Two-dimensional speckle-tracking echocardiography for evaluating left atrial remodeling in renal transplant recipients

Introduction

Cardiovascular disease (CVD) is the leading cause of death in patients with end-stage renal disease (ESRD), accounting for approximately 50% of all related deaths (1). Although kidney transplantation (KT) significantly improves patient survival, posttransplant cardiovascular events remain the primary drivers of graft dysfunction and mortality (2,3). Studies have shown that KT can effectively improve left ventricular (LV) function and reduce the risk of congestive heart failure in patients with ESRD (4). Traditionally, LV structural and functional abnormalities, such as LV hypertrophy (LVH) and impaired LV systolic and diastolic function, are considered key indicators for predicting future adverse cardiovascular events and all-cause mortality (5). The left atrium (LA) is often regarded as a passive reflector of these pathophysiological changes. In diseases such as heart failure, changes in LA size and function not only reflect LV functional status, but its own remodeling and dysfunction may also directly participate in the progression of CVD. LA size and function can directly reflect LV filling pressure and overall cardiac status, serving as an important window for cardiovascular risk (6,7). Previous studies on LA assessment have mainly relied on LA volume index (LAVI) as measured by echocardiography, but this lacks sensitivity to early fibrosis and functional impairment. Although cardiac magnetic resonance (CMR) is the gold standard for evaluating cardiac size and mass (8), its clinical application is limited due to its high cost, time-consuming nature, and low accessibility. Enabled by the development of two-dimensional speckle-tracking echocardiography (2D-STE) technology, LA strain can provide a novel perspective for assessing LA function, as it can capture subtle changes in LA reservoir, conduit, and pump functions, as well as left atrial stiffness (LASt), with high sensitivity (9). LA myocardial function parameters measured by 2D-STE are closely related to LV diastolic dysfunction (LVDD) (10) and can serve as an effective supplementary tool for cardiovascular risk stratification in patients with ESRD (11).

However, studies on LA remodeling after KT are contradictory. Huang et al. (12) found no significant changes in LA volume or ejection fraction 1 year after KT on CMR, emphasizing their association with LV remodeling, N-terminal pro-B-type natriuretic peptide (NT-proBNP) level, and systolic blood pressure (SBP). In a cross-sectional study by Yildirim et al. (13), transplant recipients had significantly higher LA reservoir strain (LASr) and conduit strain rate than did patients on dialysis, suggesting that KT may improve LA mechanical function.

In summary, the existing findings on LA remodeling after KT are inconsistent. Given the critical role of LA remodeling in cardiovascular pathophysiological processes and the unique strength of 2D-STE in the early detection of LA functional abnormalities (14), we sought to determine the effect of KT on LA structure and function. Specifically, we used 2D-STE to systematically evaluate the longitudinal changes in LA structure and function at 12 months after patients underwent KT and compared these changes to those in patients treated with maintenance dialysis over the same period. We present this article in accordance with the STROBE reporting checklist (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1613/rc).

Methods

Study population

This prospective cohort study consecutively enrolled patients with ESRD aged ≥18 years who met the Kidney Disease: Improving Global Outcomes (KDIGO) criteria for stage 5 chronic kidney disease (CKD) [estimated glomerular filtration rate (eGFR) <15 mL/min/1.73 m²] and had received regular dialysis for ≥3 months. The KT group (n=85) consisted of candidates eligible for KT as assessed by the institutional ethics committee of The Second Affiliated Hospital of Guangxi Medical University, while the maintenance dialysis group (n=78) included controls matched for baseline characteristics. Patients with atrial fibrillation, moderate-to-severe valvular disease, or poor-quality echocardiographic images were excluded (Figure 1). This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments and was approved by the Ethics Committee of The Second Affiliated Hospital of Guangxi Medical University (No. 2024-KY-0679). Written informed consent obtained from all participants (Figure 1).

Figure 1 Flowchart of patient enrollment and exclusion. AF, atrial fibrillation; CKD, chronic kidney disease; KT, kidney transplantation.

Measurement and follow-up of conventional echocardiography

All echocardiographic examinations were performed strictly in accordance with the guidelines of the American Society of Echocardiography (15). Two senior physicians conducted standardized operations with an EPIQ7C ultrasound system (Philips, Amsterdam, the Netherland) with an S5-1 probe at 2.5–5.0 MHz. Participants were placed in the left lateral decubitus position with the electrocardiogram (ECG) connected, and three cardiac cycles were recorded. The structure and function of the LV were evaluated with 2D, M-mode, and Doppler techniques through parasternal and apical views. Specific measurements included the following: (I) LV mass index (LVMI), calculated based on the Devereux formula and normalized by body surface area; (II) LV ejection fraction (LVEF), LV end-diastolic/systolic volume (LVEDV/LVESV), and LAVI obtained by the biplane Simpson method; and (III) assessment of diastolic function in the apical four-chamber view, with pulsed-wave Doppler ultrasound being used to measure the early (E-wave; after ECG T wave) and late (A-wave; after ECG P wave) diastolic flow velocities at the mitral valve orifice. Additionally, pulsed-wave tissue Doppler imaging was employed to determine the early diastolic myocardial velocity (e') at the mitral annulus of the interventricular septum and lateral wall, and the mean value was taken to finally calculate the E/e' ratio. The transplantation group underwent evaluations at two time points: 1–2 weeks during the stable period before transplantation (baseline) and 12 months after transplantation. The dialysis group was also assessed at two time points: at enrollment (baseline) and 12 months after enrollment. For the baseline assessment of patients in the dialysis group and patients in the KT group before transplantation, echocardiographic examinations were arranged as much as possible to be within approximately 24–48 hours after their regular hemodialysis treatment. This was intended to evaluate patients’ basic cardiac function under a relatively stable volume state (close to dry weight). The 12-month follow-up time point was chosen because renal function and systemic metabolic status after KT usually stabilize within 6–12 months. By this time, the clearance of uremic toxins and improvement of hemodynamics are significant, thus providing a basis for the observation of changes in cardiac structure and function (16).

2D-STE

For the assessment of LA and LV strain, speckle-tracking technology was used to analyze LA and LV function and was performed on apical two-, three-, and four-chamber views acquired via conventional 2D grayscale echocardiography. During image acquisition, patients held their breath with simultaneous ECG recording, and three consecutive cardiac cycles were digitally stored at a frame rate of 60–80 frames/second. Offline analysis was conducted with QLAB software version 13 (Philips). Cardiac cycles were defined by R-R intervals, with reference points set at the mitral annulus and apex; boundaries were automatically tracked and manually adjusted if necessary. LV global longitudinal strain (LVGLS) was calculated from the three apical views (17). LA strain was evaluated in two- and four-chamber views, with the onset of P waves and R waves serving as references (18), and LASr, LA conduit strain (LAScd), and LA contractile strain (LASct) were recorded. All parameters were derived from the same cardiac cycle, with the final results averaged over three cycles, and the analysis was performed in a blinded manner. LV and LA strain results are typically expressed as negative values; however, absolute values were used for ease of analysis and presentation (Figure 2).

Figure 2 Imaging and indices of LV GLS analysis and LA strain-related indices before and after KT. (A) Images of LV strain analysis, displaying LV GLS for the apical two-, three-, and four-chamber views and their respective averages. (B) Left atrial strain-related indices (LASr, LAScd, and LASct) before KT. (C) Left atrial strain-related indices (LASr, LAScd, and LASct) after KT, used to compare pre- and postsurgical LA function changes. GLS, global longitudinal strain; KT, kidney transplantation; LA, left atrial; LAScd, left atrial conduit strain; LASct, left atrial contractile strain; LASr, left atrial reservoir strain; LV, left ventricular.

LASt

LASt was calculated with the following formula: LASt = (E/e')/LASr (19,20), where E/e' represents the aforementioned LV filling pressure index (E-wave at the mitral valve tip measured by pulsed Doppler, with e' as the mean value of septal and lateral annular velocities obtained via tissue Doppler), and LASr denotes the reservoir strain obtained by speckle tracking (Figure 3).

Figure 3 LA strain curves, LV TDI parameters, and transmitral E wave. (A,B) LA strain curves (A4C/A2C) with LASr, LAScd, and LASct. (C,D) LV TDI of septal/lateral e' waves. (E) Transmitral E wave. LA, left atrial; LAScd, left atrial conduit strain; LASct, left atrial contractile strain; LASr, left atrial reservoir strain; LASt, left atrial stiffness; LV, left ventricular; TDI, tissue Doppler imaging.

Statistical analysis

Data were analyzed with SPSS version 27.0 (IBM Corp., Armonk, NY, USA). Normality of continuous variables was tested with the Shapiro-Wilk test, with normally distributed data being expressed as the mean ± standard deviation and nonnormally distributed data as the median with the interquartile range; meanwhile, categorical variables are expressed as frequencies (percentages). Intergroup comparisons were performed via the independent samples t-test (normal variables) or the Mann-Whitney test (nonnormal variables) for continuous variables and with the χ² or Fisher exact test for categorical variables. Longitudinal analysis was conducted to assess intra-group baseline-to-follow-up changes via paired the t-test (normal distribution) or Wilcoxon signed-rank test (nonnormal distribution). A multiple linear regression model was established to adjust for baseline confounding factors in order to isolate the independent effect of KT.

Reproducibility of parameter measurement

Ultrasonic images of 20 randomly selected patients were measured twice by two experienced attending physicians at different times. The collected data were tested via the intraclass correlation coefficient (ICC) to analyze intra- and inter-observer reliability (Table 1).

Results

A total of 163 patients were enrolled, including 78 in the dialysis group and 85 in the KT group, and 12 months of follow-up were completed. Table 2 summarizes the baseline characteristics and laboratory findings of the two groups. Compared with the dialysis group, the KT group was younger. Additionally, during pretransplant evaluation, most patients in the KT group (vs. the dialysis group) were receiving hemodialysis with a shorter dialysis duration. Notably, compared to the KT group, the dialysis group exhibited higher SBP (151.5 vs. 141.7 mmHg) and lower hemoglobin levels (98.6 vs. 108.8 g/L). No significant differences were observed between the two groups in terms of cardiovascular comorbidities, the use of antihypertensive medication, baseline DBP, renal function, lipid profiles, myocardial enzymes, or biomarkers such as NT-proBNP and high-sensitivity C-reactive protein.

The baseline LA and LV structural and functional parameters are presented in Table 3. The KT group, as compared to the dialysis group, showed significantly higher LAScd (22.4%±7.52% vs. 20.8%±14.18%), lower LASt (0.28±0.23 vs. 0.41±0.35), and higher LV GLS (19.4%±2.5% vs. 17.8%±4.1%). No significant differences were observed between the two groups in terms of LA size, volume, LV structure, ejection fraction, or traditional LV diastolic function parameters (E/A, E/e').

Table 4 compares the LA structural and functional parameters, blood pressure, and heart rate between the pre- and post-KT groups and the dialysis groups at dialysis baseline and 12-month follow-up. Longitudinal analysis revealed significant improvements in LA function after KT. For transplant recipients, compared with pretransplantation, posttransplantation had significantly increased LASr (39.0%±11.12% vs. 42.9%±13.74%) and LAScd (22.4%±7.52% vs. 25.3%±7.99%). In contrast, there were no significant changes in LA diameter (LAD), LAVI, LASct, LASt, E, or E/e' within the KT group. During the period between baseline and follow-up assessments, none of the LA parameters (LAD, LAVI, LASr, LAScd, LASct, LASt, E, or E/e') showed significant alterations in patients on maintenance dialysis (P>0.05 for all). At the 12-month follow-up, the KT group exhibited significantly better LA function and lower LASt compared with the dialysis group at follow-up, with transplant recipients having significantly higher LASr (42.9%±13.74% vs. 36.1%±13.92%); and LAScd (25.3%±7.99% vs. 20.1%±10.16%), significantly lower LASt (0.25±0.14 vs. 0.40±0.29), and lower E/e' (8.9±3.8 vs. 10.8±4.9). There were no significant differences in E, LAD, LAVI, or LASct between the two groups. After adjustments were made for confounding factors such as SBP, hemoglobin, dialysis modality, and LVGLS, LASr, LAScd, LASt, and E/e' in the KT group remained significantly superior to those in the dialysis group (Figure 4). At follow-up, SBP and DBP in the KT group were significantly lower than their own pre-transplant baseline levels. Additionally, these blood pressure indices in the KT group also differed significantly from those in the dialysis group at the same follow-up time point. The heart rate in the post-KT group was lower than that in the pre-KT group, but there was no significant difference compared with the follow-up dialysis group.

Figure 4 Bar graphs comparing LA parameters between the KT and dialysis groups. Parameters include mitral valve E peak, mitral E/e', LAD, LAVI, LASr, LAScd, LASct, and LASt. P* denotes P values after adjustment for confounding factors. KT, kidney transplantation; LA, left atrial; LAD, left atrial diameter; LAScd, left atrial conduit strain; LASct, left atrial contractile strain; LASr, left atrial reservoir strain; LASt, left atrial stiffness; LAVI, left atrial volume index.

Detailed adjusted P values are presented in Tables 1-4, statistical significance thresholds (P<0.05) are specified in the “Statistical analysis” section of the Methods.

Discussion

In this study, 2D-STE was used to evaluate LA remodeling after KT, with the principal findings being the following: (I) at 12 months after KT, patients showed significant improvements in LASr and LAScd, while no significant changes were observed in LA VI, LASct, or LASt. (II) At the 12-month follow-up, the KT group exhibited significantly better LA function (higher LASr and LAScd) and lower LASt than did the dialysis group. After adjustments were made for confounding factors, LASr, LAScd, and LASt in the KT group remained significantly superior to those in the dialysis group, but there were no differences in LAVI or LASct between the two groups. (III) At baseline, the KT group already demonstrated better LA conduit function (higher LAScd) and lower LASt than did the dialysis group and successfully maintained this advantage at 12 months postoperation.

All patients with ESRD enrolled in this study had CKD stage 5, characterized by persistent hemodynamic overload, accumulation of uremic toxins, and ionic homeostasis disorders (21). These factors promote myocardial remodeling and LVH, leading to LV systolic and diastolic dysfunction and ultimately progressing to heart failure and sudden cardiac death (22). The LA plays a key role in the pathophysiology of heart failure, and its functional and structural changes significantly affect cardiovascular morbidity and mortality in patients with diastolic dysfunction (6). LA enlargement and functional decline in patients with ESRD are mainly driven by LVH, diastolic dysfunction, and volume overload. These factors increase LV filling pressure and afterload, prompting LA dilation. Long-term high pressure not only causes dilation but also impairs LA compliance, blood storage, and contractile function, often being accompanied by fibrosis and myocardial cell hypertrophy, further damaging function. Numerous studies have demonstrated that successful KT can reverse LVH and improve LV function (23-27). However, the literature on LA remodeling after KT is inconsistent. Hewing et al. (26) examined 31 KT recipients and found that no significant changes occurred in LA reservoir, conduit, or contractile function parameters as assessed by STE after successful KT. In contrast, a prospective cohort study of 143 KT recipients found that LAVI significantly decreased at 12 and 24 months after KT (27).

In our study, longitudinal analysis indicated significant improvements in LA function at 12 months after KT, as evidenced by marked increases in LASr and LAScd, while no significant changes were observed in LAVI, LASct, or LASt. Our findings align partly with those reported by Hewing et al., who noted no changes in LA functional parameters. The lack of significant reduction in LAVI in their study may also indicate partial irreversibility of structural remodeling, as long-term ESRD-related atrial fibrosis is difficult to fully reverse after KT. Additionally, the 12-month observation period in our study may be insufficient for detecting significant reductions in LAVI, which could also be attributed to differences in sample size, baseline patient characteristics (the degree of baseline LA remodeling), measured LA parameters, and imaging techniques. LASct, which reflects the active contractile and pumping capacity of the LA, showed no significant improvement, potentially due to structural changes in the atrium itself or factors such as autonomic nervous regulation, making it relatively insensitive to the hemodynamic improvements induced by KT. The lack of significant changes in LASt similarly suggests the persistence of underlying structural alterations. Cross-sectional comparisons revealed that the KT group, as compared to the dialysis group, had significantly higher LASr and LAScd but lower LASt. This indicates that successful KT can effectively improve LA reservoir and conduit functions, delaying atrial remodeling and the progression of stiffness. These benefits arise from reduced volume load, clearance of uremic toxins, and optimized hemodynamics, which in turn improve overall hemodynamic status and LV structure and function. Notably, no differences in LAVI or LASct were observed either between groups or across time points—findings that further support the irreversibility of structural remodeling and its relative resistance to intervention. This also reflects the contradiction between the immediate improvement in hemodynamics and the lag in structural remodeling. Previous studies have suggested that LA volume is a surrogate marker for the chronicity and severity of LVDD, but LA volume alone is not a sensitive biomarker in the early stages of LVDD, as LA structural remodeling may require time to develop. Since the primary function of the LA is to regulate LV filling, it is not surprising that functional LA changes become evident in the earliest stages of LVDD (28). Although reduced volume load and clearance of uremic toxins after KT can rapidly lower LV filling pressure and reduce LA afterload, the myocardial fibrosis induced by long-term ESRD can only be reversed after a lengthy period of time. Persistence of structural stiffness limits the significance of longitudinal changes, an assertion consistent with Huang et al.’s CMR study, which found no changes in LA structural indicators at 1 year after KT. It should be noted we did not assess intravascular congestion markers (right atrial diameter, RV dimensions, pulmonary artery pressure, or inferior vena cava collapsibility). These limited our ability to fully determine whether LA function improvement post-KT stems from alleviated LV mechanical impairment or reduced congestion; nonetheless, our core conclusion (i.e., KT provides better improvement of LA function than does dialysis) remains valid, as supported by the sensitivity 2D-STE and multivariate adjustment. As Zeder et al. (29) and Wang et al. (30) have noted, capturing all cardiopulmonary indices in ESRD studies is challenging, and our focus on LA function addresses a deficiency in most KT studies, whose focus has mainly been LV. Future studies adding right ventricular or pulmonary artery pressure indices can help clarify the relevant mechanisms, yet the results from this study nonetheless provide novel evidence for KT’s LA-protective role. Additionally, posttransplant immunosuppressive agents may exert adverse effects. Calcineurin inhibitors, which form the cornerstone of post-KT immunosuppressive protocols, are known to stimulate collagen deposition via activation of the TGF-β signaling pathway (31). A similar mechanism could operate within the myocardium, impeding the reversal of LASt and potentially counteracting, at least in part, the hemodynamic benefits conferred by transplantation.

The comparison of baseline characteristics in our study showed that patients in the KT group were younger and had shorter dialysis duration, more stable blood pressure, and milder anemia. This may reflect that patients eligible for KT typically have slower disease progression, better physical reserve, and more active nutritional support and anemia management while awaiting transplantation. The lower baseline cardiovascular risk profile among patients in the KT group also accounts for the less severe manifestations of adverse cardiac remodeling, including better LAScd and lower LASt at baseline. Meanwhile, this study found that both groups had a high prevalence of hypertension at baseline, with no significant difference in antihypertensive medication use. At 12-month follow-up, the KT group had a more significant decrease in SBP and DBP than did the dialysis group, which may be related to the improvement of renal function after KT (reduced sodium and water retention) and a corresponding reduction in antihypertensive medication dosage in some patients. Previous studies have shown that effective blood pressure control can reduce LA pressure load, thereby improving LA reservoir and conduit function (32). Therefore, the more obvious blood pressure reduction in the KT group may be one of the factors contributing to the improvement of LASr and LAScd. However, after adjustments were made for baseline SBP in the multivariate linear regression model, the KT group still had significantly better LASr, LAScd, and LASt than the dialysis group, suggesting that the improvement in LA function after KT is not solely driven by blood pressure changes and also involves other mechanisms such as the clearance of uremic toxins and the alleviation of volume overload. In terms of heart rate, there was no significant difference between the two groups at follow-up, and heart rate changes had little impact on LA strain parameters, as LA strain is more preload-dependent (33). In this study, although the proportion of baseline dialysis modalities (hemodialysis/peritoneal dialysis) between the KT group and the dialysis group was matched, there remained slight differences, which potentially exerted an impact on the evaluation of LA function. Hemodialysis achieves volume control through rapid ultrafiltration, which often leads to sudden changes in LV preload. In the long term, it can increase LA pressure load and aggravate the increase of LASt. Moreover, intradialytic hypotension, oxidative stress, and inflammatory reactions may further damage LA compliance (34). Peritoneal dialysis maintains a more stable volume state through continuous low-intensity ultrafiltration, which theoretically has a less acute impact on LA load. However, long-term use of high-glucose dialysate may promote myocardial fibrosis through the accumulation of advanced glycation end products, offsetting its advantages (35). In this study, the proportion of patients undergoing hemodialysis at baseline in the KT group was slightly higher than that in the dialysis group. Notably, patients in the KT group still exhibited superior LAScd—a finding that may be attributed to stricter volume management and shorter dialysis durations among transplant candidates. During the follow-up period, after the KT group were weaned off hemodialysis, the improvement of LASr and LAScd was more significant, indirectly indicating the protective benefit of avoiding the acute load of hemodialysis. Future subgroup analyses are needed to clarify the independent impact of different dialysis modalities on LA remodeling so as to provide a reference for pretransplant dialysis management.

The study results further confirmed that compared with maintenance dialysis, KT significantly improves LA function. Even after adjustments were made for baseline confounding factors, LA function in the KT group remained significantly superior to that in the dialysis group. This persistent difference indicates that the recovery of LA function is independent of hemodynamic confounding factors, and the improvements in LASr and LAScd directly reflect the reversal of the negative effects of uremic toxicity on myocardial mechanics. However, caution is advised in interpreting these statistically significant differences in terms of their clinical relevance. Despite statistical significance, the absolute mean differences in the parameters between the two groups were relatively small. Moreover, large standard deviations for all parameters suggest high interindividual variability and a substantial data overlap between groups. Given high interindividual variability and substantial between-group data overlap, these findings suggest that while a positive trend may exist at the population level, individual measurements of parameters (e.g., a single LASr value) have limited utility for distinguishing transplant recipients from dialysis patients. For example, a patient with an LASt of 0.3 could be either a well-functioning dialysis patient or a poorly functioning transplant recipient. Thus, these parameters have limited practical value for individual patient classification or single-point clinical decision-making. Further supporting this conclusion is the fact that LASt, as the most robust biomarker, is resistant to interference from confounding factors. The significant decrease in LASt observed in this study comprehensively reflects the improvement in diastolic function, highlighting LASt’s potential as a sensitive indicator for cardiovascular risk stratification in patients with ESRD. Kurt et al. (36) were the first to propose and validate a noninvasive method for measuring LASt. They compared data from 64 patients who underwent echocardiography and right heart catheterization with those from 27 controls and found that although asymptomatic hypertensive patients with LVH and patients with diastolic heart failure (DHF) with normal LVEF showed no differences in LV mass, LA volume, or LA contractile function, DHF patients exhibited reduced LA strain and strain rate accompanied by increased LASt. LASt has been proven to have prognostic value in predicting cardiac events such as atrial fibrillation and heart failure (37,38).

Our study demonstrates that KT is associated with improved LA function, particularly reduced stiffness as compared to maintenance dialysis over 12 months. However, the observed improvements were based on surrogate echocardiographic endpoints. A key unanswered question is whether these favorable changes translate into meaningful long-term clinical benefits, such as reduced incidence of heart failure hospitalization, atrial fibrillation, or cardiovascular death. Since LA dysfunction is a known predictor of adverse outcomes, larger prospective studies with long-term follow-up are needed to determine if the improvement in LA parameters, especially LASt, can serve as noninvasive biomarkers for risk stratification and intervention assessment in the population with ESRD.

Limitations

This study involved several limitations that should be acknowledged. First, the inherent variability and substantial overlap in LA strain and stiffness measurements limit their utility for individualized patient-level interpretation, despite their showing significant group-level differences. Second, the timing of ECGs relative to dialysis sessions, while aimed at a stable state, might not have been perfectly uniform, potentially introducing variability in volume-sensitive parameters within the dialysis group and at baseline for the transplant group. Third, we did not systematically record posttransplant immunosuppressive regimens or record the key parameters related to systemic volume overload and right heart function (e.g., pulmonary artery pressure and inferior vena cava collapsibility), nor did we systematically record posttransplant immunosuppressive regimens (e.g., glucocorticoids and calcineurin inhibitors). The absence of this data limited our ability to account for the influence of cardiotoxic immunosuppressants or to more comprehensively examine the mechanisms underlying the functional improvement. Finally, the use of cross-sectional group comparisons at 12 months rather than a repeated-measures analysis of variance precluded a formal analysis of the group-by-time interaction effect; thus, we were able to demonstrate a difference at the endpoint but not a statistically distinct trajectory of change.

Conclusions

This study confirmed that KT significantly improves LA function in patients with ESRD as compared with maintenance dialysis. Its core benefits include improved LASr and LAScd and the maintenance of a lower LASt to prevent deterioration to levels in patients on dialysis. However, KT has limited influence on LA structure and active contractile function. Our findings highlight KT’s unique value in protecting LA function and delaying myocardial stiffness progression, offering new insights into its cardiovascular protective mechanisms.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1613/rc

Data Sharing Statement: Available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1613/dss

Funding: This study was supported by the Special Fund Project for Scientific Research of Postgraduate Tutors in Hospitals in 2021 (No. EFYKY2021003).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1613/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The Second Affiliated Hospital of Guangxi Medical University (No. 2024-KY-0679) with written informed consent obtained from all participants.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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