Hypertension is a major contributor to the global burden of cardiovascular disease, affecting nearly one-third of the adult population worldwide [1]. It is a key modifiable risk factor for serious complications such as myocardial infarction, stroke, heart failure, and chronic kidney disease [2]. Despite significant advances in the pharmacological management of hypertension, the residual cardiovascular risk remains high in a subset of patients, suggesting the need to explore additional biomarkers that could aid in early risk stratification and targeted intervention.

Serum uric acid (SUA), the final enzymatic product of purine metabolism, has emerged as a potential candidate in this context. Although SUA has long been associated with gout, growing evidence suggests its involvement in cardiovascular and renal pathology, particularly in hypertensive individuals [3,4]. Hyperuricemia has been proposed to contribute to vascular inflammation, oxidative stress, endothelial dysfunction, and smooth muscle cell proliferation all of which play important roles in the pathogenesis of hypertension and atherosclerosis [5].

Several large epidemiological studies have reported a positive association between elevated SUA levels and the development of hypertension, independent of other conventional risk factors [6,7]. In hypertensive patients, increased uric acid levels have been linked to target organ damage, including left ventricular hypertrophy, microalbuminuria, and arterial stiffness [8]. Moreover, SUA is known to interact with components of the metabolic syndrome, including dyslipidemia and insulin resistance, further increasing the cardiovascular burden [9].

Despite this emerging evidence, the utility of serum uric acid as a routine cardiovascular risk marker in hypertensive patients remains under debate. Most existing studies have focused on Western populations, and data from Indian settings remain limited. Considering the differences in genetic background, dietary habits, and healthcare access, region-specific studies are essential for establishing clinically relevant associations.

This study was therefore undertaken to evaluate serum uric acid levels in hypertensive patients attending a tertiary care center in North India and to explore its association with cardiovascular risk factors. The ultimate goal is to determine whether SUA could be used as a practical, low-cost biomarker for cardiovascular risk stratification in routine clinical practice.

This cross-sectional observational study was conducted over a period of one year, from August 2024 to July 2025, in the Department of Biochemistry, FH Medical College, Agra, India. A total of 200 hypertensive patients, aged between 30 and 70 years, were enrolled from the outpatient and inpatient departments of the hospital. The diagnosis of hypertension was based on the guidelines of the Joint National Committee (JNC 8), with patients having a systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg, or those already on antihypertensive treatment. Written informed consent was obtained from all participants prior to inclusion in the study.

Patients with a history of chronic kidney disease, gout, diabetes mellitus, or those currently on uric acid-lowering agents such as allopurinol or febuxostat were excluded to eliminate confounding factors. A detailed clinical history was recorded for each patient, including age, gender, duration of hypertension, medication history, lifestyle factors, and the presence of comorbidities. Anthropometric measurements such as height, weight, and body mass index (BMI) were also documented.

Venous blood samples were collected in the morning after an overnight fast. Serum uric acid was estimated using the uricase-peroxidase enzymatic method on a fully automated biochemistry analyzer. Other biochemical parameters such as fasting lipid profile (total cholesterol, HDL, LDL, triglycerides), fasting blood glucose, serum creatinine, and urea were also analyzed using standard laboratory techniques. Blood pressure readings were taken in a seated position using a calibrated sphygmomanometer, and the average of two readings taken five minutes apart was considered.

Data were entered into Microsoft Excel and analyzed using SPSS software version 25. Descriptive statistics were used to summarize the data. Pearson’s correlation coefficient was applied to assess the relationship between serum uric acid levels and other cardiovascular risk markers such as systolic and diastolic blood pressure, LDL cholesterol, and the presence of target organ damage. A p-value of less than 0.05 was considered statistically significant.

A total of 200 hypertensive patients were enrolled in the study. The mean age of the study population was 52.4 ± 9.8 years, with 120 males (60%) and 80 females (40%). The average duration of hypertension was 5.4 ± 3.1 years. Baseline characteristics, including BMI, smoking and alcohol status, are summarized in Table 1.

Table 1: Baseline Demographic and Clinical Profile of Study Participants (n = 200)

The mean serum uric acid (SUA) level among all participants was 6.8 ± 1.4 mg/dL. Elevated SUA levels (defined as >7.0 mg/dL in males and >6.0 mg/dL in females) were found in 124 patients (62%). These patients had higher total cholesterol, LDL cholesterol, triglycerides, and lower HDL cholesterol levels compared to those with normal SUA, as shown in Table 2.

Table 2: Serum Uric Acid and Biochemical Parameters

Table 3: Correlation of Serum Uric Acid with Cardiovascular Risk Factors

The prevalence of target organ damage was also higher among patients with elevated SUA levels. Left ventricular hypertrophy (LVH) was noted in 96 (77.4%) patients with high SUA, compared to 18 (23.7%) in the normal SUA group (p < 0.001). Microalbuminuria and hypertensive retinopathy were also significantly more common in the elevated SUA group. Table 4 details the association of SUA with clinical indicators of end-organ damage.

Table 4: Association of Elevated SUA with Target Organ Damage

Our study demonstrates a significant association between elevated serum uric acid (SUA) levels and the presence of cardiovascular risk factors and target-organ damage in patients with essential hypertension. Individuals with higher SUA levels were more likely to have increased systolic and diastolic blood pressure, abnormal lipid profiles, left ventricular hypertrophy (LVH), microalbuminuria, retinopathy, and impaired renal function. These findings align with earlier studies that identified hyperuricemia as an independent risk factor for hypertension-related complications, including LVH and renal damage (Kuwabara et al., 2017; Cicero et al., 2014).

The correlation between SUA and target-organ damage is biologically plausible and supported by experimental evidence. Elevated SUA levels have been shown to impair endothelial function, induce oxidative stress, and promote inflammation, all of which contribute to vascular damage, cardiac hypertrophy, and renal injury (Feig et al., 2008). In our study, the prevalence of LVH in patients with elevated SUA was markedly higher than in those with normal SUA levels. This supports previous findings by Mazzali et al. (2001), who reported that hyperuricemia directly contributes to cardiac hypertrophy through vascular smooth muscle cell proliferation and activation of the renin-angiotensin system.

Moreover, the increased occurrence of microalbuminuria and retinopathy in the hyperuricemic group further suggests a role for SUA in microvascular dysfunction. Similar associations have been reported in other cross-sectional and prospective studies, where higher SUA levels predicted renal injury and retinal vascular changes in hypertensive patients (Zoppini et al., 2012; Obermayr et al., 2008). The proposed mechanisms include uric acid-induced afferent arteriolar vasoconstriction and decreased nitric oxide bioavailability, which impair renal perfusion and glomerular filtration (Johnson et al., 2003).

Several prospective cohort studies have also established that hyperuricemia is not just a marker but potentially a mediator of future cardiovascular events. For example, in a 5-year longitudinal study, Ndrepepa et al. (2007) demonstrated that patients with SUA ≥5.2 mg/dL had a significantly higher risk of myocardial infarction and cardiovascular death. Likewise, the Rotterdam study (Strazzullo et al., 2007) found that even after adjusting for conventional risk factors, SUA was independently associated with increased risk of stroke and heart failure.

Importantly, hyperuricemia has also been implicated in the pathogenesis of hypertension itself. Experimental animal models suggest that uric acid can increase blood pressure by inducing renal vasoconstriction, stimulating smooth muscle cell proliferation, and enhancing sodium reabsorption (Feig et al., 2008). Clinical studies have supported these findings, noting that SUA predicts incident hypertension in normotensive individuals, particularly in adolescents and young adults (Chen et al., 2009; Sundström et al., 2005). In our study, we observed that hypertensive patients with elevated SUA had significantly higher blood pressure values, reinforcing this potential causal link.

From a clinical perspective, measuring SUA in hypertensive patients could offer a cost-effective and accessible tool for cardiovascular risk stratification, especially in resource-constrained settings. In environments where access to echocardiography or renal imaging is limited, elevated SUA may act as an early warning indicator for subclinical organ damage (Sánchez-Lozada et al., 2005). Additionally, some intervention trials have shown that urate-lowering therapies such as allopurinol can reduce blood pressure and improve endothelial function, particularly in younger hypertensive patients (Feig et al., 2008). However, these findings need to be validated in larger, long-term trials before routine implementation.

Despite its strengths, our study has some limitations. Being cross-sectional in design, it does not allow us to establish a cause-effect relationship between SUA and target-organ damage. Factors such as dietary purine intake, alcohol consumption, and use of diuretics—which can influence uric acid levels—were not controlled for in our analysis. Moreover, the study population was drawn from a single tertiary care hospital, which may limit the generalizability of the findings to the broader hypertensive population in India.

Our study underscores the relevance of serum uric acid as a potential biomarker of cardiovascular and renal risk in patients with essential hypertension. Elevated SUA was strongly associated with multiple indicators of target-organ damage, including LVH, microalbuminuria, and retinopathy. These findings highlight the importance of including SUA measurement in the routine evaluation of hypertensive patients. Future prospective studies are needed to explore whether early identification and management of hyperuricemia can alter the trajectory of hypertensive organ damage and improve long-term outcomes.

This study highlights a significant association between elevated serum uric acid levels and the presence of cardiovascular risk factors and target-organ damage in patients with essential hypertension. Higher uric acid levels were linked with increased blood pressure, abnormal lipid profiles, left ventricular hypertrophy, microalbuminuria, and retinopathy. These findings suggest that serum uric acid is not just a metabolic byproduct but a potential marker—and possibly a contributor—to cardiovascular morbidity in hypertensive individuals.

Given its low cost and ease of measurement, serum uric acid can be considered as an additional tool for risk stratification in hypertensive patients, especially in settings where advanced diagnostic facilities are not readily available. Regular monitoring may help identify patients at higher risk of complications, prompting earlier interventions.

However, further longitudinal and interventional studies are needed to establish causality and assess whether urate-lowering therapies can reduce cardiovascular risk and organ damage in this population.

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