CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 4, July/August 2010
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AFRICA
While not all parameters could be confirmed in the present
study, the strong association of MAU with a variety of cardio-
vascular risk markers was evident. For instance, the prevalence
of MAU in both diabetic and non-diabetic patients within the
Moroccan population appeared to be comparable, whereas diabe-
tes has been established as an important risk for MAU (OR: 1.24;
1.12–1.38) in the larger population of the global study.
14
Interestingly, the prevalence of MAU was on the other hand
particularly low in patients with more than four hours per week
of regular exercise or those with high HDL cholesterol levels.
This finding is in line with previous reports that microalbuminu-
ria is low in physically active patients and can even be reversed
when patients are motivated to exercise.
33
Therapeutic implications
A wide spectrum of treatment including statins, ACE inhibitors
and ARBs has been shown to improve endothelial dysfunc-
tion, microalbuminuria and proteinuria. In the IDNT study,
34
for example, the ARB irbesartan has been shown in patients
with hypertension, diabetes and nephropathy to prevent the
further deterioration of proteinuria in comparison to the CCB
(amlodipine). In the IRMA-2 study in patients with hyperten-
sion, diabetes and microalbuminuria, it was even shown that
early intervention resulted in a reversal and normalisation of
albumin excretion.
35
Evidence favouring ARBs over beta-blockers comes from a
sub-analysis of the LIFE trial. Ibsen and colleagues compared
atenolol and losartan with regard to the cardiovascular outcomes
in patients with MAU and showed that a reduction in MAU was
associated with a significantly reduced risk of non-fatal myocar-
dial infarction, stroke and cardiovascular death.
36
Therefore, it was of particular interest to test the differences
between antihypertensive classes with regard to MAU in clinical
practice. The interpretation of analyses was difficult because of
unknown variables and the cross-sectional nature of the study,
but it revealed that beta-blockers and CCBs were more widely
prescribed than the ARBs in MAU-positive patients. It is possi-
ble to at least assert that the choice of antihypertensive drug was
not in line with the study results discussed above.
Microalbuminuria is also a justified target for primary
prevention, as seen in evidence of recent compelling results
from the PREVENT-IT study.
37
Healthy individuals with micro-
albuminuria, but without hypertension or hypercholesterolaemia,
were treated either with placebo or RAS blockade. At four years’
follow up, microalbuminuria was effectively reduced, which was
associated with a 44% reduction in cardiovascular events.
Strength and limitations
The main strengths of our cross-sectional study included a large,
referred cohort of hypertensive patients attending a cardiologist
or internist, with validation of predefined primary and second-
ary endpoints. However, two limitations should be noted. First,
microalbuminuria could only be assessed on a single occasion
although guidelines recommend triple testing (two out of three
tests need to be positive). Therefore the present data may not
allow an exact quantification of how many patients would be
positive or negative on a second occasion. However, other data
suggest that this requirement will reduce the point prevalence
by only one-fifth,
38
up to a maximum of one-third.
39
Second, a
follow up would allow a closer investigation of the relationship
between ARB use and the development or regression of micro-
albuminuria.
Conclusions
A high prevalence of microalbuminuria was detected in a
random sample of hypertensive patients attending a cardiology
outpatient setting, indicating that high cardiovascular risk is
common in clinical practice. Early detection, in addition to a
more aggressive multifactorial treatment based on inhibitors of
the renin–angiotensin system (RAS blockade) to reduce blood
pressure as well as other cardiovascular risk factors is warranted
to facilitate not only secondary but also primary prevention.
The study was supported by sanofi-aventis. We acknowledge the support of
all participating physicians.
References
1. Pagtalunan ME, Miller PL, Jumping-Eagle S, Nelson RG, Meyers SD,
et
al
. Podocyte loss and progressive glomerular injury in type II diabetes
.
J
Clin Invest
1997;
99
(2): 342–348.
2. Deckert T, Feldt-Rasmussen B, Djurup R, Deckert M. Glomerular size
and charge selectivity in insulin-dependent diabetes mellitus.
Kidney Int
1988;
33
(1): 100–106.
3. Diercks GF, van Boven AJ, Hillege HL, Janssen WM, Kors JA, de Jong
PE,
et al
. Microalbuminuria is independently associated with ischaemic
electrocardiographic abnormalities in a large non-diabetic population.
The PREVEND (Prevention of REnal and Vascular ENdstage Disease)
study.
Eur Heart J
2000;
21
(23): 1922–1927.
4. Cuspidi C, Meani S, Valerio C, Fusi V, Catini E, Sala C,
et al.
Prevalence
and correlates of advanced retinopathy in a large selected hypertensive
population. The Evaluation of Target Organ Damage in Hypertension
(ETODH) study.
Blood Press
2005;
14
(1): 25–31.
5. Yamaji T, Fukuhara T, Kinoshita M. Increased capillary permeability to
albumin in diabetic rat myocardium.
Circ Res
1993;
72
(5): 947–957.
6. Deckert T, Feldt-Rasmussen B, Borch-Johnsen K, Jensen T, Kofoed-
Enevoldsen A. Albuminuria reflects widespread vascular damage. The
Steno hypothesis.
Diabetologia
1989;
32
(4): 219–226.
7. Pedrinelli R, Giampietro O, Carmassi F, Melillo E, Dell’Omo G,
Catapano G,
et al
. Microalbuminuria and endothelial dysfunction in
essential hypertension.
Lancet
1994;
344
(8914): 14–18.
8. Quyyumi AA. Prognostic value of endothelial function
.
Am J Cardiol
2003;
91
(12A): 19H–24H.
9. Berton G, Cordiano R, Palmieri R, Cucchini F, De Toni R, Palatini P.
Microalbuminuria during acute myocardial infarction; a strong predictor
for 1-year mortality.
Eur Heart J
2001;
22
(16): 1466–1475.
10. Lekatsas I, Kranidis A, Ioannidis G, Kalofoutis C, Tavernarakis A,
Thalassinos N,
et al
. Comparison of the extent and severity of coronary
artery disease in patients with acute myocardial infarction with and with-
out microalbuminuria
. Am J Cardiol
2004;
94
(3): 334–337.
11. Klausen KP, Scharling H, Jensen G, Jensen JS. New definition of micro-
albuminuria in hypertensive subjects: association with incident coronary
heart disease and death.
Hypertension
2005;
46
(1): 33–37.
12. Cosson E, Pham I, Valensi P, Pariès J, Attali JR, Nitenberg A. Impaired
coronary endothelium-dependent vasodilation is associated with micro-
albuminuria in patients with type 2 diabetes and angiographically
normal coronary arteries.
Diabetes Care
2006;
29
(1): 107–112.
13. Mann JF, Gerstein HC, Pogue J, Bosch J, Yusuf S. Renal insufficiency
as a predictor of cardiovascular outcomes and the impact of ramipril: the
HOPE randomized trial.
Ann Intern Med
2001;
134
(8): 629–636.
14. Böhm M, Thoenes M, Danchin N, Bramlage P, La Puerta P, Volpe M
.
Association of cardiovascular risk factors to microalbuminuria in hyper-
tensive individuals: the i-SEARCH global study.
J Hypertens
2007;
25
:
2317–2324.
15. Comper WD, Jerums G, Osicka TM. Deficiency in the detection of
microalbuminuria by urinary dipstick in diabetic patients
. Diabetes Care
