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Original Research Article
Renal Profile of Hypertensive Subjects in Melendu Hospital Isiala Mbano, Imo State,
South East Nigeria, West Africa.
Elendu MU1, Nwankwo AA2, Egwurugwu JN1, Izunwanne DI1, Ugwuezumba PC1,
Ejiofor D1, Ekweogu CN3, Ugwu PI4, Ohamaeme MC5, Ebisintei P6. Agu FU7.
1. Department of Human Physiology, Faculty of Basic Medical Sciences, College of
Medicine, Imo State University, Owerri, Nigeria.
2. Department of Physiology, College of Health Sciences, Abia State University, Uturu.
3. Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of
Medicine, Imo State University, Owerri, Nigeria.
4. Department of Human Physiology, Faculty of Basic Medical Sciences, College of
Medicine, University of Nigeria, Enugu Campus.
5. Department of Community Medicine, Nnamdi Azikiwe University Teaching Hospital,
Nnewi, Anambra State, Nigeria.
6. Department of Biological Sciences, University of Africa, Toru Orua, Bayelsa State,
Nigeria.
7. Department of Physiology, College of Medicine and Basic Health Sciences, Gregory
University, Uturu, Abia State.
©Corresponding Author: +2348067505592; elemel2002@yahoo.com
Authors contribution: EMU, NAA, EJN, OMC conceptualized and designed the study;
IDI, UPC, ED did literature search; ECN, UPI, EP and AFU did the statistical analysis.
EMU, NAA, EJN, OMC prepared the draft manuscript; all authors read and approved the
final manuscript.
Article information
Received: September 15, 2020
Accepted: December 20, 2020
Published: December 28, 2020
Doi: 10.33798/ajmas2020/vol-3-1-00313
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3(1):21-30; 2020 AJMAS 00313.
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Elendu et al ajmas2020;3(1): 21-31.
Abstract
Aim: The renal profiles of hypertensive subjects in Melendu hospital Isiala Mbano, in Imo
State, South-East Nigeria were studied.
Methodology: A total of one hundred and twenty-seven(127) adults male and female, aged
20years and above were recruited having sought and obtained their consents. They were
diagnosed, confirmed and grouped into two; hypertensive and normotensive subjects based
on the current WHO definition of hypertension and after three different consecutive blood
pressure check. Blood samples were collected with 5mls syringe and immediately emptied
into plain container for renal profile analysis.
Results: The results showed that serum levels of urea and creatinine were statistically
significant at p<0.05 among age groups 51-65years and >66. years; other age groups were
statistically insignificant. Sodium ion was statistically significant at p<0.05 among age
groups 36-50yrs, 51-65yrs and >66years; it was statistically insignificant in 20-35yr group.
Potassium ion was statistically insignificant among the age groups except >66yrs
group(p<0.05).
In conclusion, there was increase in the values of sodium ion and decrease in potassium ion
among the hypertensive subjects when compared with the normotensive subjects. Also, there
were abnormal values of urea and creatinine among the hypertensive subjects. It became
more significant with advance in age. Hence, untreated and poorly controlled hypertension
can cause renal damage which worsens with advance in age.
Key words: Hypertension, Renal profile, Normotension, Melendu Hospital, Nigeria.
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1.0 Introduction.
Blood pressure is the force exerted by circulating blood against the walls of the body’s
arteries, the major blood vessels in the body[1]. Hypertension or high blood pressure is a
condition in which the blood vessels have persistently raised pressure above systolic pressure
of 130mmHg and diastolic pressure or 80mmHg[1].
The prevalence of hypertension has increased, especially in low-and middle-income
countries. Estimates suggest that 31.1% of adults(1.39billion) worldwide had hypertension in
2020[2]. The prevalence of hypertension among adults was higher in low-and middle-income
countries(28.5%, 1.04billion people) than in high-income countries(28.5%, 349million
people) [2].
In a recent meta-analysis of blood pressure surveys in Nigeria, the documented overall
prevalence of hypertension was 28.9%, with a prevalence of 29.5% among men and 25%
among women[3]. Hypertension and its complications are responsible for about 25% of
emergency medical admissions in urban hospitals in the country and is the commonest
clinical diagnosis in elderly Nigerians, senior executives and army recruits[3]. There are about
20million cases of hypertension in Nigeria in the year 2010. This is projected to rise to
39.1million cases by the year 2030[7]. Variations in the levels of risk factors for hypertension,
such as high Sodium intake, low Potassium intake, obesity, alcohol consumption, physical
inactivity, family history of hypertension and co-existing diseases such as diabetes and renal
disease may explain some of the regional heterogeneity in hypertension prevalence. [2].
Non-communicable diseases have been purported to be a primary cause of deaths in
developing countries[4] among which diabetes and hypertension assume a lead role, being
frequently associated with a variety of co-morbid states and end organ complications
including renal impairment and cardiovascular diseases, which increase mortality[4].
Hypertension and renal impairment share a two-way cause and effect relationship, with each
one being a common etiology of the other[4].It is well known that hypertension could cause
severe renal damage including decreased glomerular filtration rate, high prevalence of renal
insufficiency and proteinuria[5,6].
Hypertension is the second leading cause of end-stage renal disease, with the risk being
substantially higher in blacks[7]. Hypertension-induced renal damage in patients with
uncomplicated essential hypertension has been separated into clinical and histological
patterns of benign and malignant nephrosclerosis[8]. Benign nephrosclerosis is the pattern
observed in the majority of patients with uncomplicated primary hypertension. The
nonspecific vascular lesions of hyaline arteriosclerosis develop slowly without overt
proteinuria. Focal ischaemic glomerular obscelence and nephron loss occur over time, renal
function is not seriously compromised except in susceptible individuals such as blacks in
whom the process tends to follow a more severe and accelerated course [8]. Malignant
nephrosclerosis is observed with very severe hypertension and has a characteristic renal
phenotype of acute disruptive vascular and glomerular injury with prominent fibrinoid
necrosis and thrombosis. Ischaemic glomeruli are frequent because of vascular injury[8].
Renal failure can develop rapidly in the absence of adequate therapy [8].
On a case study of 94patients with essential hypertension [9,10] reported an increased risk of
developing a decline in renal function was noted in blacks, in elderly patients and in those
with higher number of missed clinic visits. In retrospective study of the relationship between
recorded blood pressure data and subsequent changes in serum creatinine concentration
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Elendu et al ajmas2020;3(1): 21-31
during a mean follow up of 9.8years in a cohort of 56 patients with essential hypertension and
59control subjects; showed rate of increase in serum creatinine overtime was greater in the
subjects with essential hypertension than the control subjects. [11]. More so, association
between high blood pressure and impairment of renal function was demonstrated by[12,13].
Hypertension represents a pertinent and persistent risk factor for the development and
progression of kidney and other target organ disease particularly in the absence of appropriate
blood pressure control measures[14].Arterial hypertension can initiate progressive renal
disease and can accelerate the more moderate loss of renal function that occur with normal
aging. In addition, experimental and clinical data suggest that elevated blood pressure can
increase the rate of progression of intrinsic renal disease[14]. Despite the increasing
prevalence, the proportion of hypertension awareness, treatment and blood pressure control
are low, particularly in low-and middle-income countries and few comprehensive
assessments of renal profile and target organs. Therefore, a study to investigate renal profile
of hypertensive subjects in Isiala Mbano, Imo State will help in prevention, early diagnosis,
treatment and good prognosis of renal impairment associated with hypertension.
2.0 Materials and Methods
This study was done at Melendu Hospital Isiala Mbano, Imo State, Nigeria. The renal profiles
such as potassium ion, sodium ion, urea and creatinine were evaluated at chemistry
department Imo State Teaching Hospital, Orlu, Imo State.
2.1 Experimental design.
The American college of cardiology/American heart association, 2017 current definition of
hypertension was used to assign a diagnosis of hypertension in 80 patients who presented to
the Medical and General Out Patient Departments with symptoms and signs of hypertension
together with some that are asymptomatic. Hypertension was characterized with repeated
measurement of > 130mmHg Systolic blood pressure(SBP) or > 80mmHg Diastolic blood
pressure (DBP).
The inclusion criteria were subjects(n-80), seen by physician and diagnosed as hypertensives
based on American College of Cardiology/American Heart Association,2017 current
definition of hypertension; those who came for regular follow up and are currently on
antihypertensive medications. Some are newly diagnosed and yet to commence oral
antihypertensive medications. In addition to that, 47 normotensive and apparently healthy
subjects participated as control.
Exclusion criteria were subjects diagnosed with complications of hypertension such as
ischemic and haemorrhagic stroke, congestive cardiac failure, cardiac asthma, arrythmias,
renal failure and other co-morbidity diseases like DM, malnutrition, inflammatory, infectious
diseases, dyslipidaemia and malignant diseases.
Approval for this study was granted by the Ethical Committee of the Federal Medical centre
Owerri, Imo State (Ref. no 33/342). Informed consent was obtained from the subjects before
the collection of blood sample.
A total of one hundred and twenty-seven(127) adult male and female human subjects
participated. They were divided into hypertensive(80) and normotensive(47) subjects.
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Elendu et al ajmas2020;3(1): 21-31
Venous blood samples were collected with 5mls syringe and immediately emptied into plain
container for renal profile analysis.
2.2 Laboratory Test
Biochemical parameters analysed include:
Sodium ion – Modified colorimetric method for sodium estimation by Maruna and
Trinder[15].
Potassium ion – A new colorimetric method for the estimation of potassium by Jacob HD and
William SH[16].
Creatinine – Modified Jaff’s method of serum creatinine by Jaffe Max[17].
Urea – Modified urease-Berthelot method of serum urea estimation by Berthelot
Marcellin[18].
2.3 Data Analysis
Data generated from this study was entered into Excel sheet, cleaned, coded and analysed
using Statistical Package for Social Sciences(SPSS) version 25.
3.0 Results.
Table 3.1: Comparison of Blood Pressure (mmHg) in Age- Related Hypertensive
Subjects.
S/N
Age
groups(
Years)
Normotensive(mmHg)
(Mean±SD
N
Hypertensive(mmHg)
(Mean±SD)
N
p-value
1
20-35
28.11 4.54
4
29.25 4.35
9
0.681
0.006*
0.020*
0.649
2
36-50
42.09 3.59
16
46.38 3.69
11
3
51-65
56.76 3.63
34
59.88±4.70
17
4
66>
71.20 3.12
26
72.00 5.13
10
Mean±SD.*statistically significant (p<0.05) at the age groups of 36-50yrs and 51-65yrs
respectively.
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Elendu et al ajmas2020;3(1): 21-31
Table 3.2: Comparison of Renal Profile of Sodium ion (Na+ Meq/Ml) Between
Normotensive and Hypertensive Subjects.
S/N
Age
Groups
Normotensive subjects
(Mean±SD N
Hypertensive
Subjects
(Mean±SD) N
P-Value
1
20-35
137.78±1.20
9
140.75±1.50
4
0.457
2
36-50
138.09±3.75
11
138.50±2.28
16
0.051*
3
51-65
138.59±3.79
17
139.68±3.37
34
0.054*
4
66>
138.90±2.47
10
139.58±2.52
26
0.044*
Mean±SD* Statistically significant (p>0.05) at age groups of 36-66 yrs and above
respectively
Table 3.3: Comparison of Renal Profile of Potassium ion (K+ Meq/Ml) Between
Normotensive And Hypertensive Subjects.
S/N
Age Groups
Normotensive
subjects
(Mean±SD) N
Hypertensive
Subjects
(Mean±SD) N
P-Value
1
20-35
4.46±0.75
9
5.75±1.67
4
0.072
2
36-50
4.46±0.65
11
4.50±0.71
16
0.062
3
51-65
4.65±1.17
17
4.77±0.77
34
0.076
4
66>
4.40±0.47
10
5.43±3.27
26
0.051
Mean±SD* Not statistically significant (p>0.05) at all the age groups of 20-66 yrs and above
respectively.
Table 3.4: Comparison of Renal Profile of Urea (Ur+ Meq/Ml) between Normotensive
and Hypertensive Subjects.
S/N
Age Groups
Normotensive
subjects
(Mean±SD N
Hypertensive
Subjects
(Mean±SD) N
P-Value
1
20-35
7.01±2.58
9
8.00±2.47
4
0.533
2
36-50
10.65±4.48
11
9.08±4.50
16
0.082
3
51-65
10.45±7.36
17
9.27±4.55
34
0.04*
4
66>
9.73±4.02
10
10.12±4.13
26
0.05*
Mean±SD* statistically significant (p<0.05) at the age groups of 51-65yrs and above
respectively.
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Elendu et al ajmas2020;3(1): 21-31
Table 3.5: Comparison of Renal Profile of Creatinine (Cr- Meq/Ml) between
Normotensive and Hypertensive Subjects.
S/N
Age Groups
Normotensive
subjects
(Mean±SD N
Hypertensive
Subjects
(Mean±SD) N
P-Value
1
20-35
101.00±11.37
9
117.58±24.73
4
0.116
2
36-50
102.25±18.73
11
100.65±22.26
16
0.087
3
51-65
100.87±21.69
17
101.79±19.08
34
0.05*
4
66>
100.87±21.69
10
108.99±21.99
26
0.05*
Mean±SD* Statistically significant (p<0.05) at the age group of 51-65yrs and above
respectively.
4.0 Discussion.
Hypertension is the commonest cause of sudden unexpected natural death in Nigeria[3].
Hypertension and its complications are responsible for 25% of emergency medical
admissions in urban hospitals in Nigeria and is the commonest clinical diagnosis in elderly[3].
Untreated hypertension could cause severe renal damage including decreased glomerular
filtration rate, high prevalence of renal insufficiency, proteinuria and renal failure[5,6]. This
study investigated the renal profiles in hypertensive subjects.
The age groups of the hypertensive subjects when compared with the normotensive subjects,
showed that hypertension is commonest in 36-55years followed by 56-65years with the mean
value of 46.38 and 59.88 respectively. It goes higher with increase in age which is in
agreement with study[19]
The importance of electrolytes in the pathogenesis of hypertension is well known from the
blood pressure lowering effect of salt restriction observed in salt-sensitive individuals. There
is a strong interrelationship and interdependence between the electrolytes potassium and
sodium in the body[20]. In this present study, potassium and sodium showed
interrelationship/interdependence in their correlation among the hypertensive subjects when
compared with the normotensive subjects. The correlation was seen more as the age progress
in the hypertensive subjects. There was increase in the values of sodium ion among the
hypertensive subjects in all age groups but it was only significant in the elderly. A decrease in
Potassium ion was observed in the hypertensive subjects when compared with the
normotensive subjects. The decrease in potassium ion was only significant among >66yr age
group. This is in agreement with studies[21,22] .Increase in sodium and depletion in potassium
seen in HTN might be as a result of increased reabsorption of filtered sodium by the renal
tubules in primary HTN due to stimulation of several sodium transporters located at the
luminal membrane as well as sodium pump. Moreover, potassium depletion enhances
sodium-hydrogen exchanger by inducing intracellular acidosis and by stimulating
sympathetic nervous system and renin-angiotensin system[22]. The sodium-chloride co
transporter in the distal tubule, the epithelial sodium channel in the collecting duct and the
sodium pump are activated by Aldosterone excess in primary HTN, thereby promoting
sodium retention and potassium loss, thus worsening the HTN[21,23]. Potassium restriction
results in sodium retention, whereas potassium supplementation appears to cause a natriuresis
and prevent sodium retention. The natriuretic effect of potassium is a direct effect of
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Elendu et al ajmas2020;3(1): 21-31
potassium on sodium chloride reabsorption by the kidney. When potassium chloride is
infused into the renal artery, sodium excretion increases; this rise is mediated by reductions in
proximal sodium reabsorption, hence lowering blood pressure[24,25]. The different
mechanisms through which increase in potassium leads to lowering of blood pressure include
natriuresis effect, direct vasodilation affect and modulation of renin angiotensin aldosterone
system via increase activity of renin[26,27]
Urea and Creatinine showed correlation among the hypertensive subjects when compared
with the normotensive subjects. The correlation was moderately significant among the elderly
hypertensive subjects. This is in agreement with studies done by[27,28,29] Kidney is protected
from acute systemic increase in blood pressure by auto-regulatory mechanisms, namely by
glomerular afferent arteriole contraction due to myogenic response and by a tubulo-
glomerular feedback[8]. The extent of kidney damage due to hypertension is proportional to
the degree of arterial pressure exposure of renal microvasculature. Sustained increase in
arterial pressure as seen in hypertension disrupts the auto-regulatory mechanisms which
results in glomerular capillary overstretching, endothelial damage and elevated glomerular
protein filtration causing glomerular collapse, segmental necrosis and glomerulosclerosis.
Decreased perfusion mainly leads to glomeruli collapse, whereas increased pressure causes
either glomerular sclerosis or necrosis. Sclerosis of preglomerular vessels causes further
reduction in renal blood flow. Whereas RBF is reduced, glomerular filtration rate is
maintained and filtration fraction is increased, thus enhancing glomerular permeability to
macromolecules. Plasma proteins hyperfiltration causes both tubular reabsorption of proteins
and mesangial proliferation, thus leading to tubulo-interstitial inflammation and
glomerulosclerosis. Adaptive mechanisms in glomerular hypertension include contraction,
transcriptional activity, proliferation, remodelling and fibrosis, involving glomerular,
endothelial cells, mesangial cells, podocytes, basement membranes and extracellular
matrix[31]. Owing to overstretch, endothelial cells proliferate, remodel their shape and change
their signalling pathways, both synthesizing extracellular matrix and reorienting their
cytoskeleton[31,32]. Mesangial cells proliferate and activate the Renin angiotensin aldosterone
system, producing at the same time vascular permeability factors, tumour growth factor and
fibronectin. Podocytes modify their shape and their signallingpathway[31,32-34]. These adaptive
mechanisms become maladaptive in the long term, finally leading to glomerulosclerosis.
The glomerular filtration barrier damage causes proteinuria and podocytes effacement. As
injury persists, podocytes either detach from basal membrane or undergo apoptosis causing
denuded areas of glomerular basal membrane responsible for a marked proteinuria. The
damage of tubular basement membrane facilitates the passage of tubular-derived products
into the interstitial and peritubular capillaries space, thereby accelerating fibrosis and
inflammation, whereas several protein casts may obstruct the urinary flow, aggravating
tubule-interstitial injury[30].
Conclusion.
Untreated and poorly controlled hypertension has adverse effect on the Kidney and Kidney in
turn can worsen hypertension. In the present study, the renal profile analysed (sodium ion,
potassium ion, urea and creatinine) showed abnormal values indicating on going damage to
renal system which might eventually lead to end stage renal failure if adequate and proper
intervention is not taken on time. Therefore, renal profile evaluation should be part of routine
clinical evaluation for every hypertensive patient in other to prevent and reduce mortality rate
due to complications of hypertension.
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Elendu et al ajmas2020;3(1): 21-31
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How to cite this article.
Elendu MU, Nwankwo AA, Egwurugwu JN, Izunwanne DI, Ugwuezumba
PC, Ejiofor D, Ekweogu CN, Ugwu PI, Ohamaeme MC, Ebisintei P, Agu FU.
Renal Profile of Hypertensive Subjects in Melendu Hospital Isiala Mbano, Imo
State, South East Nigeria, West Africa. Afr J Med Allied Sci, 2020, 3(1): 21-30.
