardiovascular disease
and is associated with wide variety of acute
inflammatory conditions.
Diabetic nephropathy
Persistent proteinuria and progressive renal insuf-
ficiency are hallmarks of diabetic nephropathy.
The condition is a common complication of
diabetes which reduces life expectancy in 30 – 40
per cent of patients with type 1 diabetes. Renal
impairment is common also cause mortality in
patients with type 2 diabetes, although death in
these cases is more frequently due to cardiovascu-
lar causes (1). At the stage of persistent proteinu-
ria, careful control of diabetes and hypertension
can retard, but not arrest, the decline in renal
function.
Several years before the appearance of proteinu-
ria, however, subclinical elevation of albumin
excretion, microalbuminuria, may be detected
(2). Prospective studies (2, 3, 4, 5) have been
demonstrated that microalbuminuria is an impor-
tant marker for subsequent development of clini-
cal diabetic nephropathy. Early detection of this
forerunner may be crucial, since aggressive inter-
vention in lowering concomitant hypertension
and careful diabetic control would appear to slow
down or even arrest the irreversible progression
of diabetic nephropathy to renal insufficiency (2,
6). Therefore it is recommended that at least all
type 1 diabetic patients should have their urine
tested for albumin excretion once a year. In
microalbuminuric patients, blood glucose control
should be improved as much as possible to delay
progression to persistent proteinuria. If increased
albumin excretion still persists, ACE inhibitor
therapy should be started in both normotensive
and hypertensive patients (7).
Inflammation and trauma
Recent studies show that many acute inflamma-
tory conditions are associated with microalbum-
inuria. It is an early feature of sepsis and predicts
disease severity and outcome in children admitted
with bacterial meningitis (8). Following myocar-
dial infarction, increase of albumin excretion was
proportional to the size of the infarct (9) and in
acute pancreatitis, high levels of urinary albumin
were associated with the later development of
severe pancreatitis (10). Microalbuminuria occurs
far earlier than, for example, the rise in serum
CRP concentration, which takes 2 – 3 days to
reach a maximum. Albumin excretion increases
within 30 min of surgery and lasts only 1 – 48
hours unless there are complications. The finding
that surgery-induced microalbuminuria and incre-
ased albumin transcapillary escape rate occurs at
the same time (11) led to the hypothesis that the
changes in glomerular permeability reflect
changes in systemic vascular permeability (12).
Microalbuminuria and vascular permeability
Clinical and experimental evidence indicates that
microalbuminuria is often associated with increa-
sed vascular permeability in acute and chronic
conditions. But why is urinary albumin excretion
so sensitive to changes in systemic vascular
permeability?
The kidney is ideally placed to amplify small
changes in vascular permeability. Although fene-
strated, the endothelium lining the glomerular
membrane has similarities to the epithelium lining
the capillaries in the rest of the body. The glomeruli
Microalbuminuria: a marker of systemic disease
Aimo Harmoinen
Tampere University Hospital, Centre of Laboratory Medicine, Finland
Email: aimo.harmoinen@tays.fi
