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Table of Contents
ORIGINAL ARTICLE
Year : 2022  |  Volume : 10  |  Issue : 3  |  Page : 178-184

Evaluation of serum uric acid among new-onset primary hypertension patients – A cross-sectional study


1 Department of Medicine, Jawaharlal Nehru Medical College, Belagavi, Karnataka, India
2 Department of Obstetrics and Gynecology, Jawaharlal Nehru Medical College, Belagavi, Karnataka, India

Date of Submission28-Jul-2021
Date of Decision13-Sep-2021
Date of Acceptance29-Oct-2021
Date of Web Publication23-Feb-2022

Correspondence Address:
Dr. Arif Maldar
Department of Medicine, Jawaharlal Nehru Medical College, Nehru Nagar, Belagavi - 590 010, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ajim.ajim_80_21

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  Abstract 


Background: Hypertension is associated with a myriad of confounding factors, out of which elevated serum uric acid (SUA) profile is of interest as a biomarker. Despite a handful of studies alluding to the seminal relationship between the two, its prevalence and correlation in the Indian context have not been adequately investigated. Hence, the present study was aimed to evaluate the relationship between SUA levels and primary hypertension (HTN). Materials and Methods: This 1-year hospital-based cross-sectional study comprised 100 patients who were recently diagnosed with primary HTN and had not received antihypertensive medications, SUA levels and severity of HTN among patients were assessed along with their age, sex, body mass index, total cholesterol, and lipid profile. Results were statistically analyzed by Chi-square test, logistics regression, t-test/Welch t-test/Mann–Whitney U-test, and Pearson–Spearman rank correlation. Results: A strong correlation between SUA level with systolic blood pressure (SBP) in patients with primary HTN (r = 0.5046; P < 0.0001) was observed. The mean SBP (163.89 ± 9.99 mmHg) was significantly high (P < 0.001) in hyperuricemic patients, and raised SUA was noted in 38% of the cohort. Stage II hypertensive subjects of the 58–66 years age group were found to be a particularly vulnerable group (odds ratio of 32). History of diabetes mellitus, tobacco, and alcohol consumption showed a significant association with elevated SUA levels in males (P < 0.05). Conclusion: One in every three primary hypertensive patients is likely to present with hyperuricemia, and there exists a pertinent association between elevated SUA levels with SBP.

Keywords: Body mass index, hypertension, hyperuricemia, systolic blood pressure, uric acid


How to cite this article:
Ghali R, Maldar A, Patil P, Khursheed R. Evaluation of serum uric acid among new-onset primary hypertension patients – A cross-sectional study. APIK J Int Med 2022;10:178-84

How to cite this URL:
Ghali R, Maldar A, Patil P, Khursheed R. Evaluation of serum uric acid among new-onset primary hypertension patients – A cross-sectional study. APIK J Int Med [serial online] 2022 [cited 2022 Aug 11];10:178-84. Available from: https://www.ajim.in/text.asp?2022/10/3/178/338154




  Introduction Top


Hypertension (HTN) is a well-known risk factor for global mortality and morbidity.[1] Disease burden among adults as an outcome of HTN has doubled from 594 million in 1975 to 1.13 billion in 2015, with a disproportionately large prevalence observed in low- and middle-income countries.[2] In India, the Global Burden of Disease study attributed 1.63 million deaths as a consequence of HTN in 2016 alone.[1] Etiological factors of HTN are ubiquitous in nature; however, experimental evidence suggests that elevated serum uric acid (SUA) level was an independent predictor of HTN and progression of blood pressure (BP).[3] Nevertheless, the role of SUA as a marker, or risk factor for HTN, remains unclear.[4]

SUA level above the threshold of 6.8 mg/dL is referred to as hyperuricemia.[5] Hyperuricemia can result in gout, endothelial dysfunction, or uric acid nephrolithiasis, which further worsen the quality of life in hypertensive patients.[5],[6] SUA concentrations rise either due to increased uric acid production or decreased excretion, or a combination of the two. Increased consumption of protein, alcohol, and enzymatic abnormalities of uric acid/urate transporters in purine metabolism are key factors in increasing SUA production.[7],[8] This prolonged accrual of SUA facilitates the development of HTN by multiple pathways, such as activation of the renin–angiotensin–aldosterone pathway, influencing glomerular apparatus, uric acid-induced smooth muscle cell proliferation, or heightened hyperinsulinemia that effectuates decrease in excretion of uric acid, potassium, and sodium that results in elevated BP.[9] As the levels of SUA and BP are reflective of the inner physiology, which itself is influenced by aging, body mass index (BMI), dietary intake, and lifestyle habits, evaluating the relationship between SUA and HTN becomes a complex task.[10]

Although a couple of studies have commented on the nexus between SUA and HTN, there is a dearth of literature pertaining to the prevalence of hyperuricemia, its association, and correlation with demographic and physiological characteristics in hypertensive patients. Moreover, most of the previously conducted studies have investigated patients being treated with antihypertensive agents.[11]

Considering these facts, the present study was undertaken (1) to find the association between hyperuricemia and BP in newly diagnosed primary HTN and (2) to find the association of hyperuricemia in hypertensive patients with regard to ancillary factors of HTN such as gender, age, BMI, and high triglyceride levels.


  Materials and Methods Top


This cross sectional study was under taken at KAHER's (KLE academy of Higher Education and Research) Dr. Prabhakar Kore hospital and MRC, Belagavi, Karnataka, attached to Jawaharlal Nehru Medical College. A total of 100 adult patients diagnosed with primary HTN as per the 2017 American College of Cardiology/American Heart Association guidelines were enrolled.[12] Patients with renal failure, gout, malignancy, secondary HTN, and pregnancy-induced HTN and those receiving pharmacological treatments such as thiazides, loop diuretics, pyrazinamide, allopurinol, and ethambutol were excluded from the study. The ethical clearance was obtained from the institutional ethics committee and written informed consent was obtained from all participants

Data collection

The sample size was calculated based on the formula as mentioned below.



Where, p = prevalence of the disease which was considered as 50% due to scarcity of data on primary/essential HTN in the study area

q = 100–P = 100–50 = 50

d = Absolute error taken as 10%



n = 100

Hence, a sample size of 100 was considered for the study.

This study was conducted over a span of 1 year between January 2018 and December 2018. Demographic details of patients such as age, gender, and occupation along with a comprehensive medical history were noted. Baseline clinical features encompassing height (m), weight (kg), BMI (kg/m2), systolic BP (SBP), and diastolic BP (DBP) (mmHg) were evaluated by a thorough general physical examination. BMI was estimated by dividing the weight (kg) of patients by the square of their height (m) and subsequently classified according to overweight and obesity by BMI in adult Asians.[13] BP of patients was recorded by the digital sphygmomanometer OMRON HEM-8712 in the sitting position after a respite of 5 min. BP was recorded thrice and the mean BP was calculated.[14] A baseline SBP of 140–159 mmHg or DBP of 90–99 mmHg was recognized as Stage I HTN, whereas baseline SBP of ≥160 mmHg or DBP ≥100 mmHg was recognized as Stage II HTN.[15] Under aseptic conditions, 2 mL of venous blood was collected in ethylenediaminetetraacetic acid vials for further investigations such as SUA (mg/dL), hemoglobin (gm%), complete blood count (CBC), platelet count (/mm3), serum urea (mg/dL), thyroid stimulating hormone(mIU/L), random blood sugar (RBS) (mg/dL), total cholesterol l (mg/dL), low-density lipoprotein (LDL) (mg/dL), high-density lipoprotein (HDL) (mg/dL), and triglyceride levels (mg/dL). Early morning venous blood samples were used for SUA and lipid profile analysis. SUA was estimated by the uricase – POD enzymatic colorimetric method using the SPINREACT kit (Spinreact SAU, Girona, Spain) according to manufacturer's instructions.[16] SUA >6 mg/dL and SUA >7 mg/dL were considered as hyperuricemia for male and female, respectively. Lipid profile was ascertained based on National Cholesterol Education Program guidelines.[17] Total cholesterol, LDL, and triglyceride values above 200 mg/dL, 100 mg/dL, and 150 mg/dL, respectively, were considered to be elevated. HDL values below 50 mg/dL in females and 40 mg/dL in males were considered abnormal. SUA levels noted among patients were classified into four quartiles of <4.69, 4.69–5.58, 5.58–6.52, and ≥6.52 mg/dl, as depicted by Wei et al.[18]

Statistical analysis

The data were recorded in a Microsoft Excel spreadsheet and analyzed using R i386.3.5.1 software. Continuous data were represented as mean ± standard deviation and the categorical variables were reflected by the frequency table and analyzed by Chi-square test. Continuous data were compared using t-test/Welch t-test/Mann–Whitney U-test. Pearson's correlation between SUA levels with myriad factors such as age, SBP, DBP, total cholesterol, LDL, HDL, and triglycerides along with analysis of association logistic regression was performed. At 95% confidence interval, P < 0.050 was considered significant.


  Results Top


A study cohort comprising 100 patients showed a male preponderance of 68%. Study participants were aged between 31 and 80 years, with the majority belonging to the 61–70 age group. The overall mean age of the patients was 57.22 ± 11.46 years. [Table 1] enumerates the baseline features of patients, differentiated by their gender. The SUA noted ranged between 2.50 and 13.50 mg/dL with mean and median of 6.32 ± 2.46 mg/dL and 6.15 mg/dL, respectively. Most of the patients (37%) had a BMI between 23.00 and 24.99 kg/m2. The frequency of hyperuricemia in patients with BMI ranged between 23.00 and 24.99 kg/m2 (29.73%), 25.00 and 29.99 kg/m2 (64.71%), and ≥30 kg/m2 (100%); however, BMI was insignificant association with hyperuricemia (P = 0.4879).
Table 1: Comparison of different factors between male and female hypertensive subjects

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Overall, the SBP levels ranged between 130 and 180 mmHg with a mean and median of 156.16 ± 12.09 and 156 mmHg, respectively, whereas DBP levels varied between 80 and 100 mmHg with 93.46 ± 5.05 and 94 mmHg as mean and median values, respectively [Table 1]. Hyperuricemia characterized by raised SUA levels was seen in 38% of the patients. Comparison of mean SBP values among the sexes revealed less mean SBP in females than males (P = 0.0008). Among the females, the mean values of CBC as well as platelet count were found to be elevated (P = 0.0046, P = 0.0213). There was a significant positive correlation of influencing factors such as SBP, DBP [Figure 1], age, and RBS [Figure 2] with SUA.
Figure 1: Positive correlation of serum uric acid levels with systolic blood pressure (a) and diastolic blood pressure (b) among hypertensive patients

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Figure 2: Positive correlation of serum uric acid with (a) age among hypertensive patients (b) random blood sugar among hypertensive patients

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Out of 100 subjects, 33 patients with Stage II HTN had SUA levels ≥6.52 mg/dL, while the same was noticed in 10 Stage I HTN patients [Figure 3]. Subsequently, the association between SUA and the stage of HTN was significant (P = 0.0002). In all participants, for every one-unit increment in SUA, the odds of Stage II HTN increased by 98% after adjusting for other factors as determined by logistic regression. The odds of developing Stage II HTN were 10.72 times higher in patients with hyperuricemia than normal subjects on adjusting other factors. There was a difference predisposition of Stage II HTN for hyperuricemia among males with an adjusted odds ratio of 43.98 (P = 0.0018) and females (P = 0.0183), as shown in [Table 2]. Logistic regression of age with SUA in Stage II HTN subjects demonstrated patients in the 58–66 years age group to have a higher odds ratio of 32 than normal SUA subjects [Table 2]. In the present study, majority of patients were males (68%) and 32% were females suggesting a higher risk of primary HTN among males. However, the frequency of hyperuricemia was slightly higher in females compared to males (43.75% versus 35.29%) (P = 0.142).
Table 2: Odds ratios of acquiring hyperuricemia based on age and sex of subjects

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Figure 3: Bar graph distribution of patients having Stage I or Stage II hypertension across serum uric acid quartiles

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The elevated total cholesterol levels were noted in 59% of the patients (P = 0.6422), raised LDL levels noted in 62% of the patients (P = 0.4265), abnormal HDL levels seen in 67% of the patients (P = 0.5245), and raised triglyceride levels seen in 62% of the patients (P = 0.8041). Each of these factors displayed a weak association with hyperuricemia.


  Discussion Top


The present study involving 100 hypertensive patients was carried out to ascertain the relationship between HTN and hyperuricemia in terms of SUA levels. A wide range of SUA levels between 2.50 and 13.50 mg/dL were noted among hypertensive study participants, with over one-third (38%) of the patients presenting with elevated SUA levels. On adjusting other factors, the odds of Stage II HTN were 10 fold higher in patients with hyperuricemia in comparison to normal subjects. Hence, one out of three patients with HTN was found to have hyperuricemia in this study cohort. The mean SUA levels noted in this study were comparable to case–control study by Mishra et al (5.80 ± 2.16 mg/dL mean SUA) (P < 0.05) in patients with newly diagnosed essential HTN.[17] This concordance of results adds further validity to the notion of SUA as a predictor and cause of primary HTN. Hyperuricemia is often characterized yet not limited to exacerbated oxidative stress and amplification of the renin–angiotensin–aldosterone system. Adversarial impacts of hyperuricemia also include endothelial dysfunction, glomerulosclerosis, induction of inflammatory cascades, and cytokine expression. The consequent nephropathy and vascular abnormalities that arise stimulate the occurrence of arterial HTN.[17],[19],[20]

In the present study, SBP was recorded in a range between 130 mmHg to 180 mmHg, while DBP levels ranged between 80 and 100 mmHg. The drastically high mean values of SBP and DBP (156.16 ± 12.09 mmHg and 93.46 ± 5.05 mmHg, respectively) noted in this study closely correspond to the mean SBP and DBP levels of 159.00 ± 11.98 mmHg and 94 ± 4.62 mmHg, respectively, in the study by Mishra et al.[17] However, other studies have reported comparatively lower levels of SBP and DBP (116.0 ± 14.6 mmHg and 143.99 ± 14.28 mmHg mean SBP and 75.0 ± 8.7 mmHg and 96.61 ± 7.24 mmHg mean DBP values).[8],[9] This dissonance may arise from the fact that majority of the patients 96 (96%) had Stage II HTN and only four (4%) of the patients were diagnosed to have Stage I HTN in the current study.

Interestingly, 39.58% of the patients with Stage II HTN had hyperuricemia and none of the patient with Stage I HTN had hyperuricemia, there was a significant association between the severity of HTN and SUA levels (P < 0.05). Mean SBP (P < 0.001) was significantly high in hyperuricemic patients compared to patients with normal SUA levels, suggesting that patients with raised SUA levels were more likely to present with elevated SBP. This observation was further strengthened the correlation of SUA levels with SBP and DBP which showed a strong positive correlation between the SUA and SBP (r = 0.5046; P < 0.0001). A moderate positive correlation between SUA and DBP (r = 0.2593; P < 0.01) was noted as well. These findings are in harmony with Poudel et al. demonstrating the significant association between SUA with SBP (P < 0.001) and DBP (P < 0.01).[9] Shrivastav et al. reported similar findings where although SUA levels were significantly associated with SBP (P < 0.05), their association with DBP was insignificant (P > 0.05).[19] Hence, it is evident that every one patient out of three with HTN is likely to have raised SUA levels, reflective of the strong association between SUA with SBP. Raised SUA as a risk factor for HTN was reported by Kahn et al. In this study, about 25%–40% of adults with HTN have SUA more than 6.5 mg/dl and there was a direct relationship between SUA and SBP, a finding consistent with the present study.[3] According to Ali et al., an increase in HTN with a corresponding rise in SUA levels among patients is grouped into four quartiles.[8] These findings are congruent to the observations of the present study, thus establishing the salient interdependence between HTN and hyperuricemia.

In this study, males were found to have a higher chance of developing hyperuricemia (adjusted odds ratio of 43.98) Previous studies have reported a higher degree of hyperuricemia in males as compared to females in hypertensive patients (6.15–6.47 mg/dL in males and 4.32–4.87 mg/dL in females).[11],[21] The mean SUA levels were also slightly high among male patients compared to female patients in the present study, but again, the difference was insignificant (P > 0.05). Possible reasons for the divergence in findings may be due to sociodemographic factors such as stressful lives and inclusion of more women of postmenopausal age experiencing hormonal fluctuations. These observations suggest that, although the elevated SUA levels in patients with primary HTN are not solely influenced by sex, it is a risk factor to be monitored.

In the present study, most of the patients were aged between 61 and 70 years suggesting increased vulnerability of patients to developing hyperuricemia in their seventh decade (35%). Accordingly, a significant association was found between hyperuricemia and age (P = 0.0092). A positive correlation was also noted between elevated SUA and age among participants. The observations of Ali et al. reiterate the noteworthy association between SUA and age (P < 0.05), adding further strength to this study's results.[8] These observations partly concur with a study done by Cheng et al. who found that SUA concentration was positively associated with HTN only in the 41–50-year-old group.[22]

In the current study, a significant association was found between elevated SUA level with history of diabetes mellitus (34%, P = 0.0136), smoking (16%, P = 0.0080), alcohol consumption (17%, P = 0.0056), and tobacco chewing (26%, P = 0.0046) in male patients. However, the mean comparison of the entire cohort did not display a significant nexus of SUA with a history of diabetes mellitus, alcohol, smoking, and tobacco chewing. This variance in results may be on account of diverse differences in the sociocultural norms that influence the use of alcohol and tobacco products. These findings are suggestive of the fact that the association of SUA with lifestyle factors is multifactorial and gender specific. Dehghan et al. demonstrated that individuals with elevated SUA levels are at a greater risk of developing type 2 diabetes with hazard ratios of 1.63 and 2.83 for those in the third and fourth quartiles of SUA, respectively.[23] Rafieian-Kopaei et al. conducted a cross-sectional study on type 2 diabetics, which concluded that SUA has a strong association with SBP (P = 0.02) in type 2 diabetics.[24] With regard to smoking, these findings are in line with previous studies which have reported highly elevated levels of SUA in former smokers.[25],[26] However, Anand et al. in their case–control study reported that there is no significant difference among hypertensive males with regard to uric acid and smoking.[21] A study by Kumbhalkar and Deotale reported the absence of a significant association between tobacco chewing and SUA levels in congruence to the findings of the present study.[27] In a study by Conen et al., alcohol consumption was linked to elevated SUA levels, predominantly in men.[28] In consonance with this, the results of the present study also demonstrated a prevalence of alcohol consumption in 16 males and only one female. Regarding BMI, insignificant association with hyperuricemia was noticed in the present study (P > 0.05). In consonance with these observations, Anand et al. also concluded that though mean SUA is higher in study subjects whose BMI >25 kg/m2 than those subjects with BMI <25 kg/m2, the association is insignificant (P > 0.05).[21]

Similarly, no significant correlation could be reckoned between SUA levels and total cholesterol (r = 0.0470; P > 0.05). Despite majority of the patients having raised LDL levels, lower HDL levels, and hypertriglyceridemia, a salient significant association of these factors with hyperuricemia was missing. These findings suggest that hyperuricemia is not explicitly associated with hypertriglyceridemia. A study by Teng et al. reported similar dissociation between elevated SUA and factors such as BMI and total cholesterol levels (P > 0.05).[29] Contrary to this, a few other studies state that SUA is significantly associated with BMI, LDL, and HDL levels.[9],[11] The divergence in findings between these sets of studies is indicative that BMI and cholesterol parameters are not exclusively related to SUA and are potentially influenced by other concomitant physiological traits.

Strengths and limitations of the study

This study can help in the design of future large-scale clinical trials investigating the potential of SUA targeted therapies in the prevention and amelioration of HTN. Referring to SUA as a risk factor for HTN can expedite the screening process by clinicians as it is a robust and minimum invasive test for better patient management. Few limitations of the study are relatively smaller sample size and monocentric study design. Furthermore, the present study predominantly involved male patients and Stage II primary HTN patients in excess acting as confounding factors.


  Conclusion Top


The findings of the present study illuminate the highly significant association as well as correlation between elevated SUA profile and HTN marked as a sharp increase in SBP with SUA values. Therefore, adequate care must be taken to maintain a normal SUA profile to prevent and manage HTN. Treatment plans for HTN must include strategies to decrease SUA levels to ensure an improved quality of life and prevention of associated comorbidities.

Acknowledgments

The authors would like to acknowledge all the study participants.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

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