In the present study, the SBP, DBP, and MBP
values that were determined with ABPM were higher
in hypertensive patients who had proteinuria. It was
also found that the development of non-dipper HT
and reverse-dipper HT was more frequent in those
who had proteinuria. Creatinine and urine protein
levels were higher and there were more advanced
stages of HT in patients who had non-dipper HT and
reverse-dipper HT.
Rational management of HT begins with accurate
measurement of BP. European[7] and American[9]
guidelines recommend the use of ABPM in all
patients using antihypertensive medications. The
reasons for this recommendation of these guidelines
include the differential diagnosis of causes such as
whitecoat HT, masked HT, orthostatic HT, chronic
renal failure, autonomic dysfunction, diabetes mellitus,
and endocrine HT, as well as determining the time
of hypertensive drug use. Additionally, a relationship was detected with the progression of microvascular
diseases.[10] Ambulatory BP measurement was shown
to be more effective in indicating the development
of target organ damage.[11,12] Therefore, ABPM was
used to determine the BP values of the patients in
the present study. Furthermore, the ABPM was
found to be the most useful and effective method
in diagnosing HT, and it is also the best method
in determining the time of taking antihypertensive
medication.[7]
In the present study, the relationship between
ABPM and 24-h urinary protein excretion was
examined in patients who applied to the nephrology
clinic with complaints of HT. Similar to the literature
data, as the proteinuria level of the patients increased,
an increase in creatinine levels and a decrease in GFR
were detected.[13] The reason for this relationship
was the increase in glomerular perfusion pressure,
which may result in endothelial cell damage in the
glomerular capillaries, resulting in microalbuminuria and progressive renal damage, similar to the study
reported by Ying et al.[13]
Hermida et al.[14] reported that non-dipper or
reverse-dipper HT was more common in patients
who had resistant and uncontrolled HT. When the
renal functions of dipper HT, non-dipper HT, and
reverse-dipper HT patients were compared, GFR was
found to be lower in patients who had non-dipper and
reverse-dipper HT at significant levels. Hermida et
al.[15] reported that non-dipper HT was more common
in patients who had chronic renal failure, similar to
our study, and GFR was lower and creatinine was
elevated in those with non-dipper HT.
As a result of the increased BP at night, there
is increased peripheral resistance and thickness of
the glomerular basement membrane, which causes
cell damage in the vascular endothelium, increasing
albumin/protein excretion.[16] It was found in the
present study that as proteinuria increased, dipper HT and non-dipper HT developed in patients. Similar to
our study, Farrag et al.[17] and Guo et al.[18] reported
that the frequency of non-dipper HT increased as
proteinuria increased and proteinuria was elevated
in patients who had non-dipper HT. A recent study
that investigated the bidirectional relationship of
proteinuria and BP argued that proteinuria and BP
might influence each other, suggesting that increase
in proteinuria will cause higher BP and vice versa.[19]
Similarly, the present study found that SBP, DBP, and
MBP values that were determined with ABPM were
elevated in patients who had proteinuria. Mettimano
et al.[20] reported a significant relationship between
proteinuria and 24-h SBP, daytime SBP, and nighttime
SBP values. O’Seaghdha et al.[21] reported that this
relationship was contradictory to DBP. Similar to
our study, Hirayama et al.[22] reported a relationship
between proteinuria and SBP but not with DBP.
Differences between studies might be due to the
differences in patient age. The ages of the patients in
our study were higher compared to those in the Asian
study and other referenced studies.[21,22] Low DBP
levels reflect improved arterial stiffness in the elderly,
which may be a risk factor associated with poor renal
prognosis.[20] In other words, it may be a more practical
method to follow up patients in the elderly with SBP.
This study had some limitations. First, since the
study was conducted at a cross-sectional design,
changes over time in the relationship between
proteinuria and HT were not investigated. Second,
proteinuria was assessed with 24-h urine collection,
and spot urine protein-to-creatinine ratio was
not examined. Third, the number of patients was
insufficient since the study was conducted within a
short period.
In conclusion, the development of non-dipper
HT and reverse-dipper HT was more common in
those with proteinuria compared to those without
proteinuria. Renal dysfunction and proteinuria were
more common in patients who have non-dipper or
reverse-dipper HT. Advanced stage HT development
was detected in those who have non-dipper HT
and reverse-dipper HT compared to those with
dipper HT. Ambulatory BP monitoring was more
useful than other tests in hypertensive patients with
proteinuria, and proteinuria could be controlled with
strict BP control in such patients. However, further
multicenter studies with a larger number of patients
are needed.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Author Contributions: Idea/concept, data collection
and/or processing, literature review, writing the article,
materials, other: B.A.D.; Design, analysis and/or
interpretation, critical review, references and fundings:
M.İ.D.; Control/supervision: A.Ö.
Conflict of Interest: The authors declared no conflicts
of interest with respect to the authorship and/or publication
of this article.
Funding: The authors received no financial support for
the research and/or authorship of this article.
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