Objectives: Kidney transplant has been associated with improvements in cardiac function in patients with chronic renal failure, particularly those with clinical overload. This study aimed to assess the effect of kidney transplant on echocardiographic parameters among a group of patients with established cardiac stress.
Materials and Methods: Among 26 patients evaluated before and after kidney transplant, average age was 46.42 years. Eleven patients had fistula, and the remaining patients had other access. Echocardiographic measures, including left ventricular end-diastolic volume index, left ventricular hypertrophy, inferior vena cava collapse, and right ventricular function, were assessed. We used paired t tests to analyze changes before and after transplant.
Results: After kidney transplant, a significant decrease was observed in average left ventricular end-diastolic volume index (P = .⁰⁰²) and in left ventricular hypertrophy thickness (P < .⁰⁰¹). In addition, significant changes were observed in ejection fraction and left ventricular diameter. The left atrial volume index (P = .⁰⁰²), left atrial volume (P = .⁰⁰⁹), and size of the right ventricle (P = .⁰⁴⁶) all decreased significantly after transplant.
Conclusions: Kidney transplant significantly improved left ventricular volume and hypertrophy in patients with cardiac overload, although its effects on right ventricular and valvular function were less pronounced.

Key words : Cardiac function, Echocardiography, Left ventricular hypertrophy, Renal transplantation

Introduction
Chronic kidney diseases (CKD) are among the most prevalent health conditions worldwide and substantially impair the quality of life of patients.¹ Because renal function progressively declines in advanced stages of CKD, the kidneys lose their ability to maintain fluid and metabolic homeostasis, necessitating renal replacement therapies such as dialysis or kidney transplantation.² In this context, appropriate vascular access is critical, and the creation of an arteriovenous fistula (AVF) represents the standard method for providing durable access for hemodialysis.³ An AVF is established by surgically connecting a peripheral artery to a vein, permitting high-volume blood flow necessary for efficient dialysis. The use of AVFs as the preferred vascular access modality in patients with kidney failure has substantially improved quality of life and reduced reliance on temporary central venous catheters.⁴ Because AVFs increase peripheral blood flow and reduce the frequency of repeated cannulation procedures, AVFs have become a cornerstone of dialysis care.⁵ However, the creation of an AVF leads to substantial hemodynamic alterations, which may exert detrimental effects on cardiac function that require careful evaluation.⁶ Specifically, AVF formation results in increased cardiac output, expanded circulating blood volume, and subsequent structural cardiac adaptations.^3,7 Over time, these changes may contribute to pathological conditions such as heart failure and left ventricular hypertrophy (LVH). This issue is particularly relevant given the high prevalence of cardiovascular disease among dialysis patients and the need for optimized clinical management.⁸ Cardiovascular morbidity and mortality impose a substantial burden on health care systems, particularly among individuals undergoing dialysis or kidney transplant.⁹ Patients with CKD not only contend with the consequences of renal failure but also have elevated cardiovascular risk due to hemodynamic and metabolic disturbances.¹⁰ Consequently, the assessment of cardiac status and echocardiographic parameters in these patients is of paramount importance.¹¹ Cardiovascular complications are among the most common adverse outcomes in CKD and are strongly associated with increased morbidity and mortality.¹² In patients progressing from early to advanced stages of kidney disease requiring hemodialysis, a variety of structural and functional cardiac abnormalities develop, including LVH, ventricular dilatation with or without hypertrophy, and impaired systolic performance.^13,14 Notably, LVH is observed in more than 75% of patients at the initiation of dialysis, reflecting the substantial cardiovascular load in this population.¹⁵ Left ventricular hypertrophy represents an adaptive form of cardiac remodeling in response to increased hemodynamic stress, driven by conditions such as volume overload, anemia, and AVF creation.¹⁶ These structural and functional changes, compounded by nonhemodynamic factors such as the toxic effects of uremic metabolites, exacerbate cardiovascular dysfunction in patients with CKD. Furthermore, recent studies indicate that both hemodialysis and peritoneal dialysis contribute to the progression of LVH.^17-20 The prevalence of LVH remains high even among kidney transplant recipients, persisting despite apparent control of traditional cardiovascular risk factors.^21-24 Evidence suggests that the presence of an AVF in dialysis-dependent patients induces persistent structural and functional cardiac changes. Although these adaptations may support hemodynamic stability and optimize renal perfusion, the cardiovascular consequences of LVH remain clinically significant.^21-24 Conversely, some researchers argue that, because of potential complications such as infection and other adverse events, AVF closure after transplant may be necessary. Failure to ligate a persistent AVF could perpetuate or even exacerbate cardiac alterations such as hypertrophy and impaired function.^25-30 Despite existing evidence supporting the association between AVF creation and cardiac changes, precise echocardiographic characterization of these alterations remains incomplete. Therefore, the present study aims to comprehensively evaluate structural and functional echocardiographic changes in kidney transplant recipients with functioning AVFs. This investigation seeks to elucidate the cardiac impact of AVFs and contribute robust scientific evidence to current understanding in this domain.

Materials and Methods
This study was designed as a case-control observational investigation to evaluate changes in echocardiographic parameters before and after kidney transplant in patients with end-stage renal disease (ESRD). The study comprised 2 major groups: patients with ESRD who underwent comprehensive echocardiographic evaluation before kidney transplant and were subsequently reevaluated after transplant. Among 26 included patients, each patient was evaluated at 2 time points: before and after transplant. We used purposive (non-random) sampling to select patients. The sample size was determined based on sample size calculation formulas appropriate for case-control studies. The calculation was guided by a significance level (α) of 0.05, statistical power (1-β) of 0.80, and anticipated effect size:

Accordingly, the Z-values for the chosen significance level and power were 1.96 and 0.84, respectively. P1 and P2 represent the expected proportions of the parameter of interest before and after transplant. Based on these calculations and preliminary assumptions, 28 patients were initially selected, with all evaluated in both before and after transplant.

Inclusion and exclusion criteria
Inclusion criteria were as follows: age ≥18 years, absence of peritoneal dialysis, and no documented history of active cardiovascular disease, including left ventricular ejection fraction (EF) of <45% or significant valvular disease. All patients must have been receiving maintenance hemodialysis. Exclusion criteria included development of major cardiovascular events such as myocardial infarction during the study period, active infection at the time of evaluation, and acute graft rejection in transplant recipients.

Echocardiographic assessment
All study patients underwent a comprehensive transthoracic echocardiographic examination before kidney transplant. The echocardiographic protocol included assessment of cardiac chamber dimensions, diastolic function, pulmonary artery pressure, left ventricular mass index, cardiac index, systolic parameters such as EF, and strain measurements (including global longitudinal strain and left atrial strain). For all study patients, we recorded baseline information, including demographics, cardiovascular risk factors, duration of dialysis, medication history, and primary etiology of renal failure. Three months after kidney transplant, provided that none of the exclusion criteria were met (eg, active infection or cardiovascular events), repeat echocardiography was performed using the same protocol. The primary objective of the posttransplant evaluation was to assess the long-term effects of AVF on cardiac structure and function. We compared and analyzed echocardiographic parameters obtained at both time points for each patient.

Statistical analyses
We presented categorical variables as counts and percentages and summarized continuous variables as means and SD for normally distributed data or as medians with interquartile ranges for nonnormal distributions. For comparison of categorical variables between groups, we used the χ2 or the Fisher exact test as appropriate. We made comparisons of continuous variables by using the paired t test for normally distributed data. When data did not meet normality assumptions, we used the Mann-Whitney U test. A 2-tailed P < .⁰⁵ was considered statistically significant. We conducted all analyses with SPSS version 28 (IBM Corp).

Results

Characteristics of study patients
After inclusion and exclusion criteria were applied, a total of 26 patients were enrolled in the study. The mean age of the study population was 46.42 ± 12.46 years, with 18 male (69.2%) and 8 female patients (30.8%). Among the 26 evaluated patients, 11 (44%) had a functioning AVF. Of these 11 AVF patients, 8 (73%) had a fistula in the left arm and 3 (27%) had a fistula in the right arm. Baseline clinical assessments and medication histories indicated that 100% of patients exhibited clinically significant volume overload, reflective of substantial underlying cardiac stress in this cohort. According to functional classification based on the New York Heart Association system, 50.0% of patients were classified as class I, 7.7% as class II, and 30.8% as class I-II. A history of coronary artery disease was present in 7.7% of patients, but most patients had no prior history of chronic heart failure, myocardial infarction, or coronary artery bypass grafting. Among the cohort, 7.7% of patients had previously undergone percutaneous coronary intervention. The prevalence of metabolic and vascular risk factors was also assessed. Diabetes mellitus was present in 23.1% of patients, dyslipidemia in 30.8%, and hypertension in 88.5%. Hemodynamic parameters revealed a mean systolic blood pressure of 137 ± 21 mm Hg and a mean diastolic blood pressure of 81 ± 11 mm Hg. Before dialysis, mean systolic blood pressure and diastolic blood pressure were 125 ± 18 mm Hg and 71 ± 20 mm Hg, respectively, indicating a clinically relevant but managed cardiovascular load in these patients before transplant.

Left ventricular end-diastolic volume index
Table 1 presents paired analysis of left ventricular end-diastolic volume index (LVEDVI) before and after kidney transplant for the study cohort. The mean LVEDVI before transplant was 56.87 ± 15.47. After transplant, mean LVEDVI decreased to 45.66 ± 16.03, indicating a substantial reduction in LVEDVI after intervention. The paired correlation coefficient for pre- and posttransplant LVEDVI was 0.480, which was significant (P = .⁰¹³). Paired t test demonstrated a significant difference in measures before and after transplant, with a mean difference of 11.20 (95% CI, 4.71-17.70) (t[25] = 3.554, P = .⁰⁰²). Effect size estimates indicated a moderate effect of kidney transplant on LVEDVI, with Cohen d = 0.697 and Hedges g = 0.687, suggesting a clinically meaningful impact. These results indicated that kidney transplant was associated with a statistically and clinically significant reduction in LVEDVI in the study cohort (Figure 1). Table 2 compares LVH measurements before and after kidney transplant in the study cohort. Mean LVH index before intervention was 1.092 ± 0.1613, which decreased to 1.021 ± 0.1414 after transplant. This reduction suggested a decrease in LVH following the surgical intervention. The paired correlation coefficient between pre- and posttransplant LVH values was 0.885 and showed a significant relationship (P < .⁰⁰¹). Paired t test analysis revealed a mean difference of 0.0708 (95% confidence interval, 0.0391-0.1025), with t(23) = 4.623 and P < .⁰⁰¹. Effect size estimates demonstrated that kidney transplant had a large effect on LVH reduction, with Cohen d = 0.944 and Hedges g = 0.928, highlighting a clinically meaningful effect of the intervention on cardiac hypertrophy in this patient population. These findings underscored the potentially positive effects of kidney transplant on regression of pathological LVH (Figure 2). A description of the difference between the 2-dimensional (2D) and Simpson methods for calculating left ventricular EF was provided to clarify measurement techniques. In the 2D method, 2D images of the heart from longitudinal or cross-sectional views were used to estimate EF, relying on simplified geometric assumptions. This approach is faster but may be less accurate when the left ventricle has an irregular shape. In contrast, the Simpson biplane method divides the left ventricle into multiple discs in 2 different views (typically the 4-chamber and 2-chamber apical views) and calculates the volume of each disc. This method provides greater accuracy and is generally recommended for more precise EF assessment, especially in ventricles with irregular geometry. Table 3 compares left ventricular EF measured using both the 2D method and the Simpson method before and after kidney transplant. For the 2D method, the mean EF increased from 56.35 ± 3.33 before transplant to 58.46 ± 3.32 after transplant, with significant mean difference of -2.12 (95% CI, -4.00 to -0.23) (t[25] = -2.308, P = .⁰³⁰). The effect size for this change, as indicated by Cohen d = -0.453 and Hedges g = -0.446, reflects a small negative effect (ie, a modest increase in 2D EF posttransplant). For the Simpson method, the mean EF slightly decreased from 64.02 ± 6.17 before transplant to 61.91 ± 10.26 after transplant. However, this difference was not significant, with a mean difference of 2.11 (95% CI, -2.37 to 6.59) (t[25] = 0.971, P = .³⁴¹). Effect size estimates (Cohen d = 0.190, Hedges g = 0.188) indicated a trivial effect, suggesting minimal clinical relevance. These findings indicated that, whereas the 2D EF measurement demonstrated a significant posttransplant increase, EF measured by the Simpson method did not show a significant change. Additional comparisons were made of echocardiographic and hemodynamic parameters before and after transplant. Left atrial volume index significantly decreased after transplant (P = .⁰⁰²), indicating a reduction in left atrial size after transplant. Left atrial strain also significantly decreased (P = .⁰⁰⁹), suggesting changes in atrial deformation properties. The ascending aorta diameter significantly decreased posttransplant (P = .⁰²⁵), potentially reflecting changes in vascular loading conditions. Other parameters, such as cardiac index and E/é ratio, showed no significant differences before and after transplant. Left heart indices before and after kidney transplant were compared for several key parameters (Table 3). The cardiac index showed a mean value of 3.51 ± 1.43 before AVF creation and 3.18 ± 0.75 after transplant. Although a reduction was observed, this change was not significant (P = .¹⁵²), indicating that cardiac index was not meaningfully affected by the intervention and the observed differences may be attributed to other factors. The left atrial volume index, an important parameter for evaluating left atrial pressure and cardiac function, significantly decreased from 30.76 ± 14.91 before transplant to 21.43 ± 5.53 after transplant (P = .⁰⁰²), with mean difference of 9.33 (95% CI, 3.87-14.80), suggesting a positive impact of transplantation on left atrial pressure and volume. The E/é ratio, a surrogate marker of left ventricular filling pressure, showed a slight decrease from 13.32 to 12.24; however, this change was not significant (P = .⁰⁸⁸). Left atrial strain significantly decreased from 42.18 ± 11.42 before transplant to 36.04 ± 8.57 after transplant (P = .⁰⁰⁹). This reduction in atrial strain posttransplant may reflect favorable improvements in left atrial functional properties. The ascending aorta diameter also significantly decreased from 3.23 ± 0.37 to 3.16 ± 0.41 after transplant (P = 0.025), which may reflect subtle, indirect hemodynamic effects of the intervention on vascular structures. Table 4 compares measurements before and after transplant for right ventricle and pulmonary artery measurements. The mean right ventricular dimension significantly decreased from 3.13 ± 0.35 to 3.01 ± 0.33 posttransplant (P = .⁰⁴⁶), with a mean difference of 0.12 (95% CI, 0.00-0.23). This finding was accompanied by a moderate effect size (Cohen d = 0.430), suggesting a clinically relevant improvement in right ventricular morphology posttransplant. Mean tricuspid annular plane systolic excursion increased from 18.83 ± 6.73 to 19.74 ± 7.16 posttransplant; however, this change was not significant (P = .²⁰⁶). Right ventricular systolic motion decreased from 12.81 ± 2.13 to 12.11 ± 2.11 posttransplant, which likewise did not achieve significance (P = .⁰⁷⁰), although it may indicate a trend toward reduced right ventricular systolic excursion posttransplant. Systolic pulmonary artery pressure declined from 32.72 ± 12.64 before transplant to 28.80 ± 6.41 after transplant, but this reduction was not significant (P = .¹³¹), although the finding may hold clinical relevance. Right ventricular strain changed from -22.66 ± 5.84 to -21.29 ± 4.16 (P = .³¹²). Descriptive analysis of right ventricular functional categories demonstrated that most patients who had a “normal” right ventricular function pretransplant remained in the “normal” category posttransplant (24 patients). Only 1 patient transitioned from “normal” to “mild” dysfunction, and 1 patient with a preintervention “mild” dysfunction category improved to “normal” after transplant. These results indicated that right ventricular functional status remained largely stable in most patients, with no significant changes observed. The McNemar-Bowker test revealed no significant difference in the distribution of right ventricular functional categories (normal vs mild) before and after kidney transplant (χ2 = 1.000, degrees of freedom = 2, P = .⁶⁰⁷). This finding suggested that kidney transplant did not significantly influence right ventricular functional status in this cohort. Changes in severity of mitral regurgitation (MR) before and after transplant were evaluated across the categorical levels of “trivial,” “mild,” “mild-to-moderate,” and “moderate.” Among patients with trivial MR pretransplant, 5 patients (19.2%) remained at the same level posttransplant, and 2 patients (7.7%) progressed to mild MR. Among those with mild MR at baseline, 5 patients (19.2%) remained at the same level and 6 patients (23.1%) improved to trivial MR. In addition, 3 patients (11.5%) progressed to mild-to-moderate and 1 patient (3.8%) to moderate MR. For patients initially categorized as mild-to-moderate, 2 remained in the same category and 1 shifted to moderate. However, because of the small sample size, statistical significance could not be calculated, and these findings should be interpreted with caution. Changes in the severity of tricuspid regurgitation (TR) before and after intervention were similarly assessed at levels of “normal,” “mild,” “mild-to-moderate,” and “moderate.” Among patients with mild TR pretransplant, 3 patients (11.5%) improved to normal after transplant, whereas 14 patients (53.8%) remained at the mild level. In addition, 4 patients (15.4%) progressed to mild-to-moderate and 2 patients (7.7%) to moderate TR. Only 1 patient was categorized as moderate TR before intervention and remained at this level posttransplant. Again, because of the limited sample size, statistical significance was not calculated, and these results should be interpreted with caution. Table 5 compares inferior vena cava (IVC) collapse index measurements (in percent) before and after kidney transplant. The mean IVC collapse index increased significantly from 45% ± 12% before transplant to 55% ± 9% after transplant (P = .⁰²⁵). This finding indicated a significant effect of kidney transplant on this vascular parameter.

Discussion
Our results showed that kidney transplant leads to significant improvements in several cardiac parameters in patients with clinically significant volume overload. The LVEDVI was significantly reduced after transplant, indicating improved left ventricular function. Similarly, LVH significantly decreased, highlighting the beneficial effect of kidney transplant on left ventricular mass and overall cardiac workload. Notably, these changes were associated with moderate effect sizes, suggesting clinical relevance. Furthermore, echocardiographic measurements revealed heterogeneous results in ventricular performance after transplant. Although left ventricular EF measured by the 2D method showed a significant increase, no significant change was observed by the Simpson method, indicating potential limitations of simplified geometric assumptions in 2D assessments. Right ventricular parameters, such as size, demonstrated some reduction. Although systolic pulmonary artery pressure decreased, this change was not significant. These trends suggest that kidney transplant may help attenuate certain degrees of right-sided cardiac stress. Unlike pulmonary artery pressure, changes in IVC collapse were appreciable. Evaluation of valvular function demonstrated limited changes in the severity of MR and TR after kidney transplant. Although minor fluctuations in severity categories were observed, no notable pattern of improvement or worsening was detected. This finding may indicate that kidney transplant exerts a minimal effect on valvular regurgitation in this patient population, underscoring the need for continued surveillance and potential adjunctive treatments for managing valvular dysfunction. Significant changes in left heart parameters after kidney transplant appear to result from reductions in hemodynamic stress and improved fluid balance.³¹ In patients with renal failure, a principal contributor to increased cardiac load is elevated fluid volume and increased vascular resistance, which lead to both volume and pressure overload on the heart.³² These conditions progressively contribute to left ventricular dilation and wall thickening, commonly identified as LVH.³³ With restoration of normal renal function after kidney transplant, the body becomes capable of excreting excess fluid and better regulating blood pressure.³⁴ This process results in decreased loads on the left ventricle, leading to reductions in both LVEDVI and wall thickness.³⁵ Consequently, improvements in left ventricular volume and hypertrophy indicators are often seen after transplant.³⁶ From a physiological perspective, improvement in left heart measurements can also be explained by reductions in both preload and afterload.³⁷ Preload refers to the volume of blood entering the left ventricle at end-diastole, and afterload refers to the resistance encountered during ejection from the left ventricle.³⁸ In conditions of renal failure and uremia, both preload and afterload increase due to sodium and water retention and hormonal changes such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, which intensify cardiac stress and load.³⁹ After kidney transplant, as fluid and electrolyte balances normalize, the activity of these systems diminishes and the pressure imposed on the left ventricle decreases. This reduction in pressure and volume load permits gradual restoration toward a more physiologic state, manifested as reductions in LVEDVI and LVH.⁴⁰ Comparisons of our finding with those of Papasotiriou and colleagues showed notable similarities and differences.⁴¹ Our studies both demonstrated significant changes in left ventricular parameters, particularly LVEDVI and LVH after kidney transplant. However, unlike Papasotiriou and colleagues, our results indicated a trend toward improved left ventricular function, with reductions in LVEDD and LVH rather than in left ventricular EF.⁴¹ This discrepancy may be related to the fact that our study did not include a distinct AVF subgroup but instead focused on patients without persistent AVF function. This comparison suggests that the hemodynamic effect of AVF may differ substantially from the cardiac adaptations observed after transplant in patients without functional fistulae, indicating that AVF management in transplant recipients may be necessary to mitigate potential adverse cardiac effects.⁴¹ Our findings and those of Cridlig and colleagues provided insights into the differential cardiac effects of AVF in kidney transplant recipients.⁴² Both our study and the previous study documented significant changes in left ventricular parameters. Cridlig and colleagues identified a significant increase in left ventricular mass index and atrial dimensions, suggesting that a functioning AVF may contribute to hypertrophy and volume overload even in asymptomatic transplant recipients.⁴² In contrast, our study, which did not focus on patients with active AVF, demonstrated reductions in LVH and LVEDVI after transplant, indicating a reversal of cardiac stress. These differences imply that, while kidney transplant may reduce cardiac load in the absence of AVF, persistent hemodynamic burden from AVF may neutralize these beneficial cardiac effects, highlighting the importance of AVF management in optimizing cardiac outcomes in transplant recipients.⁴² In contrast to our study, which focused on the effect of kidney transplantation rather than AVF creation, the study by Stoumpos and colleagues observed distinct cardiac adaptations.⁴³ Our results showed improvements in left ventricular parameters after transplant, including reductions in LVEDVI and LVH.³³ This contrasts with the findings of Stoumpos and colleagues, emphasizing the distinctive hemodynamic consequences of AVF in CKD compared with the cardiac improvements observed after kidney transplantation.⁴³ Whereas AVF creation appears to prompt rapid left ventricular remodeling and increased myocardial mass, our study showed reversal of cardiac stress after restoration of renal function via transplant, suggesting that AVF management posttransplant may warrant special attention to reduce additional cardiac load.⁴³ Compared with our study, the findings of Reddy and colleagues offered important insights into discrepant effects on left and right ventricles in patients undergoing AVF/AVG placement.⁴⁴ Our study noted overall improvements in cardiac parameters, especially left ventricular dimensions, posttransplant without persistent AVF; however, Reddy and colleagues highlighted ongoing hemodynamic load on the right ventricle leading to adverse remodeling and heart failure. This comparison underscores the importance of evaluating differential effects of AVF on both right and left cardiac structures, suggesting that, in transplant recipients, the absence of AVF may allow a more balanced cardiac recovery, whereas continued presence of AVF in patients with ESRD leads to chronic right ventricular overload and related complications.⁴⁴ In contrast to our study reporting significant improvements in left ventricular dimensions and reduced hypertrophy in the absence of functional AVF, Soleimani and colleagues suggested that maintenance of AVF after transplant does not significantly worsen cardiac function.⁴⁵ However, our results indicated a more favorable cardiac remodeling profile without persistent AVF hemodynamic burden, whereas Soleimani and colleagues observed only minor, nonsignificant differences in ventricular dimensions between groups. This comparison implies that, although the presence of AVF may not severely disrupt cardiac outcomes, its absence after transplant may facilitate greater cardiac recovery, supporting potential benefits of monitoring AVF function in transplant recipients.⁴⁵ The limitations of our study included its small sample size, limiting statistical power and challenging subgroup analyses. Because our study was performed at a single center, the findings may not be generalizable to broader populations or diverse health care settings. Reliance on echocardiographic measurements may also vary with operator skill, potentially affecting the accuracy of cardiac assessments, particularly for right ventricular function. Finally, the absence of a control group restricted our ability to attribute the observed changes exclusively to the effects of kidney transplant. Despite these limitations, our study had several strengths, including rigorous cardiac evaluations before and after transplant using multiple validated echocardiographic measures. By focusing on a unique cohort of patients with clinically significant volume overload, this study offered insights into the cardiac benefits of kidney transplant beyond traditional renal outcomes. The moderate to large effect sizes observed in parameters such as LVEDVI and LVH suggested that improvements were not only statistically significant but also clinically meaningful, contributing to the management of cardiac complications in transplant candidates.

Conclusions
Kidney transplant can lead to significant improvements in certain cardiac parameters, particularly left ventricular size and hypertrophy, among patients with clinically significant volume overload. However, the effects on right heart function and valvular performance in our study were less pronounced, underscoring the complexity of cardiovascular management in kidney transplant recipients. These findings highlight the potential of kidney transplant to reduce cardiac stress, although further research is necessary to optimize cardiovascular care posttransplant.