| Abstract|| |
Left ventricular hypertrophy (LVH) is an independent predictor of mortality and its prevention can decrease cardiovascular mortality among predialysis chronic kidney disease (CKD) patients. This cross-sectional study was conducted at the Sindh Institute of Urology and Transplantation, Karachi, Pakistan, from March 2013 to October 2013 to determine the frequency of LVH and its risk factors in patients with CKD. A total of 135 outpatients with CKD duration longer than three months, were included in this study. All patients underwent laboratory investigations which included serum creatinine, blood counts, serum calcium, phosphate and uric acid, and parathormone. M-mode, two-dimensional echocardiogram in the left decubitus position was performed to document LVH. LVH was labeled when the left ventricular mass index was >131 g/m2 in men and >100 g/m2 in women on echocardiogram. LVH was found in 76 study patients (56.3%). The frequency of LVH was significantly high in patients with stage-4 CKD and those with duration of CKD above 12 months. Other risk factors included low hemoglobin, high serum calcium and phosphate levels, and decreasing estimated glomerular filtration rate. In conclusion, early detection of LVH and control of risk factors may help to achieve a decrease in cardiovascular morbidity and mortality in patients with CKD.
|How to cite this article:|
Ali T, Idrees MK, Shoukat, Akhtar SF. Left ventricular hypertrophy among predialysis chronic kidney disease patients: Sindh institute of urology and transplantation experience. Saudi J Kidney Dis Transpl 2017;28:1375-80
|How to cite this URL:|
Ali T, Idrees MK, Shoukat, Akhtar SF. Left ventricular hypertrophy among predialysis chronic kidney disease patients: Sindh institute of urology and transplantation experience. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2019 Dec 11];28:1375-80. Available from: http://www.sjkdt.org/text.asp?2017/28/6/1375/220856
| Introduction|| |
Chronic kidney disease (CKD) is considered a coronary heart disease risk equivalent and cardiovascular diseases contribute to increased morbidity and mortality among CKD patients when compared to the general population. Majority of CKD patients die from cardiovascular disease before they require renal replacement therapy. Cardiovascular disease accounts for twice the mortality among CKD patients as compared with those not having renal disease. Left ventricular hypertrophy (LVH) is an independent predictor of mortality and prevention of LVH can decrease cardiovascular mortality among predialysis CKD patients. Hypertension, anemia, parathyroid hormone (PTH) excess, arteriovenous fistula, and ischemia are the physiological stimuli for LVH in CKD. Predialysis CKD patients have high frequency/prevalence of LVH. A study from Japan noted a lower prevalence (21.7%) among patients with CKD stages 3–5 who were being treated by nephrologists. The prevalence of LVH increases with increasing loss of renal function that is reflected by 51% in patients with CKD stage 1–2 and 78% in those with CKD stage 3–5. A study from India showed prevalence of LVH ranging from 71% among those with CKD stage 1–3 to 96% among those with CKD stage-5.
There is now increasing attention toward LVH in patients with early CKD where measures can be taken to prevent or retard its progression. There are various studies conducted worldwide, but no such data are available in Pakistan. Since there is a very high frequency of LVH in CKD patients as revealed by international studies, this study was conducted to determine the frequency of LVH in CKD patients on follow-up at the CKD clinic (outpatient department) of the Sindh Institute of Urology and Transplantation (SIUT), Karachi, Pakistan. This study will help highlight the atrisk population in whom early measures can be undertaken to treat LVH and prevent associated morbidity and mortality. It will also provide a base for the future detailed studies.
| Patients and Methods|| |
This cross-sectional study was conducted at the CKD clinic of the Sindh Institute of Urology and Transplantation in Karachi, Pakistan, from March 2013 to October 2013. It included 135 adult patients (>18 years old) of either gender with CKD stage 2–4, on followup for at least three months and who had never received any form of renal replacement therapy. These patients were chosen by nonprobability, purposive sampling, and it excluded patients with uncontrolled hypertension, valvular and other congenital heart diseases, those with abnormal left ventricle wall motion on echo or with poor echo window. Patients with blood pressure (BP) >150/90 mm Hg were excluded from the study.
All patients underwent laboratory investigations including serum creatinine, creatinine clearance/estimated glomerular filtration rate (eGFR), calculated by the Cockroft–Gault formula. M-mode, two-dimensional echocardiogram in left decubitus position was performed by the same senior echocardiographer. LVH was diagnosed when the left ventricular mass index was >131 g/m2 in men and >100 g/m2 in women.
The data were collected on predesigned pro forma and analyzed on Statistical Package for the Social Science (SPSS) version 15.0 (SPSS Inc., Chicago, IL, USA). The quantitative variables such as age, weight, duration of CKD, creatinine clearance, and serum creatinine level were presented as their mean ± standard deviation values. The qualitative variables such as gender, stages of CKD, and LVH were presented by their frequencies and percentages. Stratification for known confounders was made at the time of data analysis (age, sex, duration of CKD, creatinine clearance, and different stages of CKD) through Chi-square test. The P ≤0.05 was considered statistically significant.
| Results|| |
This cross-sectional study included a total of 135 patients (93 males and 42 females) with CKD on outpatient follow-up for at least 3 months, who fulfilled the inclusion criteria. Descriptive statistics are given in [Table 1]. The average age of the patients was 42.08 ± 11.19 year (range 18 to >60 years). Fifty-six patients (41%) were below 40 years of age while 44 (32.5%) were between 40 and 50 years of age and 31 patients (23%) were between 51 and 60 years of age. Only five patients (3.7%) were above 60 years of age. The mean age was similar in the two groups (P = 0.906). The duration of CKD was highly variable and ranged from four to 138 months. The mean duration of CKD was 26.29 ± 22.64 months. The highest number of the patients (66.7%) had CKD stage-3, 22 (16.3%) had stage-2, and 23 (17%) had stage-4 CKD. Primary disease included chronic glomerulonephritis (bilateral small kidneys at presentation) in 65 patients, diabetes mellitus in 27, renal stones in 23, polycystic kidney disease in 12, and miscellaneous in others.
LVH was recorded in 76 patients (56.3%) with CKD. The frequency of LVH increased with increasing age and it was present in 50% patients above 30 years of age and increased to 80% among those over 60 years of age, but this difference was not statistically significant (P = 0.26). The frequency of LVH was higher among females and was found in 48 males (51.6%) and 28 females (66.7%). However, this difference was not statistically significant (P = 0.103). The frequency of LVH was significantly high in stage-4 CKD (P = 0.0003). Similarly, LVH was significantly higher (P = 0.0005) in those cases whose duration of CKD was above 12 months and it was present in virtually 100% of patients whose duration of CKD was more than two years. The mean creatinine clearance was 34.7 ± 9.85 mL/min in patients with LVH and 56.2 ± 12.0 in those without LVH. Both systolic BP (SBP) and mean arterial pressure (MAP) were significantly higher among patients who had LVH. The risk factors are tabulated in [Table 2].
| Discussion|| |
The prevalence of LVH increases as kidney function worsens and may be as high as 70%–80% before initiation of dialysis., In our study, LVH was documented in 76 CKD patients (56.3%). About 73% of the patients were below 50 years of age and 66% were in CKD stage-3. The frequency of LVH was significantly high among those with CKD duration of more than 12 months.
Yilmaz et al reported that LVH was detected in 67.6% of patients with CKD stages-3 and -4 at the baseline and increased to 89.7% in one year (P = 0.011). It concurs with our results that the frequency of LVH was significantly high among our study participants who had CKD for more than one year. The comparatively lower frequency of LVH in our study could be due to the exclusion of patients with high BP. In contrast, a study from Nigeria found that 95.5% patients with CKD stage-4 and 5 had LVH at first evaluation by a nephrologist.
A study from Brazil showed that 53% of CKD patients had LVH and more than 60% had CKD stage-4. The mean age was 60 ± 13 years. Our results closely resemble this study except that our study population is younger with a mean age of 42 years. CKD is more prevalent among relatively younger population in our country and it is further supported by a study from Pakistan that included diabetic CKD patients and showed that most of the patients with CKD were young (mean age 38 ± 12.5 years). Similarly, CKD and dialysis requirement is reported to occur at a younger age in other South Asian countries including India.
Our results show that there is significant difference in hemoglobin, serum calcium, phosphate, eGFR, duration of CKD (>12 months), and decline in renal function (stages of CKD) among those with and without LVH. A study from Karnataka, India, showed that 69% patients with CKD had LVH and its frequency increased with deteriorating renal function. The prevalence of LVH increases with progressive decline in renal function, drop in hemoglobin and rise in SBP.
Anemia was a significant factor among patients who had LVH. However, the hemoglobin level was not optimal even in patients without LVH. Most of our patients had adequate iron, folate and Vitamin B12 levels, and erythropoietin use was suboptimal due to financial constraints. A study from Karachi (Pakistan) found that 28.9% of CKD patients were anemic, and the mean Hb was 9.2 ± 2.3 g%. Patients with LVH had significantly higher SBP and MAP as compared to those who did not have LVH on echocardiography. We had excluded patients with BP more than 150/90 mm Hg and most of the patients included in the study had their BP controlled with antihypertensive drugs. Had we included CKD patients with high BP, the frequency of LVH might have been higher in our study population. Sustained lowering of SBP leads to regression of LVH as shown in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) BP trial. This study has shown that intensive lowering of SBP (≤120 mm Hg) leads to greater reduction of LVH (electro-cardiographic) as compared with standard BP lowering (≤140 mm Hg).
Serum calcium and phosphate were significantly higher in patients with LVH when compared with CKD patients who did not have LVH. Hyperphosphatemia contributes to cardiovascular morbidity and mortality, and it can lead to vascular calcification when accompanied by hypercalcemia.
Intact PTH (iPTH) levels were higher among CKD patients who had LVH than those not having LVH. However, this difference was not statistically significant (P = 0.0663). Elevated PTH has been implicated in LVH among CKD patients.
A study showed that iPTH level in patients with CKD stages-3 and -4 is an important and independent risk factor for LVH and is associated with an increased incidence of cardiovascular events, independent of calcium and phosphorous levels.
Similarly, anemia was found to be a risk factor for LVH among our study participants and it is well documented in literature.,
Most of our study parameters resemble those reported from other parts of the world and particularly in patients of South Asian region. Of note is the high proportion of young people of productive age having CKD which is much more pronounced than in the Western world where middle aged to old age population is affected predominantly. This young age population is to be the target of our future strategy to control the epidemic of CKD.
| Conclusion|| |
There is a high frequency of LVH among CKD patients in our population, and it is strongly associated with hemoglobin level, calcium and phosphate levels, stages of CKD, and duration of CKD (more than 12 months). Early detection of LVH and control of risk factors may help to achieve a decrease in cardiovascular morbidity and mortality in these patients.
| Limitations|| |
This study did not include the effect of interventions and control of risk factors identified in the study to regress the LVH.
Conflict of interest: None declared.
| References|| |
Briasoulis A, Bakris GL. Chronic kidney disease as a coronary artery disease risk equivalent. Curr Cardiol Rep 2013;15:340.
Dangri P, Agarwal S, Kalra OP, Rajpal S. Echocardiographic assessment of LVH in patients with chronic renal failure. Indian J Nephrol 2003;13:92-3. [Full text]
Wright J, Hutchison A. Cardiovascular disease in patients with CKD. Vasc Health Risk Manag 2009;5:714-8.
Shlipak MG, Fried LF, Cushman M, et al. Cardiovascular mortality risk in chronic kidney disease: Comparison of traditional and novel risk factors. JAMA 2005;293:1737-45.
Bregman R, Lemos C, Pecoits Filho et al. Left ventricular hypertrophy in patients with chronic kidney disease under conservative treatment. J Bras Nefrol 2010;32:83-8.
Levin A, Thompson CR, Ethier J, et al. Left ventricular mass index increase in early renal disease: Impact of decline in hemoglobin. Am J Kidney Dis 1999;34:125-34.
Nitta K, Iimuro S, Imai E, et al. Risk factors for increased left ventricular hypertrophy in patients with chronic kidney disease. Clin Exp Nephrol 2013;17:730-42.
Paoletti E, Bellino D, Cassottana P, Rolla D, Cannella G. Left ventricular hypertrophy in nondiabetic predialysis CKD. Am J Kidney Dis 2005;46:320-7.
Datta S, Abraham G, Mathew M, et al. Corre-lation of anemia, secondary hyperparathyroidism with left ventricular hypertrophy in chronic kidney disease patients. J Assoc Physicians India 2006;54:699-703.
Yilmaz BA, Mete T, Dincer I, Kutlay S, Sengül S, Keven K, Ertürk S. Predictors of left ventricular hypertrophy in patients with chronic kidney disease. Ren Fail. 2007; 29: 303-7.
Ulasi II, Arodiwe EB, Ijoma CK. Left ventricular hypertrophy in African Black patients with chronic renal failure at first evaluation. Ethn Dis 2006;16:859-64.
Rachel B, Carla L, Roberto PF, et al. Left ventricular hypertrophy in patients with chronic kidney disease under conservative treatment. J Bras Nefrol 2010;32:85-90.
Hassan M, Idrees MK, Ahmad F. Metabolic syndrome in patients with diabetic chronic kidney disease. Rawal Med J 2012;37:365-9.
Jha V. Current status of end-stage renal disease care in India and Pakistan. Kidney Int 2013; 3:157-60.
Kumar S, Jeganathan J, Miryala L. Left ventricular hypertrophy in chronic kidney disease. Int J Med Public Health 2014;4:364-6. [Full text]
Levin A. Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis. Semin Dial 2003;16:101-5.
Wasti AZ, Iqbal S, Fatima N, Haider S. Hematological disturbances associated with chronic kidney disease and kidney transplant patients. Int J Adv Res 2013;1:48-54.
Soliman EZ, Byington RP, Bigger JT, et al. Effect of intensive blood pressure lowering on left ventricular hypertrophy in patients with diabetes mellitus: Action to control cardiovascular risk in diabetes blood pressure trial. Hypertension 2015;66:1123-9.
Toussaint ND, Pedagogos E, Tan SJ, et al. Phosphate in early chronic kidney disease: Associations with clinical outcomes and a target to reduce cardiovascular risk. Nephrology (Carlton) 2012;17:433-44.
Rasoulzadegan MH, Rafiei M, Bashardoost N, Akbarian S. Relation between secondary hyperparathyroidism and left ventricular hypertrophy in hemodialysis patients. Iran J Kidney Dis 2011 ;5:69.
Lishmanov A, Dorairajan S, Pak Y, Chaudhary K, Chockalingam A. Elevated serum parathyroid hormone is a cardiovascular risk factor in moderate chronic kidney disease. Int Urol Nephrol 2012;44:541-7.
Muhammad Khalid Idrees
Department of Nephrology, Sindh Institute of Urology and Transplantation, Karachi
[Table 1], [Table 2]