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ORIGINAL ARTICLE

JNEPHROL 2010; 23 ( 05 ) : 547-555


www.sin-italy.org/jnonline www.jnephrol.com

Pattern of urinary sediments and comparison


with dipstick urinalysis in hypertensive Nigerians
Timothy O. Olanrewaju, Ademola Aderibigbe

Division of Nephrology, Department of Medicine,


University of Ilorin Teaching Hospital, Ilorin - Nigeria
Division of Nephrology, Department of Medicine, University of Ilorin Teaching Hospital, Ilorin - Nigeria

Introduction

Abstract
Background: Urinary sediment examination and dipstick urinalysis are an integral part in evaluating hypertensive patients. This study aims to determine the
prevalence of urinary sediment abnormalities and
compare this result with dipstick urinalysis in hypertensive Nigerians.
Methods: 138 newly diagnosed, adult, hypertensive
Nigerians were studied. They were compared with
an age- and sex-matched non-hypertensive control
group from the general population. The subjects urine
samples were analyzed by dipstick test and microscopy (bright field), enhanced by Sternheimers stain.
Significant sediments were defined as 3/hpf and dipstick proteinuria or hematuria as 1+.
Results: Mean age was 43.219.64 yrs and 43.199.55
yrs in patients and controls respectively with 76 (55%)
males in the patients and 80 (58%) in controls. Microscopic hematuria (3/hpf) was detected in 15.2% of
the patients and 3.6% of the control group (p=0.0009).
Other elements present in insignificant quantities
in patients and controls, respectively, were: leukocytes (7.2%, 9.4%, p=0.513); hyaline casts (5.8%,
8%, p=0.476), granular casts (1.4%, 0%) and crystals
(6.5%, 5.1%, p=0.606). Dipstick proteinuria with hematuria was found in 6.55% and proteinuria alone in
1.45% of cases, while the control group showed 2.2%
and 1.45% of hematuria and proteinuria, respectively;
47.6% of hypertensive patients with urinary sediment
hematuria were not detected by dipstick test.
Conclusions: Hypertensive Nigerians showed a high
prevalence of microscopic hematuria which may be
suggestive of sub-clinical kidney damage at diagnosis. There is a high false-negative rate with dipstick
urinalysis, underscoring the need for routine examination of urinary sediment in the assessment of hypertensive patients.
Key words: Dipstick tests, Hypertension, Nigerians,

Urinary sediments

Systemic hypertension is a major health problem worldwide and Blacks are more prone to its complications (1,
2). About 4.33 million Nigerians aged 15 years and above,
corresponding to 9.3% of the population, are hypertensive
based on a systolic blood pressure of 160 mmHg and a
diastolic pressure of 90 mmHg (3, 4). However, when the
World Health OrganizationInternational Society of Hypertension (WHO/ISH) guidelines of 1999 were applied to the
above data, the estimated prevalence of hypertension was
17% to 20% or more (5, 6). Although the prevalence rate is
lower than the figure reported for the United States (>25%)
(7), the mortality associated with the disease in Nigeria has
been observed to be higher (8). Hypertension has a cause
and effect relationship with kidney disease and is a major
factor responsible for progression to End-Stage Renal Disease (ESRD) (9-12). The risk factors that have been found
to predispose hypertensive to developing ESRD include:
Black race, positive family history, long-standing or severe
hypertension, age of onset of hypertension between 25 and
45 years old, presence of hypertensive retinopathy, and left
ventricular hypertrophy (13). Many studies in Nigeria have
shown that hypertension and chronic glomerulonephritis
topped the list of common causes of chronic renal failure
(CRF) (14-16). In a prospective study of 1,980 patients,
Ojogwu (16) observed that the most common cause (43%
of cases) of chronic renal failure was hypertensive nephrosclerosis. This was followed by obstructive uropathy (33%)
and chronic glomerulonephritis (18%). He observed that
the frequency and severity of hypertension in Nigerians and
their propensity to develop renal failure are similar to what
obtains in American Blacks. Similarly, Akinsola et al (17)
reported that hypertension was second to chronic glomerulonephritis as a cause of chronic renal failure, the care
of which is unaffordable to the majority of patients. This
underscores the need to emphasize strategies for preventing the development of progressive renal disease with early
recognition of clinical markers of chronic kidney disease

2010 Societ Italiana di Nefrologia - ISSN 1121-8428

547

Olanrewaju and Aderibigbe: Urinary sediment evaluation in hypertension

(18). In a developing nation like Nigeria, such strategies


involve a simple urine test to detect early renal damage.
Early detection of patients with glomerulonephritis will attract appropriate intervention measures to prevent or delay
progression to ESRD.
There are many markers for assessing renal damage.
These range from very sensitive endogenous markers such
as cystatin C, microalbuminuria and proteinuria to serum
urea, creatinine, uric acid, creatinine clearance and urinary sediment. While some of these markers are indeed
sensitive, they can be expensive as a screening tool for
early detection of renal damage. The examination of urinary sediments under the microscope for abnormalities is
a recognized method for assessing renal damage irrespective of the cause, and some characteristic features of the
sediment have been used to determine the type and possibly the severity of renal disease (19). The findings in the
sediment of red blood cells or red blood cell casts, white
blood cells or white blood cell casts, oval fat bodies or fatty
casts and broad casts are almost diagnostic of glomerulonephritis, pyelonephritis, nephritic syndrome and renal
failure, respectively (19). Thus, urinary sediment analysis
tends to give information about the etiology of renal diseases, helps in prognostication, and may offer a simpler
index for evaluating the stage of renal damage in patients
with newly diagnosed hypertension. The facilities are readily available, the samples can be collected anywhere and
its collection is noninvasive. Urinary sediment examination
has therefore been recommended for evaluation of hypertension in order to determine the cause and/or effect relationship (5, 20, 21).
Though some studies have been done on urinary abnormalities in Nigeria, most of them were carried out on children and
adolescents using dipstick urinalysis (22-26). There is paucity of published studies on urinary sediments among Nigerians and in particular, adult hypertensive patients. Hence
this study was designed to evaluate the pattern of urinary
sediments and compare the results with dipstick urinalysis
in newly diagnosed, adult Nigerian hypertensive patients.

Materials and methods


Study design and location
This was a cross-sectional study of consecutively recruited, consenting patients. The study was carried out at the
General Out-patient Department (GOPD), Medical Outpatient Department (MOPD), Accident and Emergency (A/E)
Department of the University of Ilorin Teaching Hospital
548

(UITH) and the Federal Staff Clinic at the Federal Secretariat in Ilorin. Ilorin is the capital city of Kwara State, which
is one of the states in the north-central zone of Nigeria.
UITH Ilorin serves both Kwara State as well as five other
adjoining states.

Selection of subjects
The inclusion criteria for patients were newly diagnosed,
adult hypertensive patients aged 18 years and above with
average systolic blood pressure of 140 mmHg and/or a
diastolic pressure of 90 mmHg who were not on drugs
and who consented to the study by filling in the consent
form. The exclusion criteria included (i) patients with diabetic mellitus, sickle cell disease, history of/or established
renal disease, malignancy and clinical evidence of connective tissue disease; (ii) women who are pregnant, in peuperium or those menstruating; (iii) patients who are on antihypertensive drugs; and (iv) those who have just completed
rigorous exercise or are on any medications. For the control
group, the inclusion criteria were healthy, non-hypertensive,
age- and sex-matched individuals who have not undergone
rigorous exercise; and the exclusion criteria included individuals with high blood pressure and those that fulfilled the
exclusion criteria as stated for the subject group.

Ethical clearance
An approval was obtained from the ethical and research
committee of the University of Ilorin Teaching Hospital before commencing the study. All patients and controls who
participated in the study signed the informed consent before recruitment.

Evaluation and investigation protocols

Clinical
Detailed biodata and socio-demographic parameters were
obtained from the patients and controls using structured
questionnaires. Weight (WT) was measured using the portable SECA weighing scale placed on a flat, hard surface
with the subjects wearing light clothing and height measured with subjects standing without shoes. Body mass index was calculated from height and weight. Blood pressure
was measured in sitting position with a mercury sphygmomanometer with standard cuff (25 cm x 12 cm) on the right
arm after 5 minutes of rest. Korotkoff phases I and V were
taken as systolic blood pressure (SBP) and diastolic blood
pressure (DBP), respectively. Hypertension was defined

JNEPHROL 2010; 23 ( 05 ) : 547-555

based on the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of
High Blood Pressure (JNC VII) (1). Two measurements were
taken at least 5 minutes apart and the value of the mean
was used for the study. The mean arterial pressure (MAP)
and pulse pressure (PP) were also determined.

Serum biochemistry and urine culture


Blood samples for urea and creatinine were collected in
heparinized bottles and analyzed at the Chemical Pathology Laboratory of the hospital using an RA-50 spectrophotometer (Bayer, Germany). Urea (Ur) was analyzed by
diacetyl monoxime method while Jaffes reaction was used
for creatinine (Cr). Also, fasting plasma glucose (FPG) samples were collected in a fluoride oxalate bottle and analyzed at the same laboratory by glucose oxidase method.
Urine culture was done to exclude urinary tract infections.
Glomerular filtration rate (GFR) was estimated by the Cockroft and Gault formula which has been validated in Nigerian
patients (27).

Dipstick urinalysis
About 10 mL of early morning, clean catch urine was collected in a sterile test tube. The urine was examined physically and tested with urinanalysis reagent strips (Multistix
10 SG; Bayer, Leverkusen, Germany). Each parameter
tested (e.g., protein, blood, leukocytes, and nitrite) was read
manually within the specified time limit as indicated by the
manufacturer of the dipsticks. Protein 1 + and blood more
than trace were considered to be significant.

Urine sediment microscopy


This procedure was carried out in the renal laboratory by the
investigator with the assistance of an experienced laboratory technologist. A standard urinary sediment Atlas produced
by Fogazzi et al (19) was used for clarification as deemed
necessary. A 10 mL early morning, first void, clean catch
urine was collected in a sterile tube and centrifuged for 5
minutes at 2000 rpm. The supernatant was decanted leaving approximately 0.5 mL volume of the sediment. In order
to enhance the identification of the constituent elements
of the sediment, Sternheimers stain was applied. Sternheimers stain is one of the most popular supravital stains
which, in the absence of a phase contrast microscope,
helps to partly overcome the limitations of the bright field
microscope (28). It is a mixture of Copper-phthalocyanine
dye, national fast blue and a xanthene dye called pyronin

B. A drop of this stain was added to the 0.5 mL sediment


and left for 10 minutes to allow the staining to develop and
increase in intensity. This enhances a good differentiation of
red blood cells, white blood cells, epithelial cells, and casts.
The stained urine sediment was resuspended by gentle agitation and a drop was pipetted using a micropipette onto a
clean glass slide and covered with a clean cover-slip. The
sediment was then examined under the bright-field microscope, first under low (x 100 magnifications) and then high
power (x 400 magnifications). Ten to fifteen fields were examined in the low and high power objectives. Each of the
constituent elements of the sediment was recorded as an
average number per high power field (hpf). The presence of
sediment cells >2/hpf and casts or crystals as indicated by
a plus (+) were considered significant.

Data analysis
The data were analyzed by SPSS version 12.0.1 (SPSS Inc.,
Chicago, IL, USA). Means and standard deviations were
used to summarize numerical/quantitative variables. The
statistical significance of differences in patients and control groups was estimated using chi-square for categorical
variables and Students t-test for continuous variables. The
proportion of patients with abnormal urinary sediment was
determined. The level of statistical significance was taken
as a p value of < 0.05.

Results
The demographic, clinical and laboratory characteristics
of the patients and control subjects are shown in Table
I. There was no difference between the mean age of the
patients and the control subjects, showing that they were
well matched. There was also no difference in the fasting
plasma glucose between the two groups. However, the patient group had significantly higher values of weight, BMI,
SBP, DBP, MAP and PP than control subjects (p<0.05).
Also, estimated GFR was significantly lower in the patients
(107.6 0 52.85 mL/min/1.73m2) than the control subjects
(122.1744.3 mL/min/1.73m2) (p=0.0134). The prevalence
and pattern of urinary sediment cells are depicted in Figures 1 and 2; while those for casts and crystals were shown
in Table II. Ninety patients (65.2%) had no red blood cells
(RBC) in their urinary sediment, twenty-seven (19.6%)
had insignificant RBC (1-2/hpf) in the urine, while twentyone (15.2%) had significant RBC (>2/hpf) with a range of
3-10/hpf. In the control group, 119 (86.2%) had no RBC,
14 (10.2%) had 1-2/hpf and only 5 (3.6%) had > 2/hpf of
RBCs in the urinary sediment (Fig. 1). The difference in the
549

Olanrewaju and Aderibigbe: Urinary sediment evaluation in hypertension

Fig. 1 - Urinary sediment red blood cells per high power field
(hpf) in study subjects. White columns = patient; black columns = control.

Fig. 2 - Urinary sediment white blood cells per high power


field (hpf) in study subjects. White columns = patient; black
columns = control.

microscopic hematuria between the patients (15.2%) and


controls (3.6%) was significant (p=0.001).White blood cells
(WBC) of 1-2/hpf were detected in 10 (7.2%) of the pa-

tients while the remaining 128 (92.8%) had no WBC. In the


control group, 13 (9.4%) had 1-2/hpf of WBC while 125
(90.6%) had no WBC (Fig. 2). Granular casts of 1-2/hpf

TABLE I
CLINICAL AND LABORATORY CHARACTERISTICS OF THE SUBJECTS
Characteristics
Age (years)
Gender: male, n (%)

Patients

Control

43.21 9.64

43.19 9.55

p value
0.9862

76 (55)

80 (58)

Weight (Kg)

72.63 14.29

69.34 12.55

0.0431

Body Mass Index (kg/m2)

26.18 5.12

23.34 9.02

0.0015

154.32 17.2

119.44 11.94

< 0.001

Systolic Blood Pressure (mmHg)


Diastolic Blood Pressure (mmHg)

98.67 16.87

76.11 6.14

< 0.001

Pulse Pressure (mmHg)

59.64 19.79

43.33 11.32

< 0.001

90.55 6.65

< 0.001

Mean Arterial Pressure (mmHg)

114 14.21

Urea (mmol/L)

5.27 1.39

4.86 1.24

0.0102

76.06 22.49

67.55 15.9

0.0003

96 1.29

0.2926

122.17 44.3

0.0134

Creatinine (umol/L)
Fasting plasma glucose (mmol/L)
Glomerular filtration rate (ml/min/1.73m2)
550

4.12 1.23
107.6 0 52.85

JNEPHROL 2010; 23 ( 05 ) : 547-555

were present in only 2 (1.4%) of the patients and none in the


control subjects, while hyaline casts of 1-2/hpf were found
in 8 (5.8%) patients and 11 (8%) control subjects (Tab. II).
Crystals were detected in 9 patients (6.5%) and 7 (5.1%)
of the control subjects (Tab. II). RBC cast, WBC cast, waxy
and broad casts were not found in either patients or control
subjects. Significant proteinuria (1+) was found in 11 (8%)
of the patients with 8 (5.8%) and 3 (2.2%) of them having
1+ and 2+, respectively (Tab. III). In the control group, only
2 (1.45%) had significant proteinuria. Significant hematuria
1+) was present in 9 (6.5%) of the patients with 7 (5.1%)
and 2 (1.45%) of them having 1+ and 2+, respectively, while

only 3 (2.2%) of the controls had significant hematuria. Table IV shows the proportion of subjects with significant dipstick findings as compared with microscopic findings. All
the 9 patients with dipstick hematuria had proteinuria and
all the 11 patients with dipstick proteinuria had significant
microscopic hematuria. Ten patients out of the twenty-one
(47.6%) that had significant microscopic hematuria were
not detected by dipstick urinalysis. Similarly, the 2 controls
that had significant proteinuria also had hematuria and the
3 controls that had hematuria also had microscopic hematuria. Two control subjects who had significant microscopic
hematuria were not detected by dipstick urinalysis.

TABLE II
URINARY SEDIMENT CASTS AND CRYSTALS AMONG PATIENTS AND CONTROLS
Parameters (per hpf)

Patients
n (%)

Controls
n (%)

P value

Hyaline cast:


Granular cast:


Crystals

130 (94.2)
8 (5.8)
-
136 (98.6)
2 (1.4)
-
129 (93.5)
9 (6.5)
-

127 (92)
11 (8)
-
138 (100)
-
-
131 (94.9)
7 (5.1)
-

0.4757
0.4757
0.6064
0.6064
-

Nil
1-2
> 2
Nil
1-2
> 2
Nil
1-2
> 2

Red blood cell and White blood cell casts were nil.
hpf = high power field.

TABLE III
DIPSTICK URINALYSIS FINDINGS IN PATIENTS AND CONTROLS

Patients
n (%)

Controls
n (%)

P value

Protein


Nil
1+
2+
3+

127 (92)
8 (5.8)
3 (2.2)
-

13 (98.65)
2 (1.45)
-
-

0.0106
0.0106
-

Blood


Nil
1+
2+
3+

129 (93.5)
7 (5.10)
2 (1.45)
-

135 (97.8)
3 (2.2)
-
-

0.0766
0.0766
551

Olanrewaju and Aderibigbe: Urinary sediment evaluation in hypertension

TABLE IV
PROPORTION OF SUBJECTS WITH SIGNIFICANT DIPSTICK FINDINGS AND MICROSCOPIC HEMATURIA

Patients
n (%)

Controls
n (%)

p value

Dipstick proteinuria

11 (8)

2 (1.45)

0.0106

Dipstick hematuria

9 (6.5)

3 (2.2)

0.7656

21 (15.2)

5 (3.6)

0.0010

Microscopic hematuria

Discussion
The pattern of urinary sediment in newly diagnosed,
adult Nigerian hypertensive patients was found to be microscopic hematuria in 34.8%, out of which 15.2% was
significant in spite of moderately elevated blood pressure; leukocyturia in 7.2%, of which none was present in
significant quantity (Figs. 1 and 2). Other findings were
granular casts in 1.4%, hyaline casts in 5.8% and crystals
in 6.5% of patients, all of which were present in normal
quantities (Tab. II). When these parameters were compared with the control group, only the microscopic hematuria showed a statistically significant difference. This
suggests that the urinary sediment manifestation of early
hypertensive renal damage is microscopic hematuria. In a
similar study by Ratto et al (29), the prevalence of urinary
sediment alterations in their patient population at baseline
was 12.2% (leukocyturia 6.6% and microhematuria with
or without leukocyturia 5.6%). The prevalence of microhematuria of 15.2% in our patients is significantly higher
than the approximately 5.6% obtained in their study. This
wide difference may be related to the racial difference of
the study populations. While our study was conducted in
a predominantly Black population, the study by Ratto et al
was carried out among Caucasians. Blacks are known to
have a high prevalence of hypertensive renal damage and
they experience more rapid progression to ESRD. For example, the gender- and age-adjusted incidence of ESRD
due to hypertension in Blacks is 8 times the rate among
the Caucasians (30). Furthermore, it has been shown that
hypertension at any level exacts a greater degree of cardiovascular and renal damage in Blacks than Whites and
these target- organ complications occur much earlier in
life among Blacks (31). The Ratto et al study found that
the microhematuria in some of their patients was due to
552

renal diseases such as nephrosclerosis, interstitial disease, glomerulonephritis, etc. but the relative proportion
of these underlying diseases was not documented. The
prevalence of leukocyturia of 7.2% in our patients is comparable to the findings of Ratto et al (6.6%). Also important is the fact that the leukocyturia in our patients was
present in an insignificant quantity and so it is difficult to
ascribe it to an underlying renal disease, although Ratto
et al ascribed leukocyturia in some of their female patients
to urinary tract infection. Granular casts and crystals were
present more in the study subjects while hyaline casts
were more present in the control group. However, the difference was not statistically significant, hence, possible
primary glomerular disease could not be ascribed to the
elevated blood pressure in the study subjects. The presence of granular casts is suspicious in the 2 patients in
whom they were found, although they were present in
normal quantities. A follow-up of these patients will be
necessary to determine their relevance in the long term,
since although casts and crystals were not analyzed by
Ratto et al, their study showed an increased prevalence
of microhematuria (5.6% to 7.4%) and leukocyturia (6.6%
to 17%) after a 6.6-year follow-up of their patients. Red
blood cell, white blood cell and epithelial cell casts were
not detected in our patients or the control subjects. This is
not so surprising, because they are almost always present
in active renal disease in most cases such as proliferate or
acute glomerulonephritis, urinary tract infections or acute
renal tubular disease which had already been excluded in
our patient population as confounding factors.
The prevalence of abnormal urinary sediment in newly diagnosed hypertensive Nigerians was therefore found to be
15.2%, essentially consisting of microhematuria. This figure is substantially higher than the 3.6% found among the
normotensive controls. Although the authors are not aware
of any similar studies previously carried out in this group

JNEPHROL 2010; 23 ( 05 ) : 547-555

of patients in our environment to compare this prevalence


rate, this value is rather high. The high prevalence rate
shows that a significant number of Nigerian hypertensive
patients already have subtle renal damage at the point of
diagnosis, even though the other markers of renal damage such as serum creatinine and urea may still be within
the normal limits. Moreover, a more sensitive marker of hypertensive renal damage such as microalbuminuria would
probably detect a much higher number of these patients
if this test was used. Indeed Olatunde et al (32) found the
prevalence of microalbuminuria in their hypertensive patients to be 17.4% despite the fact that 70% of the patients
were already on antihypertensive drugs. The prevalence of
microhematuria and microalbuminuria in hypertensive patients are comparable perhaps because the mechanisms
of their formation are almost similar, involving injury to the
glomerular endothelium, although microhematuria requires
greater and more intense injury and structural alterations.
Routine screening of newly diagnosed hypertensive patients for microalbuminuria would be rather costly for the
majority of our patients in the developing world who are
poor. The ISH-WHO of 1999 and the JNC guidelines for
the management of hypertension have advocated routine
urinalysis (both dipstick and microscopy) in the initial evaluation of hypertensive patients so that renal damage can
be detected early. The findings in this study suggest that
a urinary microscopic could be a valuable screening tool
not only for hypertensive renal damage but for renal conditions that have potential for renal vascular injury. Dipstick
proteinuria was detected in 8% of the patients and 1.45%
of controls. Although the prevalence rate among patients
in this study was rather lower than the figure obtained by
Kannel et al (18%) (33), Bulpitt et al (16%) (34) and Ljungman et al (17%) (35), it is comparable to the findings of
Wollf et al (10%) (36) and Samuelsson et al (6%) (37) but
higher than the report by Lewin et al (4%) (38). A recent
general population screening to detect renal disease in
Germany reported a prevalence of persistent proteinuria of
12% (104 of 856 participants with self-reported dipstickpositive proteinuria were confirmed by family physicians)
and 45% of these have essential hypertension (39). The
much higher prevalence observed in this study compared
to ours may be due to differences in the study methodology and sensitivity of the test strips used to detect proteinuria. The majority of previous studies on dipstick proteinuria
in Nigeria were done mainly on children and adolescents
(22-26). While Ajasin (23) found the prevalence of isolated
proteinuria among primary school children to be 8.6%,
Akinkugbe FM et al (24) and Asani et al (26) obtained prevalences of 5.4% and 1.95%, respectively, using similar cri-

teria. Among the adolescents, Akinkugbe (22) reported a


prevalence of 3.2% while Oviasu (25) obtained 4.7% with
similar age ranges of 12 to 22 years and 13 to 20 years,
respectively. These studies showed that the prevalence
of proteinuria among the young age groups varies significantly, probably influenced by the geographical location.
However, there seems to be a reduced prevalence among
the older children. This observation cannot be applied to
adulthood, in which there is higher predisposition to renal damage from various conditions such as hypertension.
Dipstick hematuria was found in 9 (6.5%) patients and in
only 3 (2.2%) of the control group in this study but the
difference is not statistically significant (p=0.0766). In his
study on adolescent students, Oviasu found a prevalence
of 0.55%. It is however difficult to compare these groups
because of the difference in the population characteristics. All the patients and controls with dipstick hematuria
had proteinuria. The 21 (15.2%) patients that had microscopic hematuria were inclusive of the 11 (8%) that had
dipstick proteinuria. This implies that about 47.6% of patients with abnormal urinary sediment were not detected
by the dipstick method. Similarly, 2 out of the 5 controls
with microscopic hematuria were not picked out by the
dipstick test. This high false- negative rate with dipstick
urinalysis is higher than the 6.5% to 36% obtained in the
literature (40-43). The difference might be due to the characteristics of the population of the patients studied. While
this study focused on hypertensive patients, the majority
of the other study populations were unselected cohorts.
These high false- negative rates show that the sensitivity
of dipstick test in detecting microscopic hematuria in adult
hypertensive patients is poor.There has been a protracted debate on the usefulness of urinary microscopy compared with dipstick urinalysis in screening for diagnosis
of asymptomatic disease. While some authors are of the
opinion that microscopic examination of urinary sediment
should be limited to those patients with abnormalities in
the dipstick test, others strongly recommend its use as an
initial evaluation of patients to forestall the high false-positive and false-negative rates associated with the dipstick
method which have been discussed earlier. Our findings
in this study support the opinion that microscopy of the
urine should be part of the initial evaluation of not only
systemic hypertension but also other patients at a high risk
for kidney damage. There was a significantly lower value
of GFR in the patients than in the control subjects, which
is in agreement with the higher serum creatinine in these
patients. This suggests that renal function in hypertensive
patients is depressed compared with normotensive controls. In conclusion, significant proportions of newly di553

Olanrewaju and Aderibigbe: Urinary sediment evaluation in hypertension

agnosed hypertensive Nigerians have sub-clinical kidney


damage, as evidenced by microscopic hematuria. There
is a high false-negative rate with dipstick urinalysis among
this patient population, which underscores the need for a
routine examination of urinary sediment in addition to a
dipstick test in the assessment of hypertensive patients. It
is recommended, however, that supravital stains should be
used for sediment identification in the absence of a phase
contrast microscope.

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Financial support: No financial support.


Conflict of interest statement: None declared.

Address for correspondence:


Timothy O. Olanrewaju, MD
Division of Nephrology
Department of Medicine
University of Ilorin Teaching Hospital
PMB 1459, Ilorin, Nigeria
timothysegun@yahoo.com

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Received: July 25, 2009
Revised: October 19, 2009
Accepted: October 20, 2009

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