|Year : 2022 | Volume
| Issue : 1 | Page : 17-23
Echocardiographic manifestations in patients on renal replacement therapy and renal transplant recipients
PL Vidya1, Satish Chandra Mishra1, Ananthakrishnan Ramamoorthy1, Arijit Kumar Ghosh1, Priyanka Singh1, Ishan Sharma2, Nitin Bajaj1
1 Department of Cardiology, Army Institute of Cardiothoracic Sciences, Pune, Maharashtra, India
2 Department of Medicine, Indian Naval Hospital Ship Asvini, Mumbai, Maharashtra, India
|Date of Submission||03-Jan-2021|
|Date of Decision||11-Jan-2021|
|Date of Acceptance||20-May-2021|
|Date of Web Publication||21-Jan-2022|
Col (Dr) Nitin Bajaj
Department of Cardiology, Army Institute of Cardiothoracic Sciences, Pune - 411 040, Maharashtra
Source of Support: None, Conflict of Interest: None
Background: Chronic kidney disease (CKD) patients have 20–30 times greater risk of cardiovascular morbidity and mortality. Echocardiography is quintessential in cardiovascular evaluation and monitoring in CKD patients. This study was designed to determine the echocardiographic manifestations in patients on renal replacement therapy (RRT) and recipients of renal transplantation. Materials and Methods: An observational cross-sectional study was undertaken in a tertiary care hospital. All CKD patients on RRT or post renal transplant were included. Patients with known cardiac disease, malignancy were excluded. Demographic details, thorough history, physical examination and 2D echocardiography were performed for the patients. Results: Of the 51 patients, 60% were on dialysis and remaining were post renal transplant recipients. The mean age of study population was 44.16±13.66 years, with 64.7% males. 47% of patients were of age group of 41 years to 60 years. The most common etiology of CKD was hypertension in 16 (31.4%) followed by diabetes in 11 (21.6%). Only 8 patients (15.7%) had normal echocardiograms. LVH (80.4%) was most common abnormality, followed by diastolic dysfunction (74.5%), systolic dysfunction (13.7%), mitral regurgitation (13.7%) and pericardial effusion (5.8%). Around 95.2% had concentric hypertrophy. Diastolic dysfunction was observed in 90.2% and 80.9% of cases with LVH and hypertension respectively and was significantly associated with both (p=0.001, p=0.003 respectively). Conclusions: Left ventricular hypertrophy was the most common abnormality in CKD patients and renal transplant recipients. Diastolic function was affected in majority of patients. Early identification of cardiac abnormalities by echocardiography prior to manifestation of cardiac complications may result in better prognosis for this patient population.
Keywords: Diastolic function, echocardiography, hemodialysis, left ventricular hypertrophy, renal transplant recipients
|How to cite this article:|
Vidya P L, Mishra SC, Ramamoorthy A, Ghosh AK, Singh P, Sharma I, Bajaj N. Echocardiographic manifestations in patients on renal replacement therapy and renal transplant recipients. J Mar Med Soc 2022;24:17-23
|How to cite this URL:|
Vidya P L, Mishra SC, Ramamoorthy A, Ghosh AK, Singh P, Sharma I, Bajaj N. Echocardiographic manifestations in patients on renal replacement therapy and renal transplant recipients. J Mar Med Soc [serial online] 2022 [cited 2022 Oct 4];24:17-23. Available from: https://www.marinemedicalsociety.in/text.asp?2022/24/1/17/336191
| Introduction|| |
Chronic kidney disease (CKD) is a significant health problem worldwide affecting all age groups. Patients with CKD have been shown to have 20–30 times increased risk for cardiovascular morbidity and mortality., Owing to cardiovascular disease development at earlier stages of CKD, more than 70% have left ventricular hypertrophy (LVH) and over 40% of the hemodialysis patients have clinical evidence of coronary artery disease or heart failure, associated with worse prognosis. Conventional echocardiography is a safe and noninvasive diagnostic tool in cardiology used for the evaluation of CKD patients. The present study aims to determine the various echocardiographic abnormalities in CKD patients receiving renal replacement therapy (RRT) and posttransplant recipients.
| Materials and Methods|| |
An observational cross-sectional study was undertaken at the Department of Medicine in a tertiary care hospital setting at western India from October 2016 to September 2017. All individuals of end-stage renal disease on RRT or postrenal transplant were included in the study. Patients with known preexisting heart disease, malignancy, and those who refused consent were excluded. Patient's demographic details, complete history along with physical examination, were carried out. Blood investigations including hemogram, renal function tests, chest X-ray, and electrocardiography were performed in all patients. Two-dimensional echocardiography was done by Esaote, MyLab™ 30Gold Cardiovascular echocardiographic machine in the left lateral position. The following parameters were obtained in all patients.
The fractional shortening (FS) and left ventricular ejection fraction (EF) were taken as measures of left ventricular systolic function.
- Fractional shortening: FS = (LVEDD − LVESD) ÷ LVEDD × 100%; LVEDD: Left ventricular end-diastolic dimension (mm), LVESD: Left Ventricular end-systolic dimension (mm)
- Left ventricular EF: Calculated by Teichholz's formula, using Simpson's biplane method.
EF = SV ÷ LVEDV × 100%; SV: Stroke volume, LVEDV: Left ventricular end diastolic volume
Patients with EF <50% or FS ≤25% were classified as having systolic dysfunction.
It was assessed using Doppler studies of mitral inflow and annular velocities (peak early filling (E-wave) and late diastolic filling (A-wave) velocities and annular E' velocity) as well as deceleration time (DT). The grading scheme is Grade I (impaired relaxation pattern), Grade II (pseudonormal), and Grade III (restrictive filling) depending on E/A ratio, E/E' ratio values, DT, and change after Valsalva maneuver [Table 1].
Left ventricular mass
LVM = 0.8 × (1.04× [LVEDD + PWd + IVSd]3 − LVEDD3) +0.6; LVEDD: Left ventricular end-diastolic dimension, PWd: left ventricular posterior wall thickness at end-diastole, IVSd: interventricular septal wall thickness at end diastole.
Left ventricular mass index
LVMI (g/m2) = LVM ÷ body surface area
Normal reference value of LVMI for female is 43–95 (g/m2) and male is 49–115 (g/m2), were taken for evaluation of study population.
Relative wall thickness
Relative wall thickness (RWT) = (2 × PWd) ÷ (LVEDD).
RWT was used to categorize of an increase in LV mass as either.
- Concentric hypertrophy: RWT >0.42 or
- Eccentric hypertrophy.: RWT <0.42.
Discrete categorical data were tabulated as n (%). Continuous data were presented as mean ± standard deviation and range or median and interquartile range, as appropriate. Analysis was conducted using SPSS software Version 22.0 (IBM Corp, Armonk, NY, USA). Pearson correlation coefficient and univariate analysis were done as applicable. A P < 0.05 was considered significant.
| Results|| |
A total of 51 patients satisfied the inclusion criteria. Among them, 31 (60.8%) patients were receiving hemodialysis and 20 patients (39.2%) were postrenal transplant recipients. The average age of our study population was 44.16 ± 13.66 years, ranging from 21 to 73 years [Figure 1]. There were 33 (64.70%) males and 18 (35.30%) females. The male: female ratio was 1.83:1. Hypertension was present in 92.2% and 33.3% patients were diabetic. Both hypertension and diabetes were present in 17 patients (33.3%). The most common etiology of CKD was hypertension in 16 (31.4%) patients followed by diabetes in 11 (21.6%). The various causes for CKD in our study population are depicted in [Figure 2].
Out of 51 patients with CKD, only 8 patients (15.7%) had normal echocardiograms. Out of 43 patients with cardiac abnormality on echocardiogram, 39 (90.7%) cases had more than one abnormality. Most frequent abnormality was LVH, seen in 80.4% patients, followed by diastolic dysfunction in 74.5%, systolic dysfunction in 13.7%, and mitral regurgitation in 13.7%. Pericardial effusion was seen in 3 (5.8%) cases. Various mean echocardiographic parameters documented in the study population are shown in [Table 2]. The mean value for LVMI value in our study population was 123.51 ± 23.49 g/m2 (range: 58.9–179.9 g/m2). Minimum value for EF was 45% and maximum value 79% with mean value of 64.41 ± 5.37%.
|Table 2: Mean echocardiography parameters in patients of chronic kidney disease|
Click here to view
Left ventricular hypertrophy
From all patients of LVH (80.4%), 4.9% had eccentric hypertrophy and 95.1% had concentric hypertrophy. In hypertensive patients with CKD, LVH was found in 85.1% of cases. There was statistically significant association between hypertension and LVH (P = 0.021). LVH was observed with higher frequency in diabetic CKD patients (94.1% vs. 5.9%) but this difference was not statistically significant (P = 0.135). Only 5 (12.2%) patients with LVH had systolic dysfunction. Relation of LVH with systolic dysfunction was not significant (P = 0.612). Diastolic dysfunction was more prevalent in patients with LVH, reported in 37 (90.2%) of cases, compared to only one (2.6%) without LVH and this relation was statistically significant (P = 0.001). The correlation of various echocardiographic findings in relation with comorbidities and LVH is elaborated in [Table 3].
|Table 3: Correlation of various echocardiographic findings with presence or absence of left ventricular hypertrophy|
Click here to view
Systolic dysfunction was observed in 7 (13.7%) patients. Six (12.8%) patients with hypertension and only one (5.9%) patient of diabetes mellitus had systolic dysfunction. Comparison of various parameters with systolic dysfunction is shown in [Table 4]. The observed mean value of LVMI in those with systolic dysfunction is 121.23 ± 21 g/m2 and for those without systolic dysfunction is 123.88 ± 24.07 g/m2. Mean value of LVEF in those with and without systolic dysfunction is 57.14 ± 6.47 and 65.57 ± 4.21, respectively. 85.7% of patients with systolic dysfunction also had presence of diastolic dysfunction (P = 0.662).
|Table 4: Correlation of risk factors and various echocardiographic findings with left ventricular systolic and diastolic function|
Click here to view
Diastolic dysfunction was present in 38 (74.5%) cases. Out of these 22 (57.9%) patients had Grade I diastolic dysfunction, 9 (23.6%) patients had Grade II, and 7 (18.4%) patients had Grade III diastolic dysfunction. Hypertensive patients had higher prevalence of diastolic dysfunction, seen in 38 (80.9%) of cases (P = 0.003). Among diabetic patients, there was no significant difference for the presence of diastolic dysfunction (P = 0.175) [Table 4]. The relation of LVMI with diastolic dysfunction was significant (P = 0.001). There was higher prevalence of diastolic dysfunction in patients with LVH (90.2%) and was statistically significant compared to those without diastolic dysfunction (P = 0.001). The mean E/A in those with and without diastolic dysfunction was 1.07 ± 0.53 and 1.09 ± 0.41 (P = 0.352), respectively.
| Discussion|| |
Cardiac structural and functional changes detected by echocardiography are the rule in patients with CKD on RRT and have been identified as important predictors of outcome. Early detection and treatment of these cardiac complications may help modify the outcome. Studies reveal that LVH was seen in 70%–80% of patients with CKD and indicates worse prognosis. This study provides range of echocardiographic abnormalities in patients on RRT and its correlation with etiological and various cardiac parameters.
The age and gender distribution of our study group were comparable to previous studies as shown in [Table 5]. Majority of patients (47%) belonged to middle age group of 41 years to 60 years, as was seen in the study by Rao et al., corresponding to the most vulnerable population for both cardiovascular and renal disease morbidity. Male preponderance (male:female = 1.83:1) has been shown in several studies including ours.,,
|Table 5: Comparison of echocardiographic manifestations in various studies among end-stage renal disease patients|
Click here to view
The most common etiology of CKD in our study was hypertension, seen in 16 (31.4%) patients. Most common etiologies observed in literature by various authors are shown in [Table 5]. Hypertension, often in conjunction with diabetes remains the most important and first common cause of CKD today. Hypertension in CKD is caused due to sodium retention leading to renin-angiotensin system activation. Renal failure has been attributed to raised plasma catecholamine and sympathetic nervous system activation., Hypertension also results in cardiac damage in CKD through LVH induction.
Out of 51 patients with CKD, only 8 (15.7%) patients had normal echocardiograms. The percentage of echocardiography abnormality observed was high in our study (86.3%), with 93% of them having more than one cardiac abnormality. On the contrary, higher percentage of normal echocardiogram (34.8%) as demonstrated by Kale et al. could be explained by differences in demography and sample size. Results for mean EF value and mean FS in different studies is shown in [Table 5]. Our findings conform to findings of Agarwal et al., Laddha et al., and Rao et al., in terms of FS with slightly higher value of mean EF.,, In our study, we found the prevalence of pericardial effusion in 3 patients (5.88%), it was mild in all of them. In literature, it varies between 6.5% and 17% [Table 5].
In literature, patients on hemodialysis have increased prevalence of LVH ranging from 40% to 80% in various studies., Kidney transplant candidates have an estimated prevalence of LVH of 60%-70% with studies showing partial regression of LVH after 1 year of transplantation. Parfrey et al. hypothesized that the increased prevalence of anemia and hypertension in patients with CKD may additionally contribute to the higher prevalence of LVH in such patients. The prevalence of LVH in our study also conform to results of Laddha et al., However, the relatively wide disparity in the prevalence of LVH in various studies can be attributed to several differences with respect to the characteristics of the population studied (age, RRT or earlier stage of CKD, prevalence of hypertension and prevalence of cardiovascular diseases), the technique used to estimate glomerular filtration rate (GFR), the cutoff of GFR chosen to enroll the patients and last but not least, the definition of LVH.
The pattern of LVH in our study was majorly concentric (95.2%) which was similar to Dangri et al. (87%) while eccentric hypertrophy (69%) was more common in the study by Debnath et al. This mixed pattern of LVH was reported by Nardi et al., in their study about LVH and the modified geometry in hypertensive patients with CKD. Further, they found that along with the worsening of renal function, instead of the expected eccentric ventricle that may occur due to volume overload, they found a significant prevalence of both concentric and mixed LVH, due to increase in wall thickness.
Majority of the studies have shown systolic dysfunction in CKD patients between 14% and 28%, as depicted in [Table 5] while Rao et al. reported in 55.2%. Systolic functions were well preserved in hypertensive and even in diabetic patients with CKD in our study. LV systolic dysfunction has been a poor prognostic predictor in patients on RRT and posttransplant patients. It is notable that manifested systolic dysfunction is independent of LV mass, and both these changes contribute to cardiovascular outcome and a heightened risk is seen in patients with an association of both.
Diastolic dysfunction was present in 38 (74.5%) cases. We have reported similar incidence of diastolic dysfunction in comparison to previous studies [Table 5]. In the study by Laddha et al., diastolic dysfunction was found in 72.9% of the hypertensive patients and in 42.9% of the normotensive patients with CKD. Significant relation of hypertension with diastolic dysfunction was reported by them which is similar to our study (P = 0.003). LV diastolic dysfunction is well known among CKD patients and results in cardiac failure leading to mortality. In the present study diastolic dysfunction was more frequent in diabetic CKD patients seen in 15 (88.2%) cases, though not statistically significant (P = 0.175). In contrast to our study, Miyazato et al. suggested that LV diastolic dysfunction is commonly seen in diabetic patients with CKD.
LV diastolic dysfunction develops in CKD patients at very early stages. Nardi et al. focused that CKD patients develop diastolic impairment much earlier, even without LVH. They evaluated diastolic function in 156 hypertensive patients, with and without CKD. They reported that the group with CKD (mean GFR 37 ml/min) had significantly worse diastolic function and also demonstrated an independent correlation between renal function and diastolic function. Diastolic dysfunction in these patients is multifactorial due to various causes such as impaired myocardial relaxation, poor compliance, increased preload, transvalvular pressure gradient, and passive elastic properties of the myocardial wall.
Small sample size is a major limitation of the study, and results of this study need to be validated over a large study group for better understanding of cardiac changes in patients on RRT and posttransplant recipients.
| Conclusion|| |
Cardiovascular structural abnormalities on echocardiogram were present in large number of patients on RRT and renal transplant recipients. LVH was seen most commonly in these patients. Diastolic function was frequently affected in this group. In the present study, 92.2% had hypertension suggesting that it might also have contributed toward the development of diastolic and systolic dysfunction. Early identification of cardiac abnormalities with the help of echocardiography before manifestation of definite cardiac symptoms may result in improved prognosis in these patients.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med 2004;351:1296-305.
Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J, Culleton B, Hamm LL, et al.
Kidney disease as a risk factor for development of cardiovascular disease: A statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Circulation 2003;108:2154-69.
Foley RN, Parfrey PS, Harnett JD, Kent GM, Martin CJ, Murray DC, et al.
Clinical and echocardiographic disease in patients starting end-stage renal disease therapy. Kidney Int 1995;47:186-92.
Foley RN, Parfrey PS, Kent GM, Harnett JD, Murray DC, Barre PE. Serial change in echocardiographic parameters and cardiac failure in end-stage renal disease. J Am Soc Nephrol 2000;11:912-6.
Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al.
Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015;16:233-71.
Nagueh SF, Smiseth OA, Appleton CP, Byrd BF 3rd
, Dokainish H, Edvardsen T, et al.
Recommendations for the evaluation of left ventricular diastolic function by echocardiography: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2016;29:277-314.
Marwick TH, Gillebert TC, Aurigemma G, Chirinos J, Derumeaux G, Galderisi M, et al.
Recommendations on the use of echocardiography in adult hypertension: A report from the European Association of Cardiovascular Imaging (EACVI) and the American Society of Echocardiography (ASE)†. J Am Soc Echocardiogr 2015;28:727-54.
Foley RN, Curtis BM, Randell EW, Parfrey PS. Left ventricular hypertrophy in new hemodialysis patients without symptomatic cardiac disease. Clin J Am Soc Nephrol 2010;5:805-13.
Rao T, Karwa M, Wanjari A. Left ventricular dysfunction among chronic kidney disease patients: A cross sectional study. Int J Adv Med 2018;5:1093-9.
Ahmed H, Yassein Y, Zaki S, Al Qersh A, Fahim F. Study of echocardiographic changes among adult patients on maintenance hemodialysis. Menoufia Med J 2016;29:44. [Full text]
Laddha M, Sachdeva V, Diggikar PM, Satpathy PK, Kakrani AL. Echocardiographic assessment of cardiac dysfunction in patients of end stage renal disease on haemodialysis. J Assoc Physicians India 2014;62:28-32.
Shivendra S. Echocardiographic changes in patients with ESRD on maintenance hemodialysis – A single centre study. J Cardiovasc Dis Diagn 2014;2:165. [doi: 10.4172/2329-9517.1000165].
Arjona Barrionuevo JD, Gonzáles Vargas-Machuca MF, Gómez Pulido F, Gil Sacaluga L, Gentil Govantes MA, Martínez-Martínez A. Transthoracic echocardiographic findings in patients with chronic kidney disease awaiting kidney transplantation. Transplant Proc 2010;42:3123-5.
Agarwal S, Dangri P, Kalra O, Rajpal S. Echocardiographic assessment of cardiac dysfunction in patients of chronic renal failure. J Indian Acad Clin Med. 2003;4(4):297.
Dangri P, Agarwal S, Kalra O, Rajpal S. Echocardiographic assessment of left ventricular hypertrophy in patients of chronic renal failure. Indian J Nephrol 2003;13: 92-7. [Full text]
Kale S, Kulkarni N, Gang S, Ganju A, Shah L, Rajapurkar M. Left ventricular disorders in patients of end stage renal disease entering hemodialysis programme. Indian J Nephrol 2001;Indian J Nephrol 2001;11:12-6.
Owen WF, Madore F, Brenner BM. An observational study of cardiovascular characteristics of long-term end-stage renal disease survivors. Am J Kidney Dis 1996;28:931-6.
Collins AJ, Foley RN, Gilbertson DT, Chen SC. United States Renal Data System public health surveillance of chronic kidney disease and end-stage renal disease. Kidney Int Suppl (2011) 2015;5:2-7.
Guyton AC, Coleman TG. Quantitative analysis of the pathophysiology of hypertension. Circ Res 1969;24:1-9.
Zoccali C, Mallamaci F, Tripepi G, Parlongo S, Cutrupi S, Benedetto FA, et al.
Norepinephrine and concentric hypertrophy in patients with end-stage renal disease. Hypertension 2002;40:41-6.
Neumann J, Ligtenberg G, Klein II, Koomans HA, Blankestijn PJ. Sympathetic hyperactivity in chronic kidney disease: Pathogenesis, clinical relevance, and treatment. Kidney Int 2004;65:1568-76.
Locatelli F, Bommer J, London GM, Martín-Malo A, Wanner C, Yaqoob M, et al.
Cardiovascular disease determinants in chronic renal failure: Clinical approach and treatment. Nephrol Dial Transplant 2001;16:459-68.
Pakfetrat M, Roozbeh J, Nikoo MH, Asem Z, Malekmakan L, Nikoo MA. Common echocardiography findings in pretransplant dialysis patients and their associations. Hong Kong J Nephrol 2013;15:15(2):68-74. Available from: https://cyberleninka.org/article/n/1134552
. [Last accessed on 2020 Jul 28].
Hernández D. Left ventricular hypertrophy after renal transplantation: New approach to a deadly disorder. Nephrol Dial Transplant 2004;19:1682-6.
Parfrey PS, Foley RN, Harnett JD, Kent GM, Murray DC, Barre PE. Outcome and risk factors for left ventricular disorders in chronic uraemia. Nephrol Dial Transplant 1996;11:1277-85.
Debnath A, Chaudhury SR, Chaturvedi AN, Sarkar S, Mandal S, Saha TK. Echocardiographic assessment of left ventricular systolic dysfunction in chronic kidney disease patients of a rural tertiary medical care centre in West Bengal. IOSR J Dent Med Sci 2014;13:69-73.
Nardi E, Palermo A, Mulè G, Cusimano P, Cottone S, Cerasola G. Left ventricular hypertrophy and geometry in hypertensive patients with chronic kidney disease. J Hypertens 2009;27:633-41.
Zoccali C, Benedetto FA, Mallamaci F, Tripepi G, Giacone G, Cataliotti A, et al.
Prognostic value of echocardiographic indicators of left ventricular systolic function in asymptomatic dialysis patients. J Am Soc Nephrol 2004;15:1029-37.
London GM. Left ventricular alterations and end-stage renal disease. Nephrol Dial Transplant 2002;17 Suppl 1:29-36.
Miyazato J, Horio T, Takiuchi S, Kamide K, Sasaki O, Nakamura S, et al.
Left ventricular diastolic dysfunction in patients with chronic renal failure: Impact of diabetes mellitus. Diabet Med 2005;22:730-6.
Albakri A. Electrolyte/Renal abnormalities cardiomyopathy: A review and pooled analysis of pathophysiology, diagnosis and clinical management. Clin Med Investig 2019;5:1-6.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]