Received: 24 October 2022 | Revised: 19 November 2022 | Accepted: 2 January 2023
DOI: 10.1002/hsr2.1053
OR I G I NA L R E S E A R CH
Serum leptin levels in patients with chronic kidney disease
and hypertensive heart disease: An observational
cross‐sectional study
Emmanuel K. Ofori1 | Christian N. Adekena1,2 | Vincent Boima3 |
Henry Asare‐Anane1 | Ernest Yorke3 | Eric N. Y. Nyarko1 |
Bismark N. Mohammed1 | Emmanuel Quansah2 | Sisitha U. Jayasinghe4 |
Seth D. Amanquah1
1Department of Chemical Pathology,
University of Ghana Medical School, Accra, Abstract
Ghana Background and Aim: Adipocytes secrete a peptide hormone called leptin, which
2University of Ghana Medical Center, Accra,
plays a crucial role in controlling appetite and energy expenditure. Alterations in
Ghana
3Department of Medicine and Therapeutics, leptin concentrations are associated with CKD‐related cardiovascular problems such
University of Ghana Medical School, Accra, as hypertensive heart disease (HHD). Despite the link, data on the precise function
Ghana
of leptin in people with CKD and HHD is scant.
4School of Health Sciences, University of
Tasmania, Hobart, Tasmania, Australia Methods: An observational cross‐sectional study involving a total of 108
participants (72 CKD patients with HHD and 36 healthy controls). Their
Correspondence
demographic and anthropometric information was collected using a standardized
Emmanuel K. Ofori, Department of Chemical
Pathology, University of Ghana Medical questionnaire. Certain clinical measures such as blood pressure and body mass index
School, Accra, Ghana. (BMI) were assessed. Fasting blood samples were analyzed for levels of plasma
Email: ekofori1@ug.edu.gh
glucose (FPG), lipids, creatinine, and leptin. Data were analyzed with SPSS v23.
Results: Leptin, FPG, creatinine and triglyceride levels were all significantly higher in
CKD patients with HHD compared to controls (p < 0.01 for all). Furthermore,
advanced CKD status (being in stage 5), having a 6‐year diagnosis of HHD, being
female, having a higher BMI, and elevation in levels of HDL and FPG contributed
significantly to the variance in serum leptin levels in the case group (β = 0.37, 0.22,
0.19, 0.18, 0.27, 0.28; p < 0.05 for all). In the control group, the female gender had
the biggest unique effect on circulating leptin levels, followed by BMI and eGFR
(β = 0.71, 0.34, −0.22; p < 0.01 for all).
Conclusion: Patients with CKD who also had HHD reported considerably higher
circulating leptin levels. Significantly higher blood leptin levels were shown to be
associated with CKD stage 5 in the case group. These results are consistent with the
role of leptin in the metabolic complexity seen in CKD patients. There needs to be
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium,
provided the original work is properly cited.
© 2023 The Authors. Health Science Reports published by Wiley Periodicals LLC.
Health Sci. Rep. 2023;6:e1053. wileyonlinelibrary.com/journal/hsr2 | 1 of 9
https://doi.org/10.1002/hsr2.1053
2 of 9 | OFORI ET AL.
more research into treatments that aim to lower leptin levels in CKD patients
with HHD.
K E YWORD S
body mass index, chronic kidney disease, glomerular filtration rate, hypertension, leptin
1 | INTRODUCTION fertility28–30 although the mechanics of these secondary actions
remain to be fully elucidated. Accordingly, relatively little research
Chronic kidney disease (CKD), is associated with a gradual decline in has been conducted to investigate the link between elevated blood
glomerular filtration rate (GFR). It is a debilitating condition that leptin levels and CKD, with the majority reporting higher than normal
affects millions of people all over the world.1–4 The ineffective levels of leptin in CKD patients,31,32 alongside a sleuth of
management of risk factors for the vast majority of chronic cardiovascular complications.33,34
nephropathies and the ongoing progression to end‐stage kidney Specifically, the interface between CKD, leptin, and HHD has
disease (ESKD) both contributes to an increase in the incidence of received much less attention considering the enormity of the CKD
CKD over the world.4–6 epidemic. Given the significant economic burden on countries,35–37
Major risk factors for developing CKD include diabetes mellitus, and the negative health outcomes associated with leptin and
high blood pressure, and other cardiovascular‐associated diseases.7,8 CKD,38–40 as well as the role of both leptin and CKD in CVD
These risk factors can only explain a portion of the increased fatality mortality, more research into the role of leptin in CKD and HHD are
rates in CKD patients. The last two decades have seen considerable merited. Therefore, the main purpose of this study is to report on
technological and pharmacological CKD therapy advancements, levels of serum leptin and identify the characteristics that predispose
although these innovations have not yet resulted in any substantial CKD patients with HHD to have altered leptin concentrations in the
changes in CKD survival rates.9,10 Sub‐Saharan African nations, blood.
including Ghana, have a particularly higher prevalence of CKD
ranging from 5% to 17%.5,11 The rising prevalence of CKD is a public
health emergency in Ghana, despite a significant scarcity of pertinent 2 | MATERIALS AND METHODS
knowledge regarding its epidemiology, prognosis, and treatment.12,13
Amongst a myriad of reasons including low levels of public 2.1 | Study site, design participants
awareness, unpreparedness to cope with the cardiovascular conse-
quences of CKD, and the lack of access to renal replacement therapy, The Renal Dialysis Unit of the Korle‐Bu Teaching Hospital (KBTH) in
are considered major contributors to the CKD epidemic in Ghana and Accra was the site where the study was carried out. Patients
other sub‐Saharan nations.14,15 suffering from acute and chronic renal failure are under the care of
Hypertensive heart disease (HHD) is a group of changes in the the Unit's management. A total of 72 patients with CKD who also had
left ventricle, left atrium, and coronary arteries caused by high blood HHD (i.e., had a documented diagnosis of HHD by a qualified
pressure that lasts for a long time. It is linked to heart failure, ischemic specialist and/or were on chronic hemodialysis) and 36 healthy
heart disease, stroke, and deaths caused by hypertension.16,17 HHD individuals (hospital staff) were recruited into this study using the
is characterized by anatomical and physiological changes in the simple random sampling technique. CKD patients were required to
myocardium in the absence of other primary anomalies in the have an eGFR of <60mls/min for more than 3 months, and/or have
cardiovascular system, resulting in a collection of responses from an ultrasound scan showing small kidneys measuring less than 9 cm.
target organs ranging from systolic and diastolic dysfunctions to left Individuals between the ages of 30 and 70 who did not have CKD,
ventricular hypertrophy (LVH) and their clinical manifestations were not on admission to the hospital, or had been diagnosed with a
(arrhythmias and heart failure).18,19 CKD patients are highly specific condition for which they were receiving the medicine were
susceptible to HHD.20,21 considered to be healthy adults for this study and were included as
Leptin is a peptide hormone that controls how much energy the controls. Patients with CKD who were undergoing transplantation, as
body uses.22,23 It is mostly made by adipocytes (mostly white well as those who had a history of Mycobacterium tuberculosis,
adipocytes and less often brown adipocytes) and plays a big role in autoimmune illness, gout, allergies, cancer, urinary tract infection, or
controlling the body's energy balance and reducing hunger.24,25 acute cardiovascular events, were not allowed to participate in the
Leptin in the bloodstream may be complexed with proteins or it may study. A structured questionnaire was used to collect data on the
circulate freely.26,27 Leptin is involved in a wide variety of different participants, including their sociodemographics and clinical histories
physiological processes in addition to its primary function of (Supporting Information file). The College of Health Sciences Ethical
regulating the amount of fat stored in the body. These activities and Protocol Review Committee at the University of Ghana approved
include bone formation, immunological function, angiogenesis, and every step of the research process (CHS‐Et/M.3‐P2.7/2017–2018).
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OFORI ET AL. | 3 of 9
Before being recruited for the study, participants were needed to fill 3 | RESULTS
out a consent form stating their willingness to participate. They were
also informed of the following before consent: the duration of the Seventy‐two CKD patients with HHD and 36 controls made up the
study, the benefit of the study, the materials used in sample total number of participants used in this study. Tables 1 and 2 reflect,
collection, and the potential risks involved with the sampling respectively, the demographic and clinical (categorical) characteristics
technique. of the study participants. Approximately half of the participants in the
case group were men (52.8%), and 45.8% of them had completed a
postsecondary degree. Approximately 42% of the cases were in the
2.2 | Clinical assessment and laboratory fourth stage of the disease. Moreover, one‐third (37.5%) had suffered
procedures HHD for 1 to 3 years. Only a minority (9.7%) of the patients with
CKD have been on dialysis for more than 3 years. Ischemic heart
Participants' height (in m) and weight (in kg) were measured disease (IHD) was seen in the majority (44.4%) of CKD patients.
respectively with a calibrated wall‐mounted stadiometer (Secca) The clinical (continuous) and biochemical characteristics of the
and a medical scale (Seca GmBh) using standardized procedures. To patients in the study are presented in Table 3. Using a t‐test on
determine the participants' BMI, we divided their total body weight independent samples, we found that the case group were older and
by the square of their height (kg/m2). An automated cuff blood had a higher BMI, blood pressure, FPG, total cholesterol, triglyceride,
pressure machine (OMRON) was used to take blood pressure
readings of volunteers after they had sat still and relaxed for at least
TABLE 1 Clinical features (categorical) of the study participants
10min before the testing.
A trained phlebotomist collected venous blood (5 ml) from all CKD group
Clinical features Number %
participants after an overnight fast (8–12 h). One milliliter (ml) of
blood was aliquoted into a sodium fluoride‐containing tube, and CKD stage
the resulting plasma was obtained for glucose measurement. The Stage 3A 7 9.7
remaining 4 mls of whole blood were placed in serum separator Stage 3B 21 29.2
tubes, spun, split into aliquots, and stored at −20°C until assayed.
Stage 4 30 41.7
Fasting plasma glucose (FPG), total cholesterol (T. cholesterol),
triglycerides (TG), high‐density lipoprotein (HDL) cholesterol, and Stage 5 14 19.4
creatinine concentrations were measured using the auto‐analyzer Period with CKD
of the VITROS system (Ortho Clinical Diagnostics). To determine Less than 1 year 23 31.9
the amount of leptin, present in the sera, an enzyme‐linked
1–3 years 29 40.3
immunosorbent assay (ELISA) was carried out in the solid phase
(GenWay Biotech Inc). A previously established algorithm was More than 3 years 20 27.8
utilized to calculate a value for the estimated glomerular filtration Period on dialysis
rate (eGFR).41 Nondialysis CKD 39 54.2
Less than 1 year 5 6.9
2.3 | Statistical procedures 1–3 years 21 29.2
More than 3 years 7 9.7
Data were analyzed with the Statistical Package for the Social HHD category
Sciences (SPSS) version 23 (IBM SPSS Statistics for Windows,
LVH 20 27.8
2018). Descriptive statistics were applied to summarize the
CHF 20 27.8
demographic and clinical characteristics of the participants. To
analyze the differences in clinical and biochemical parameters that IHD 32 44.4
exist between the cases and the controls, an independent t‐test Period with HHD
was carried out. Further, the magnitude of the observed effect was
Less than 1 year 21 29.2
determined using the η2 test statistic. A multiple regression
1–3 years 27 37.5
analysis was carried out to identify the features that make both
groups more likely to have altered amounts of leptin in their blood. Greater than 3–6 years 13 18.1
A preliminary investigation was carried out to establish whether or More than 6 years 11 15.3
not the data exhibited any deviations from normality, linearity,
Abbreviations: CHF, congestive heart failure; CKD, chronic kidney
residual independence, or homoscedasticity. p < 0.05 were con- disease; HHD, hypertensive heart disease; IHD, ischemic heart disease;
sidered statistically significant. LVH, left ventricular hypertrophy.
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4 of 9 | OFORI ET AL.
TABLE 2 Sociodemography and clinical characteristics (categorical) of participants
CKD Controls Chi‐square
Variables N = 72 (%) N = 36 (%) (χ2) p Value
Age (years)
<50 31 (43.1) 24 (66.7) 5.354 0.021
≥50 41 (56.9) 12 (33.3)
Gender
Male 38 (52.8) 19 (52.8) 1.0 × 10−7 0.98
Female 34 (47.2) 17 (47.2)
Educational status
No formal education 1 (1.4) 0 (0.0) 7.487 0.058
Primary 13 (18.1) 2 (5.6)
Secondary 25 (34.7) 8 (22.2)
Tertiary 33 (45.8) 26 (72.2)
Occupation
Self‐employed 50 (69.4) 11 (30.6) 10.800 0.005
Gainfully employed 20 (27.8) 23 (63.9)
Unemployed 2 (2.8) 2 (5.6)
BMI (kg/m2)
Normal weight (18–24.9) 30 (41.7) 33 (91.7) 24.750 <0.0001
Overweight (25.0–29.9) 39 (54.2) 3 (8.3)
Obese (>30) 3 (4.2) 0 (0.0)
Blood pressure
Normotensive 4 (5.6) 36 (100.0) 91.800 <0.0001
Hypertensive 68 (94.4) 0 (0.0)
Note: Data are presented as numbers (percent). Categorical variables were compared using the χ2 test. p < 0.05 is considered statistically significant.
Abbreviations: CKD, chronic kidney disease; χ2, Chi‐Square test.
low‐density lipoprotein, creatinine, and leptin levels than the control The findings of the regression analysis for the control group are
group (p < 0.05 for all, two‐tailed). Unsurprisingly, the eGFR in the outlined in Table 5. Female gender, age, BMI, blood pressure, FPG,
group with CKD and HHD was significantly lower than that of the TG, LDL, HDL, and eGFR were all included in the conventional
control group (p < 0.05, two‐tailed). multiple regression model. This model was able to explain 89.4% of
The results of the regression analysis conducted on the case the variance in the levels of leptin in the blood. Female gender
group are presented in Table 4. The standard multiple regression contributed the most significantly (β = 0.709, p < 0.001), followed by
model contained the following variables: CKD stage, HDL‐ BMI (β = 0.341, p < 0.001), and eGFR (β = −0.222, p < 0.05).
cholesterol, FPG, HHD category and diagnosis, blood pressure, years
of CKD diagnosis, gender, BMI, LDL‐cholesterol, and triglycerides.
The model was able to explain 79.2% of the variation in terms of the 4 | DISCUSSION
mean levels of leptin found in serum. Being at CKD stage 5 had the
biggest contribution (β = 0.370, p < 0.001) after adjusting for con- A primary goal of this research was to report on serum leptin levels in
founding factors. Other factors that significantly contributed to the CKD patients with HHD and to find out some characteristics that
overall variation in mean serum leptin levels include HDL (β = 0.269, predispose CKD patients with HHD to have altered leptin concen-
p < 0.001), FPG (β = 0.267, p < 0.01), HHD diagnosis of more than trations in their blood. We found that the cases (CKD patients with
6 years (β = −0.217, p < 0.05), systolic BP (β = 0.201, p < 0.05), female HHD) had considerably greater levels of leptin in their blood when
gender (β = 0.191, p < 0.01), BMI (β = 0.180, p < 0.05), and LDL compared to the control group (Table 3), which suggests that CKD is
(β = 0.177, p < 0.05). a key factor in boosting serum leptin levels. This was somewhat
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OFORI ET AL. | 5 of 9
TABLE 3 Comparison of clinical and biochemical parameters longitudinal study that lasted for 7 years. This is a considerable
between cases and controls amount of time for the body to develop mechanisms that lower
Variables CKD Controls p Value blood leptin levels. The research that was conducted by Wahba
49
Age 52.29 ± 12.98 43.83 ± 11.40 0.0012 and Mak in 2007, which found that the expression of the gene
that codes for leptin were reduced in the adipose tissues of
BMI (Kg/m2) 25.35 ± 2.733 22.86 ± 1.046 <0.0001
patients with CKD, provides support for the existence of this
Blood pressure potentially adaptive phenomenon.
SBP (mmHg) 162.3 ± 19.20 113.3 ± 4.889 <0.0001 All of the CKD patients in this research also had HHD.
DBP (mmHg) 99.90 ± 11.97 75.08 ± 3.729 <0.0001 Evidence to date has shown that leptin is associated with the
development of cardiovascular problems by increasing cellular
Lipid profile
enzymatic activities which in turn increases the proliferation,
T. Cholesterol (mmol/L) 6.104 ± 1.440 4.544 ± 0.581 <0.0001 calcification, and migration of vascularized cells.50,51 The regres-
Triglycerides (mmol/L) 1.900 ± 0.661 1.492 ± 0.439 0.0011 sion model that took into account the predictor factors was able to
HDL‐cholesterol 1.342 ± 0.189 1.467 ± 0.167 0.0011 explain 79.2% of the variation in serum leptin levels among those
(mmol/L) who had CKD and HHD. Importantly, the most significant addition
LDL‐cholesterol 3.894 ± 1.182 2.383 ± 0.447 <0.0001 to the model was being at CKD stage 5 which predicted the
(mmol/L) existence of increased blood leptin levels and accounted for 8.47%
VLDL (mmol/L) 0.868 ± 0.297 0.683 ± 0.201 0.0011 of the observed variation (Table 4). This result that being at CKD
stage 5 is related to greater blood leptin levels may bestow a
Renal function test
survival advantage on this cohort of CKD patients. High levels of
Serum creatinine 292.8 ± 136.6 72.89 ± 10.39 <0.0001 leptin have been observed in other contexts to predict favorable
eGFR 27.33 ± 12.12 117.1 ± 18.51 <0.0001 outcomes in patients who are receiving hemodialysis.48 That said,
FBG (mmol/L) however, it is difficult to conclude if identifying CKD stage 5 as a
predictor of higher serum leptin levels is relevant for this
Both 6.276 ± 1.973 4.733 ± 0.638 <0.0001
population at this time because the information on which such
Male 5.939 ± 1.644 4.647 ± 0.611 0.0017 an inference may be made is insufficient, necessitating additional
Female 6.653 ± 2.252 4.829 ± 0.672 0.0021 studies to complete knowledge gaps.
Leptin (ng/ml) It is noteworthy that the time elapsed since the diagnosis of
HHD was a significant predictor of serum leptin in CKD patients.
Both 25.42 ± 12.92 5.683 ± 3.929 <0.0001
Thus, in this cohort of CKD patients, being diagnosed with HHD for
Male 22.45 ± 11.78 2.500 ± 0.574 <0.0001 more than 6 years was related to lower serum leptin levels. This
Female 28.96 ± 13.50 9.241 ± 2.814 <0.0001 finding collaborated with an earlier study in 207 women with normal,
Note: Data presented as mean ± standard deviation (SD). Continues impaired, or type 2 diabetes where lower leptin levels predicted
variables compared using unpaired t‐test and p < 0.05 considered increased cardiovascular mortality during a 7‐year follow‐up dura-
statistically significant. tion.52 While HHD diagnosis in a CKD patient for more than 6 years
Abbreviations: CKD, chronic kidney disease; DBP, diastolic blood may compensate for the aberrant kidney's reduced ability to take up
pressure; SBP, systolic blood pressure; VLDL, very low‐density
leptin from circulation,53,54 it is quite unclear whether such
lipoprotein.
reductions in serum leptin levels could predict improved outcomes
in CKD patients diagnosed with HHD, as proposed by Scholze et al.48
anticipated given the proclivity for poor renal clearance of blood This is because HHD on its own is not connected with any favorable
leptin among CKD patients leading to the higher circulating leptin outcomes.19,55
concentrations observed.32,42,43 According to the findings of this study, high levels of HDL and
Elevated levels of leptin can be associated with a range of LDL cholesterols, both of which have been connected with a variety
metabolic complications. For instance, some studies have estab- of cardiovascular events,56–58 substantially predicted elevated levels
lished a connection between elevated leptin concentrations and of serum leptin in the case group, with each factor contributing
hyperglycemia, a rise in blood pressure, natriuresis, and renal 5.15% and 1.35% respectively to the overall variation observed
dysfunction.44,45 Indeed, elevations in levels of leptin have also (Table 4). Furthermore, this study identified elevated FPG as a
been shown to enhance kidney endothelial cell proliferation, significant predictor of increased serum leptin levels in patients with
indicating a potential role in renal glomerulosclerosis.46,47 Never- CKD and a risk factor for metabolic diseases.59,60 The relationship
theless, contradictory findings have been reported by Scholze between FPG and serum leptin has been looked at in prior studies
et al.48 where lower serum leptin levels were associated with with the latter exerting effects on the homeostasis of glucose and
lower GFR among CKD patients on hemodialysis therapy. The insulin, some of which were independent of whole‐body adiposity
research that Scholze and colleagues conducted in 2007 was a and of specific regions of the body.61,62
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6 of 9 | OFORI ET AL.
TABLE 4 Predictors (regression analysis) of increasing blood leptin levels among the CKD group
Unstandard Standard
Variables beta (β) beta (β) 95% CI for beta (β) p Value
CKD stage
CKD stage 4 ref
CKD stage 5 12.98 0.370 8.12–17.83 0.0001
CKD stage 3A 0.58 0.130 −6.29–7.44 0.8570
CKD stage 3B −0.25 −0.011 −4.84–4.33 0.9040
HDL‐cholesterol 19.86 0.269 10.37–29.34 0.0001
FBG 1.89 0.267 0.86–2.92 0.0012
Years of HHD diagnosis
<1 year ref
1–3 years HHD diagnosis −4.29 −0.150 −8.91–0.34 0.0690
4–6 years HHD diagnosis −2.03 −0.056 −8.03–3.99 0.501
>6 years HHD diagnosis −8.37 −0.217 −15.35–1.37 0.020
Systolic BP 0.15 0.201 0.20–0.27 0.0320
Diastolic BP −0.09 −0.07 −0.29–0.15 0.3920
Female gender 5.31 0.191 1.61–9.00 0.0059
BMI 0.92 0.180 0.17–1.67 0.0170
LDL‐cholesterol 2.09 0.177 0.14–4.05 0.0368
Years on dialysis
Nil ref
≤3 2.84 0.009 −3.62–9.29 0.3820
>3 years of dialysis −2.62 −0.06 −11.53–6.30 0.5580
CHF −3.86 −0.125 −8.89–1.16 0.1294
IHF −3.37 −0.121 −7.68–0.94 0.372
Years CKD diagnosis
<1 ref
≤3 years CKD diagnosis 2.22 0.079 −2.47–6.91 0.346
>3 years CKD diagnosis 6.15 0.198 −0.72–12.99 0.078
Note: N = 72; df = 71; F = 13.898; R2 = 0.854; Adj. R2 = 0.792; p < 0.05 is considered significant.
Abbreviations: BMI, body mass index; BP, blood pressure; CHF, congestive heart failure; CKD, chronic kidney disease; FBG, fasting blood glucose;
HHD, hypertensive heart disease; IHF, ischemic heart failure.
Some studies have reported BMI63,64 and female gender65,66 as of eGFR studies have focused on metabolic risk,70,71 resistin,72,73
determinants of increasing serum leptin in health and disease states. adiponectin,74,75 serum creatinine, serum cystatin C, and lean tissue
According to the findings of this study, these two factors are reliable mass.76,77 In light of these findings, it is of the utmost importance to
indicators of increased blood leptin levels not just in patients with emphasize the requirement for more research into the association
CKD and HHD but also in persons who appear to be in good health. between GFR and serum leptin, in addition to advancements in
Furthermore, eGFR was shown to predict leptin levels among the methodologies for accurate GFR prediction.
control group and corroborated prior studies conducted in Japan and The condition of multicollinearity was violated by the measured
Taiwan.67,68 On the other hand, an experimental early‐stage type 2 total cholesterol and triglycerides, and as a result, were not included
diabetic mouse model showed a correlation between elevated leptin in the regression model. This was done to avoid producing an
levels and an increase in GFR,69 contrary to what was observed overdispersion of the data, which would have put the reliability of the
among our control cohort. It is important to mention that the majority conclusions drawn from the data at risk. Therefore, the proportions
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OFORI ET AL. | 7 of 9
TABLE 5 Predictors (regression analysis) of increasing blood AUTHOR CONTRIBUTIONS
leptin levels among the control group Emmanuel K. Ofori: Conceptualization; supervision; writing – original
Unstandard Standard draft; writing – review & editing. Christian N. Adekena: Formal
Variables beta (β) beta (β) 95% CI for β pValue analysis; investigation; writing – original draft. Vincent Boima:
Female gender 5.51 0.709 4.37–6.64 0.0001 Conceptualization; supervision; writing – review & editing. Henry
Asare‐Anane: Writing – review & editing. Ernest Yorke: Writing –
BMI 1.28 0.341 0.70–1.86 0.0001
review & editing. Eric N. Y. Nyarko: Writing – review & editing.
FBG 0.06 0.009 −0.85–0.97 0.899
Bismark N. Mohammed: Investigation; methodology. Emmanuel
eGFR −0.22 −0.222 −0.08–0.02 0.012 Quansah: Investigation; methodology. Sisitha U. Jayasinghe: Writing –
Age 0.03 0.062 −0.04–0.08 0.414 review & editing. Seth D. Amanquah: Supervision; writing – review
& editing.
Systolic BP 0.11 0.131 −0.02–0.23 0.076
Diastolic BP 0.01 0.003 −0.15–0.16 0.952
ACKNOWLEDGMENTS
Triglyceride −0.64 0.071 −2.22–0.94 0.404 The authors wish to thank the Renal Unit staff at Korle‐Bu Teaching
LDL‐ −1.16 −0.131 −2.61–0.30 0.114 Hospital's Department of Medicine and the Biomedical Scientists at
cholesterol Accra's Eastwing Clinic. The authors would also like to express their
HDL‐ 0.81 0.034 −2.76–4.37 0.636 appreciation to the University of Ghana Medical School's Department
cholesterol of Chemical Pathology for their support.
Note: N = 36; df = 35; F = 30.398; R2 = 0.924; Adj. R2 = 0.894; p < 0.05 is
considered significant. CONFLICT OF INTEREST
Abbreviations: BMI, body mass index; BP, blood pressure; eGFR, The authors declare no conflict of interest.
estimated GFR; FBG, fasting blood glucose.
DATA AVAILABILITY STATEMENT
The corresponding author will provide the interested party with
that remained unexplained in these models may be accounted for by access to the data sets that were used throughout this study upon
the missing components, in addition to additional variables that were reasonable request.
not studied in this work.
In summary, individuals with CKD who also had HHD exhibited TRANSPARENCY STATEMENT
higher blood leptin levels. In the case group, the presence of The lead author Emmanuel K. Ofori affirms that this manuscript is an
CKD stage 5 and high HDL cholesterol showed as the greatest honest, accurate, and transparent account of the study being
predictors of serum leptin. Within the control group, the greatest reported; that no important aspects of the study have been omitted;
predictors of blood leptin levels were found to be female gender, and that any discrepancies from the study as planned (and, if relevant,
high BMI, and eGFR. More research is needed to fully understand registered) have been explained.
the consequences that elevated leptin levels in CKD patients
might have. ORCID
This study has several drawbacks. A larger number of study Emmanuel K. Ofori http://orcid.org/0000-0001-7375-8830
participants could not be sampled due to the specific character-
istics of the target research group including our inability to obtain REFERENCES
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