Saudi Journal of Kidney Diseases and Transplantation

: 2020  |  Volume : 31  |  Issue : 4  |  Page : 750--758

Echocardiographic Evaluation of Left Atrial Volume Index in Patients with Chronic Kidney Disease

Syed Rizwan Bokhari1, Abeera Mansur2, Muhammad Zaman Khan Assir3, Afshan Ittifaq2, Shahbaz Sarwar2,  
1 Department of Nephrology, Tulane University, New Orleans, Louisiana, USA
2 Department of Nephrology, Doctors Hospital and Medical Center, Lahore, Pakistan
3 Department of Nephrology, Allama Iqbal Medical College, Lahore, Pakistan

Correspondence Address:
Abeera Mansur
Department of Nephrology, Doctors Hospital and Medical Center, Lahore


Chronic kidney disease (CKD) patients are at high risk of developing cardio vascular disease. Left atrial volume index (LAVi) is an indicator of left ventricular diastolic dysfunction. We conducted this study to find out the correlation of LAVi and other echocardio- graphic parameters with estimated glomerular filtration rate (eGFR). We prospectively enrolled 170 individuals: 69 patients with CKD and 101 controls. Echocardiographic parameters including systolic and diastolic volumes of left ventricle, LAVi, ejection fraction (EF), pulmonary artery systolic pressure (PASP), and E/e ratio were measured in all participants. The demographic, clinical, and echocardiographic parameters were examined. From the total of 170 individuals, 69 (40.5%) patients had CKD and 101 (59.5%) had normal renal profile. There were 38 (55.07%) males in the CKD group and 71 (70.29%) in the control group. Patients with CKD had higher median LAVi [33.33 mL/m2 ± 11.71 vs. 22.54 mL/m2 ± 5.82; P < 0.001], higher median E/e ratio [10.41 ± 6.28 vs. 7.48 ± 2.28; P < 0.001], higher median PASP [42.47 ± 13.64 vs. 33.59 ± 12.51; P < 0.001], and lower median EF [52.79% ± 14.37 vs. 60.7% ± 8; P < 0.001]. There was a statistically significant negative correlation of eGFR with LAVi (r = -0.515, P < 0.001), PASP (r = -0.44, P = 0.001), and E/e ratio (r = -0.331, P = 0.001). Patients with CKD have higher LAVi, PASP, and E/e ratio and lower EF as compared to individuals without CKD. There is a significant negative correlation between eGFR and LAVi.

How to cite this article:
Bokhari SR, Mansur A, Khan Assir MZ, Ittifaq A, Sarwar S. Echocardiographic Evaluation of Left Atrial Volume Index in Patients with Chronic Kidney Disease.Saudi J Kidney Dis Transpl 2020;31:750-758

How to cite this URL:
Bokhari SR, Mansur A, Khan Assir MZ, Ittifaq A, Sarwar S. Echocardiographic Evaluation of Left Atrial Volume Index in Patients with Chronic Kidney Disease. Saudi J Kidney Dis Transpl [serial online] 2020 [cited 2023 Feb 8 ];31:750-758
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Full Text


Patients with chronic kidney disease (CKD) are prone to premature cardiovascular diseases.[1] The left atrium (LA) is taken as a crucial risk indicator, as its physiology is closely linked with left ventricular (LV) filling and performance. The LA acts as a reservoir to collect the pulmonary venous return and also as a conduit for the passage of stored oxygenated blood to the LV during the early diastolic phase of the cardiac cycle.

Recent studies and guidelines[2] suggest that left atrial volume (LAV) measurements provide clinically relevant data about other cardiac parameters, and increased levels of LAV and LAV index (LAVi) are significantly associated with increased risks of cardiovascular events.[3] The major causes for increased LAV include volume overload, atrial fibrillation, and impaired left ventricular systolic and diastolic function.[4]

Echocardiography has the utmost importance in foreseeing the risk of developing cardiovascular complications in patients, as well as to guide timely treatment.[5],[6],[7] Various LA and ventricular structural and functional abnormalities, i.e., LA dilatation (LAD), left ventricular dilatation (LVD), left ventricular hypertrophy (LVH), and left ventricular systolic dysfunction (LVSD), have been identified using echocardiography in ESRD patients and are termed as uremic cardiomyopathies. These confer poorer prognosis independently in these patients.[8],[9] Increased LAVi is observed very commonly in patients with CKD. Two previous studies by Gardin et al[10] and Ristow et al[11] express that LAD [corrected in relation with body surface area (BSA)] assessment, using echocardiography as a diagnostic tool, is itself an independent predictor of mortality not only in patients with CKD and hypertension (HTN) but in the general population as well.

We can use multiple diagnostic tools to measure different cardiac parameters, i.e., echocardiography and cardiovascular magnetic resonance imaging (CMR). CMR imaging is a reliable, authentic, and reproducible tool for the measurement of LAV using biplane area- length method.[2],[12] CMR provides both volume- dependent and volume-independent measurements of atrial and ventricular structure and is taken as the most precise method for the assessment of cardiac dimensions in patients with early stages of CKD as well as CKD stage 5.[13],[14] We have used echocardiography to measure LAVs and LAVi in our study.

The aim of this study was to find out the changes in cardiac parameters, particularly the increased LAVi in patients with CKD, using echocardiography, and to compare the results with the previously established echocardiographic parameters.


We enrolled 170 patients including case and control groups in this prospective single- centered case–control study conducted over a period of one year (from April 2015 to March 2016) at the Departments of Nephrology, Cardiology, and HTN at Doctors Hospital and Medical Centre, Lahore, Pakistan, in collaboration with a consultant cardiologist performing echocardiography of the enrolled patients. The grouping of the patients was done as follows:

  1. Control group (n = 101): This group consisted of 101 patients with glomerular filtration rate (GFR) more than 60 mL/min and no echocardiographic abnormality
  2. Study group (n = 69): This group consisted of 69 patients with CKD. CKD patients were identified using GFR, estimated by an equation developed by the CKD-Epidemiology collaboration.

The exclusion criteria for both control and study groups consisted of the following:

  • Valve lesions (mitral stenosis or mitral regurgitation)
  • Atrial fibrillation and atrial flutter
  • Bundle branch block (left)
  • Intracardiac shunt
  • LV ejection fraction (LVEF) ≤35%
  • Any history of congestive cardiac failure that required hospitalization or ultra- filtration[15]
  • Unclear acoustic window.

The study protocol was approved by the ethical review board, and informed written consent was obtained from all the patients enrolled in the study. Baseline demographic data regarding age; gender; smoking; previous hospitalization and clinical data about HTN, diabetes mellitus (DM), ischemic heart disease (IHD), dyslipidemia, and CKD were obtained using a self-administered and ethically approved questionnaire for each individual included in the present study. The complete and thorough analysis of all the individuals was done by:

• Echocardiographic examination

Left atrium Measurements

The study patients underwent echocardio- graphy, using Toshiba, Aplio 300 system, Model TUS-A300. All patients were examined in the left lateral position. Transthoracic echo (TTE) is the recommended approach for assessing LA size and it was used in our study. Transesophageal echo was not used because the entire LA frequently cannot fit into the image sector. LA size is measured at the end of LV systole, when the LA chamber is at its greatest dimension. Care was taken to avoid foreshortening of the LA. Acquisition of the LA from the apical approach was done. Care was taken to have the base of the LA at its largest size so that the imaging plane passes through the maximal short-axis area. LA length was also maximized to ensure alignment along the true long axis of the LA. The lengths of the long axes measured in the two and four- chamber views were almost similar. When tracing the borders of the LA, the confluences of the pulmonary veins and the LA appendage were excluded. The atrioventricular interface was represented by the mitral annulus plane and not by the tip of the mitral leaflets. LA volume is measured using the disc summation method.[16] The LA endocardial borders were traced in both the apical four- and two-chamber views. Gender differences in LA size were accounted for by indexing to BSA.

LAV was taken as the volume of blood in the LA at the end of the systole, just prior to the opening of mitral valve. Standardized planimetry was used to trace the borders of the LA and LV. LAVi was computed by dividing the LAV by the BSA of the individuals, as shown by the following formula:

LAVi = LAV (mL)/BSA (m2)

• Left ventricular measurements: TTE in the left lateral decubitus position was performed in all the participants enrolled in the present study. LVEF was calculated as the difference of volumes in the LV during systolic and diastolic phases of cardiac cycle, by using apical four- and two-chamber views. LV volume is measured to calculate the EF. LV volumes are measured using two-dimensional (2D) echo (2DE). Volume calculations derived from linear measurements may be inaccurate because they rely on the assumption of a fixed geometric LV shape such as a prolate ellipsoid, which does not apply in a variety of situations. Volumetric measurements are based on tracings of the interface between the compacted myocardium and the LV cavity. At the mitral valve level, the contour is closed by connecting the two opposite sections of the mitral ring with a straight line. LV length is defined as the distance between the bisector of this line and the apical point of the LV contour, which is most distant to it. The longer LV length between the apical two- and four-chamber views is used, which is recommended. LV volumes are measured from the apical four- and two-chamber views. 2D echo- cardiographic image acquisition is aimed to maximize LV areas, while avoiding foreshortening of the LV, which can result in volume underestimation. The method used for 2D echocardiographic volume calculations is the biplane method of disc summation (modified Simpson’s rule), which is the recommended 2D echocardio- graphic method. EF is calculated from EDV and ESV estimates, using the following formula: LVEF = EDV–ESV/EDV χ 100

LV volume estimates are derived from 2DE, as described above. The biplane method of discs (modified Simpson’s rule) is the currently recommended 2D method to assess LV EF by consensus and is used in our study protocol.[17]

Other parameters computed from the echo- cardiography were mitral regurgitation, LVH, E/e ratio, and pulmo-nary artery systolic pressure (PASP).

 Statistical Analysis

All the data generated were entered and analyzed by using IBM SPSS Statistics 20.0 software (IBM Corp., Armonk, NY, USA). Data were expressed as mean ± standard deviation (SD) for different parameters. Quantitative variables were expressed as mean ± SD, whereas qualitative variables were expressed with numbers and percentages. Comparison of various cardiac parameters in both the control and study groups was done by “unpaired Student’s /-test.” Linear regression analysis was done to predict the effect on LAVi caused by decreasing GFR. Degree of freedom and P values were also obtained. The results of P values for different parameters were expressed as follows:

  • P > 0.05 = not significant
  • P < 0.05 = significant
  • P ≤ 0.001 = highly significant.

Confidentiality of all the patients was maintained at each step. Informed consent was obtained from all the participants regarding use and publication of data obtained from them. All the patients were referred to a cardiologist for the best possible management regarding changes in cardiac parameters occurring in them.


The study comprised of 170 individuals, of which 69 40.6%) patients had CKD and 101 (59.4%) patients had normal renal profile. Among the CKD patients (GFR > 60 mL/min), 39 (56.5%) (were male and 30 were female (43.5%). There were 101 individuals with GFR > 60 mL/min, of which 73 were male (72.3%) and 30 were female (27.7%). The mean age of the patients with CKD was 40.92 ± 17.03 and 65.29 ± 11.99 years in the control group.

HTN was seen in 15 (14.8%) in the control group vs 46 (66.6%) in the study group (P < 0.001). DM was found in 14 (13.8%) in the control group vs 35 (50.7%) in the study group (P < 0.001) and IHD was present in 14 (13.8%) in the control group vs 32 (46.4%) (P < 0.001), mean GFR was 106.77 mL/min ± 21.29) in the control group vs (28.88 mL/ min ± 17.42) in the study groups (P < 0.001. The baseline demographic data are summarized in [Table 1].{Table 1}

We compared the means of different echo- cardiographic parameters among patients with GFR > 60 mL/min and the individuals in the control group with GFR > 60 mL/min using unpaired Student’s /-test [Table 2]. It showed that patients with GFR <60 mL/min had higher mean ± SD of the studied echocardiographic parameters with a statistically significant P < 0.001 as compared to the individuals with GFR > 60 mL/min. The study patients had higher mean for LAVi (33.23 ± 11.71) as compared to control group (22.51 ± 5.82; P < 0.001), lower mean EF (52.79 ± 14.37 vs. 60.71 ±8; P < 0.001), higher mean for E/e ratio (10.34 ± 6.2 vs. 7.45 ± 2.27; P < 0.001), and higher mean for PASP (42.47 ± 13.6 vs. 33.59 ± 12.51; P < 0.001).{Table 2}

The correlation between variables was examined by Pearson’s correlation coefficient. Correlation of GFR was done with LAVi, EF, E/e ratio, and PASP. A lower GFR correlated [Table 3]; negatively with LAVi (r = -0.515) P < 0.001, positively with EF (r = +0.381) P < 0.001). In addition there was negative correlation with E/e ratio (-0.331) P < 0.001, negative correlation with PASP (r = -0.44) P < 0.001{Table 3}

After fulfilling all the regression assumptions and requirements, a linear regression analysis was run. GFR was taken as a dependent variable, and regression analysis was run with LAVi values. The following linear regression model was used to interpret the results:

Y = α + β χ X + e

where Y = dependent variable, X = independent variable, α = y-intercept, β = slope of the line, and e = error. The result show a negative value of Beta (-0.515); P < 0.001, which supports our data, that with the decrease in GFR in patients with CKD, there is a significant increase in LAVi, which concludes that there is a significant negative correlation between estimated GFR (eGFR) and LAVi [Figure 1].{Figure 1}

It was also shown that LAVi value increased progressively with a higher CKD stages [Figure 2].{Figure 2}


It is proven by previous studies that premature cardiovascular abnormalities are more common among patients with CKD ire- spective of the stage as compared to normal healthy population.[1] In earlier studies, researchers used to predict the risk of cardiovascular events in hemodialysis patients by primarily focusing on the left ventricular characteristics, i.e., LVH[18] and LV systolic dysfunction.[19] LVH is also a very commonly occurring cardiac change in patients with CKD, approximately present in 70% of patients,[20] and it is considered the most common change associated with uremic cardiomyopathies leading to higher LAVi. It can independently lead to cardiac failure, sudden cardiac arrest, arrhythmias, and death, not only in patients with CKD receiving hemodialysis but also in healthy individuals.[9],[16] Recent studies have emphasized that LA dilatation is represented by LAVi, measured by 2D echocardiography, and is directly related to the duration of the left ventricular dysfunction.[21] LAVI, in addition to LA and left ventricular strain measurements, is a reliable indicator of involvement of myocardium in CKD patients. Fibrosis of myocardium in CKD can be attributed to renin–angiotensin-aldosterone system activation inrelation to changes in LA dimensions in CKD patients.[22]

We have evaluated diastolic function in all our patients by using four parameters (2016 Guidelines), and LAVi is one of the parameters. By using LAVi alone, we are utilizing an anatomical parameter which would be less effected by loading conditions.[23] LAVi correlates better with all-cause mortality.[11] Against this background knowledge from previous studies, we prospectively assessed the direct correlation between the renal and cardiac parameters, specifically the LAVi. In our study, we observed a higher mean LAVi (33.33 ± 11.71 mL/m2) in patients with GFR <60 mL/min as compared to lower mean LAVi (22.54 ± 5.82) in the control group. Increased LAVi in our study reflects the long-term effects of increased left ventricular filling pressure and chronic volume overload that is quite comparable with the studies conducted previously by Simek et al[21] and Tsang et al,[24] showing results similar to our study. A study conducted by Tripepi et al[25] concluded that LAVi was higher in patients undergoing hemodialysis than that in healthy individuals of same age and gender. They also pointed out that LA size is largely correlated with the underlying LVH and systolic dysfunction.[25] This provides us the information that the echocardiographic assessment of LA not only provides us information about the anatomic changes that may help in the prediction and interpretation of cardiomyopathies (uremic cardiomyopathies) in CKD patients but also may prove beneficial in risk stratification and prognosis.[26]

The present study indicates that the increased levels of LAVi and LAV are inversely proportional to the GFR values (negative correlation, r = -0.515) in the study group. LAVi and LAV measured by echocardiography are markedly increased in CKD Stages 3–5 with decreased GFR, which independently predict the incidence of other cardiovascular events in patients with CKD. LA enlargement is generally overlooked in complex echocardiogra- phic evaluation of altered cardiac parameters in CKD patients. eGFR also showed a negative correlation with PASP (r = -0.44) and E/e ratio (r = -0.33). Moreover, LAVi is considered the most stable indicator of diastolic function, and it explains that it is productively superior over E/e ratio but very sensitive to acute changes in preload.[27],[28] E/e ratio is considered the most accurate and reliable noninvasive cardiac parameter for estimating end-diastolic left ventricular pressure.[27],[28]

After fulfilling all the assumptions of regression analysis, a linear regression analysis was done between GFR and LAVi. It showed an inverse relationship between these two variables pointing that with the significant decrease in GFR, there is a sufficient volume overload that increases the LAVi proportionately.

It is still not clear that whether the changes in LAV specifically have any prognostic significance in patients with CKD. This uncertainty is due to the fact that factors affecting LAV, i.e., extracellular volume overload, valvular heart diseases, and changes in left ventricular mass (LVM), are very common in patients undergoing dialysis. These parameters may be modified by drug therapy or dialysis. Thus, identifying whether the changes in LAV has a relationship with death and cardiovascular complications and if these associations are independent of ongoing changes in LVM and LV function, is a significant question that can be of clinical significance in CKD or ESRD patients. In one study of 49 CKD (3–5) patients, LAVi was significantly larger in the CKD group and was a predictor of adverse cardiac events. In addition, patients with LAVi > 32 mL/m2 had significantly lower event-free survival than patients with normal (<28 mL/ m2) or mildly dilated LAVi (28–32 mL/m2).[29] In another abstract presented by our department at the American Society of Nephrology meeting in 2018, unadjusted logistic regression analysis revealed that cardiovascular mortality in dialysis patients correlated with a higher LAVi. LA volume emerged as the only echocardiographic index independently associated with mortality in a low-risk dialysis population in whom strict volume control was achieved by dietary salt restriction.[30]

Tripepi et al[25] demonstrated that increase in LA volume predicts cardiovascular events in dialysis patients, independent of baseline LA volume or LV mass.

Future studies, with larger number of patients, including both CKD Stages 3–5 and CKD 5D and adjusting for other clinical and echocardiographic parameters, are warranted.


Although the mean LAVi was higher in the study population, it was less than the cutoff value of 34 ml/m2 proposed by the European Society of Cardiology.[3] However, in a study evaluating mean LAVi in healthy patients, the mean LAVi was 21.96 ± 4.189 mL/m2.[31] This is slightly lower than the mean LAVi found in the control group in this study, which also included CKD Stages 1 and 2. Thus, in our population, the cutoff of normal LAVi may be lower.

Although CMR provides better volume- dependent and volume-independent measurements of atrial and ventricular structure, we did not use it due to financial constraints.


It is concluded that LA enlargement is highly associated with the LA dysfunction, resulting in higher LAVi in patients with CKD Stages 3-5. We also postulate that in CKD patients, the increased LAVi and LAV are highly associated with chronic volume overload due to expansion in intravascular volume in all the stages of CKD. Patients with CKD have higher LAVi, PASP, and E/e ratio and lower EF as compared to individuals without CKD. There is a significant negative correlation between eGFR and LAVi. LA serial monitoring should be added in echocardiographic parameters that may help in refining risk stratification in CKD patients.

Conflict of interest: None declared.


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