Klinisk Biokemi i Norden Nr 2, vol. 14, 2002 - page 29

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Klinisk Kjemi i Norden 2, 2002
receive 25 % of the cardiac output. Of the 70 kg of
albumin that pass though the kidneys every 24 h,
less than 0.01% reaches the glomerular ultrafiltrate
(i.e. less than 7 g / 24 h) and hence enters the renal
tubules (13). Almost all filtered albumin is reabsor-
bed by the proximal tubule via high-affinity, low-
capacity endocytotic mechanism (14), with only 10
– 30 mg / 24 h appearing in the urine. Assuming
that 7 g of albumin is filtered every 24 h, a 1 %
increase in systemic vascular permeability in
response to an inflammatory stimulus would result
in an additional 70 mg of albumin passing into the
filtrate. Since tubular mechanisms for albumin
reabsorption are near saturation, urinary albumin
excretion would increase from a maximum of 30 to
100 mg / 24 h (15) and this kind of increase is very
easily detected by the measurement of microal-
buminuria.
Cardiovascular diseases
Both hypertensive and diabetic patients with
microalbuminuria show increased vascular
permeability to radiolabelled albumin (16). Thus
urinary albumin albumin excretion is closely
linked to vascular endothelial function, making
microalbuminuria a possible marker of vascular
disease (17). Endothelial dysfunction may lead to
impaired insulin action as well as to capillary lea-
kage of albumin, features possibly linked to a pre-
disposition to cardiovascular disease (18).
Attention has been drawn to the predictive power of
microalbuminuria for cardiovascular mortality.
Microalbuminuria may be a risk factor implicated in
the development of cardiovascular disease and may
therefore have a role in screening programmes (19).
The condition is, however, so frequent in many
acute and chronic diseases that this non-specifity
fatally limits its usefulness in this setting (15).
Applications of microalbuminuria
measurements
As mentioned earlier during the last two decades
microalbuminuria has found its place as an indi-
cator of "incipient" nephropathy of diabetes.
Although it is sensitive marker of vascular perme-
ability, it reflects a phenomenon which is present
in many conditions; its diagnostic value is there-
fore limited. However, albumin excretion can be
used to assess disease severity and progression.
Increased vascular permeability follows major
inflammatory insults such as trauma, sepsis and
surgery. Leakage of albumin and water from
capillary to interstitial space increases the gap
between the capillary and the cell, across which
oxygen and other substances have to travel. In
uncomplicated cases this effect is transitory, and
excess interstitial fluid is lost within few hours
when vascular permeability returns to normal. In
patients with prolonged and excessive capillary
leak, the distance between the capillary and the
cell becomes large enough to compromise oxy-
gen delivery, and single or multiple system organ
failure ensues (20). In elective aortic surgery,
urine albumin excretion four hours after the start
of the operation predicts those patients who will
develop pulmonary dysfunction 24 hours later (21).
Similar results have been obtained for urine albu-
min excretion 4 – 8 hours post-trauma (22).
Early identification of excessive capillary lea-
kage will influence surgical and medical mana-
gement, including the choice crystalloid or col-
loid for resuscitation, depending on capillary
patency.
References
1) Viberti GC, Walker J. Diabetic nephropathy:
etiology and prevention. Diabetes Metab Rev
1988; 4: 147- 62
2) Parving H-H, Oxenboll B, Svedsen PA,
Christiansen JS, Andersen AR. Early detec-
tion of patients at risk of developing diabetic
nephropathy. A longitudal of urinary albumin
excretion. Acta Endocrinol (Copenh) 1982;
100: 550-5
3) Viberti GC, Hill RD, Jarret RJ, Argiropoulos
A, Mahmoud U, Keen H. Microalbuminuria
as a predictor of clinical nephropathy in insu-
lin-dependent diabetes. Lancet 1982; i: 1430-
2
4) Mogensen CE, Christensen C. Predicting
diabetic nephropathy in insulin-dependent
patients. New Engl J Med 1984; 311: 89-93
5) Mathiesen ER, Oxenboll B, Johansen K,
Svedsen PA, Deckert T. Incipient nephro-
1...,19,20,21,22,23,24,25,26,27,28 30,31,32,33,34,35,36
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