Chronic kidney disease (CKD) is a condition characterized by persistent abnormalities in kidney structure or function lasting more than 3 months. Several pathophysiological processes in CKD contribute to a progressive decline in renal function, often leading to kidney failure.¹

In the United States, the number of patients with progressive CKD requiring renal replacement therapy has increased over the past two decades.² According to data from Riskesdas (2018), the prevalence of CKD in Indonesia was 0.38% of the total population, affecting approximately 713,783 individuals.³ The risk of cardiovascular disease in patients with CKD increases by 15%. Several studies have shown that more patients with CKD die from left ventricular enlargement and congestive heart failure than from coronary heart disease (CHD).^4-6

Research by Said (2014) on the relationship between CKD and cardiovascular risk demonstrated that electrocardiography (ECG) abnormalities are common in patients with CKD and may predict future cardiovascular events, including left ventricular hypertrophy (LVH).^7,8 Other studies have reported wide variations in the prevalence of ECG abnormalities, including prolongation of the Q wave and QRS complexes, which reflect ventricular electrical activity.⁹

Previous research by Taddei et al. on hypertension, LVH, and CKD reported a high prevalence of LVH among patients with CKD, regardless of the initial severity of the disease. This finding is largely attributed to the multifactorial pathogenesis of LVH in individuals with CKD.¹⁰ Abnormal arterial stiffness and systolic hypertension increase afterload pressure by opposing left ventricular ejection, thereby contributing to the development of LVH. Moreover, older patients with CKD often present with ECG abnormalities — particularly ventricular hypertrophy — which are associated with a significantly higher risk of mortality compared to older individuals without CKD. This is especially evident in those aged 40 years or older, who face an elevated risk of developing CHD.^11,12

LVH can be detected using various modalities, including ECG and echocardiography. Echocardiography is widely regarded as the gold standard for diagnosing LVH due to its superior accuracy in assessing left ventricular mass.¹³ However, in resource-limited settings, the use of echocardiography may be restricted by its higher cost, the need for specialized equipment, and the requirement for trained personnel.¹⁴ ECG presents a more practical and accessible alternative. It is less expensive, easier to perform, and can serve as an initial screening tool for LVH, particularly in under-resourced health care environments.¹³

To date, no studies in Indonesia have investigated the detection of LVH by ECG in patients with CKD. Therefore, this pilot study aims to explore the relationship between CKD and LVH as diagnosed by ECG.

The mean age of respondents was 58.31 ± 7.73 years in the case group and 60.03 ± 8.14 years in the control group. An independent t-test revealed no statistically significant difference in age between the two groups (Table 1).

In terms of sex distribution, the case group consisted primarily of women (51.4%), while the control group was predominantly male (57.1%). A chi-square test indicated no significant difference in sex distribution between the groups. Additional sociodemographic data are presented in Table 1, and a summary of the study's key findings is illustrated in Central Illustration.

As shown in Figure 1 and Table 2, analysis using the Sokolow–Lyon criteria demonstrated that the case group had a significantly higher score compared to the control group (p = 0.03). This finding indicates a statistically significant association between the Sokolow–Lyon score and CKD.

The mean age of participants with CKD in this study was 58.31 years. Similar findings were reported by Delima et al. (2017), who observed a higher likelihood of CKD in individuals over the age of 52.¹⁵ This aligns with previous theories suggesting that, beginning at age 40, the number of functioning nephrons decreases by approximately 10% every 10 years.¹⁶ As individuals age, kidney function progressively declines, resulting in reduced glomerular excretory capacity. When this decline occurs extensively, it can lead to a range of clinical symptoms and ultimately the development of CKD.¹⁷ One contributing factor is the physiological mechanism of oxidative stress, which is commonly observed in aging. The combined effects of oxidative stress and inflammation during the aging process increase glomerular permeability, thereby elevating the risk of CKD.⁶

According to research by Abdelhafiz et al. (2010), two main theories explain the association between aging and increased risk of CKD: vascular changes and renal structural alterations. With advancing age, the arterial tunica intima tends to harden and develop endothelial dysfunction. In the tunica media, there is proliferation of smooth muscle cells, a reduction in elastin content, and progressive medial fibrosis.¹⁸ These vascular changes contribute to increased intima-media thickness, vascular wall calcification, and stiffness of the aorta and large arteries.¹⁹ Thickening of the tunica intima is considered an early marker of atherosclerosis, which is a known predictor of cardiovascular disease.¹⁸ The rising prevalence of cardiovascular conditions with advancing age is closely linked to the increased prevalence of CKD.²⁰ With regard to renal changes, aging is associated with both structural and functional alterations in the kidneys. Previous research by Tauchi et al. demonstrated a significant reduction in kidney mass in autopsies of individuals aged 40 years and older.²¹ This decline in renal mass, along with the progression of glomerulosclerosis observed with aging, supports the theory that increasing age is related to a decrease in glomerular filtration rate.²²

Regarding the analysis of sex, the results showed that women were more affected by CKD than men. This finding is consistent with previous research by Sundari et al. (2014), which also reported a higher prevalence of CKD in women.²³ According to the National Kidney Foundation, women may be more susceptible to CKD due to the shorter anatomical structure of the female urinary tract compared to males.^24,25 In women of reproductive age, CKD is often linked to disruptions in the hypothalamic–pituitary–ovarian axis, leading to hormonal imbalances and irregular menstrual cycles.²⁶ Additionally, postmenopausal women have an increased risk of developing CKD. Interestingly, a longer reproductive lifespan has been associated with a lower risk of CKD, suggesting that prolonged estrogen exposure during reproductive years may offer cumulative protective effects against the disease.²⁷

This study also demonstrated varying Sokolow–Lyon scores, with a higher average score observed in participants with CKD (22.49 mm). These findings are consistent with a review by Cerasola et al. (2011), which reported a higher prevalence of LVH among individuals with CKD.²⁸ Similarly, a study by Han et al. (2020) showed the prevalence of LVH in patients with CKD is notably high, affecting between 29% and 74% of individuals, depending on the severity of renal impairment.²⁹ Furthermore, previous research by Losi et al. (2010) indicated that patients with CKD are prone to developing diastolic dysfunction — a type of left ventricular functional impairment — that results in fluid accumulation within the left ventricular space, ultimately contributing to the development of LVH.³⁰

Bivariate analysis revealed a significant difference in Sokolow–Lyon scores between the CKD and non-CKD groups, with the CKD group exhibiting a significantly higher mean score. These findings are consistent with recent research conducted in Ghana, which demonstrated that ECG using the Sokolow–Lyon criteria effectively identified a high prevalence of LVH among patients with CKD.¹⁴ The Sokolow–Lyon criteria are known for their high specificity, reported to range from 93% to 100% across various studies.^31,32 Ogunlade and Akintomide (2013) reported a sensitivity of 58.6% and a specificity of 60.66% for the Sokolow–Lyon criteria, surpassing the Cornell voltage criteria, which had a sensitivity of 51.72%.³³ However, other studies such as Ahn et al. (2015) reported much lower sensitivity, with rates as low as 3.3%.³⁴ In CKD populations, factors such as obesity and comorbid conditions may further reduce the sensitivity of the Sokolow–Lyon criteria, as noted by Snelder et al. (2020).³⁵ Therefore, while the Sokolow–Lyon criteria are valuable for detecting LVH, it is recommended that they be used in conjunction with other diagnostic tools, such as the Cornell voltage criteria, in order to improve overall diagnostic accuracy.³⁶

These findings indicate a significant difference in the S and R wave amplitudes measured using the Sokolow–Lyon criteria between the two groups, which suggests a strong association between LVH on ECG and CKD. This relationship may be explained by the inflammatory and vascular calcification processes commonly observed in individuals with CKD. These pathological changes can lead to increased afterload and/or preload, ultimately resulting in LVH.^37,38 Figure 2 displays the proposed mechanisms contributing to the development of LVH in patients with CKD.

This study has several limitations that should be acknowledged. First, there were constraints in collecting supporting data on key variables such as renal function and glomerular filtration rate. Ideally, the assessment of LVH should be compared against well-supported, established gold-standard methods.

Additionally, the case–control design may have affected the robustness of our findings since it limits the ability to establish causality. Future studies should aim to incorporate gold-standard diagnostic tools, such as echocardiography, and address methodological gaps to improve the validity and clinical relevance of results. Moreover, the relatively small sample size may limit the generalizability of our findings to broader populations. These limitations underscore the need for further research to validate our results and to better understand the complex interplay between renal function and cardiac health.

In conclusion, our findings demonstrate a significant association between LVH as assessed by the Sokolow–Lyon score on ECG and CKD. This suggests a potential relationship between cardiac structural changes and CKD. We propose that the Sokolow–Lyon score may serve as a reliable tool for detecting LVH in patients with CKD, particularly in resource-limited settings where access to echocardiography is restricted.

Future studies should consider additional factors that may influence the Sokolow–Lyon score, such as the duration of hemodialysis and the stage of CKD. The incorporation of alternative diagnostic criteria (e.g., the Cornell voltage criteria) could enhance the accuracy of LVH detection and help differentiate true LVH from other ECG abnormalities.

To strengthen the validity and generalizability of findings, future research should also consider alternative study designs, such as prospective cohort studies, larger sample sizes, and multi-center settings. These approaches would allow for more comprehensive and representative conclusions regarding the relationship between CKD and LVH.