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 Table of Contents  
Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 11-16

Study of the Prevalence of Microalbuminuria in Patients of Essential Hypertension and its Correlation with Left Ventricular Hypertrophy and Carotid Artery Intima-media Thickness

1 Department of Internal Medicine, VMMC and Safdarjang Hospital, New Delhi, India
2 Department of Cardiology, VMMC and Safdarjang Hospital, New Delhi, India

Date of Web Publication11-Jan-2018

Correspondence Address:
Dr. Rita Rani Maggon
Department of Internal Medicine, VMMC and Safdarjang Hospital, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCPC.JCPC_22_17

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Background: Limited evidence is available among Indian patients regarding significance of microalbuminuria (MA) in context of hypertension and future cardiovascular morbidity. Therefore, the current study was undertaken to determine the prevalence of MA in hypertensive patients and to examine its correlation with severity of hypertension, left ventricular hypertrophy (LVH), and common carotid intima-media thickness (CCIMT). Material and Methods: Fifty treatment-naïve hypertensive patients (16–80 years of age) were prospectively enrolled. All patients underwent basic metabolic profile, urine evaluation, echocardiography, and measurement of CCIMT, and the data were evaluated. Results: MA (defined as urinary albumin excretion in the range of 30–300 mg/24 h) was present in 44% of patients with newly detected essential hypertension. A significant number of patients with MA had abnormally high mean left ventricular mass index as compared to those without MA. In addition, a positive correlation was also observed between MA and LVH. Furthermore, mean CCIMT was found to be higher in patients with MA (P < 0.001), with 69.2% of the patients with MA having elevated mean CCIMT. The CCIMT had a positive correlation with both MA and LVH. Conclusions: This study demonstrates the presence of MA in a significant number of newly detected and untreated patients of essential hypertension. Further, MA had a statistically significant relationship with LVH and CCIMT. Thus, screening of all recently diagnosed patients of essential hypertension for MA may be a reasonable strategy to predict the presence of future cardiovascular risk.

Keywords: Carotid artery intima-media thickness, essential hypertension, microalbuminuria

How to cite this article:
Maggon RR, Malik R, Jain N, Isser H S. Study of the Prevalence of Microalbuminuria in Patients of Essential Hypertension and its Correlation with Left Ventricular Hypertrophy and Carotid Artery Intima-media Thickness. J Clin Prev Cardiol 2018;7:11-6

How to cite this URL:
Maggon RR, Malik R, Jain N, Isser H S. Study of the Prevalence of Microalbuminuria in Patients of Essential Hypertension and its Correlation with Left Ventricular Hypertrophy and Carotid Artery Intima-media Thickness. J Clin Prev Cardiol [serial online] 2018 [cited 2022 Nov 26];7:11-6. Available from: https://www.jcpconline.org/text.asp?2018/7/1/11/222921

  Introduction Top

Hypertension is a disorder of circulatory regulation. Sustained hypertension causes accelerated atherosclerosis with consequent coronary heart disease (CHD), heart failure, and stroke and renal failure. If untreated, approximately 50% of patients develop heart disease, 33% develop stroke, and 10%–15% develop renal failure.[1]

Microalbuminuria (MA), defined as urinary albumin excretion (UAE) in the range of 30–300 mg/24 h, is seen in patients with established essential hypertension and is a predictor of higher risk of cardiovascular and renal dysfunction.[2] Klausen et al. showed that even a slightly raised levels of albumin well within microalbuminuric range relates to increased cardiovascular risk, i.e., increased risk for myocardial infarction, stroke, cardiovascular death, heart failure, and peripheral vascular resistance.[3] Detection of increased UAE could be the best index of an increased global cardiovascular risk in a given patient.[4]

Hypertension affects the heart by increasing afterload causing the left ventricular hypertrophy (LVH) and stiffening of the left ventricle leading ultimately to increase in the left ventricular mass (LVM). LVH is the most common abnormality in patients with hypertension and significant marker of subclinical cardiovascular disease.[5],[6] A positive correlation between MA and LVH has been documented in few studies.[4] Hypertension accelerates atherosclerosis and also independently causes vascular damage affecting large and small vessels. Common carotid intima-media thickness (CCIMT) represents a marker of sub-clinical atherosclerosis and helps in detection of atherosclerosis in presymptomatic atherosclerotic individuals. Despite Indians having increased predisposition for cardiovascular deaths, there are very few Indian studies which have examined the correlation of MA and essential hypertension. One study by Hitha et al. in South India studied relationship between MA and target organ damage in hypertension. They concluded that the prevalence of MA is 26.67%, and patients with MA have high odds for developing target organ damage such as stroke, LVH, and hypertensive retinopathy. This study did not take into account correlation of MA and CCIMT.[7] Therefore, our study was undertaken to determine the prevalence of MA in hypertension and to examine its correlation with severity of hypertension, LVH, and CCIMT.

  Material and Methods Top

A total of 50 patients satisfying inclusion and exclusion criteria, attending the medical OPD and ward of a tertiary care hospital were studied. They were subjected to detailed history and physical examination (including vitals, weight, height, and body mass index [BMI]), with special emphasis on the examination of cardiovascular system.

Inclusion criteria

  • Age: 16–80 years
  • Both sexes
  • Essential Hypertension of any grade as defined by the Seventh report of the Joint National Committee 7 (JNC 7) guidelines[8]
  • Patients who were treatment naive.

Exclusion criteria

  • Diabetes mellitus or impaired fasting glucose or impaired glucose tolerance
  • Renal diseases
  • Urinary tract infection
  • Tobacco use
  • Fever (current or within the past on month)
  • Serum creatinine >1.5 mg/dl
  • Positive for albumin by dipstick, i.e., MA
  • Overweight as defined by BMI >25
  • Major cardiovascular and cerebrovascular events in the past 6 months such as coronary artery disease (CAD), congestive heart failure (CHF), valvular heart disease, atrial fibrillation, cerebrovascular accidents, and myocardial infarction.

All patients were subjected to following laboratory investigations

  • CBC with ESR
  • Urine albumin by dipstick
  • Urine routine and microscopic examination
  • 24 h urinary albumin
  • Blood urea and serum creatinine
  • Plasma glucose – fasting and postprandial
  • Serum electrolytes–sodium and potassium
  • Serum uric acid
  • Serum calcium and phosphate
  • Lipid profile
  • X-ray chest
  • Electrocardiography
  • Ultrasonography abdomen (for kidney size)
  • Echocardiography
  • Fundus examination
  • Doppler examination of the neck.

MA, defined as UAE in range of 30–300 mg/24 h, was measured by hemocue albumin technique.

Echocardiography was done in all patients using Philips, Sonos 5500 USA. LVM was calculated by following formula developed by Devereux et al.:

LVM = 0.80 × (1.04 [IVST + PWT + LVID]3 − LVID3) + 0.6 g


IVST is the interventricular septal thickness,

PWT is posterior wall thickness,

LVID is the left ventricular internal diameter,

1.04 = specific gravity of the myocardium and 0.8 is the correction factor.[9]

LVM index (LVMI) was calculated by dividing LVM by body surface area of the patients and represented as g/m2. LVH was considered to be present when LVMI was ≥131 g/m2 in men and LVMI ≥100 g/m2 in women.[10]

CCIMT was measured in all patients included in the study (US scanner Philips HDI 4000) with a linear transducer of 5–12 MHz with resolution of 0.001. The common carotid artery was scanned and measurements were taken at one point 15 mm proximal to the bifurcation (manual measurement). A total of six readings (three on each side) were taken. The average value of CCIMT of both sides was calculated, and finally, average of both sides was taken as final value of CCIMT. Images were recorded in diastole. In this study, CCIMT >0.08 cm was taken as raised CCIMT.[11]

The study was designed to observe the prevalence of MA in these patients and its correlation with LVH and CCIMT.

Statistical analysis

Chi-square test was used to analyze nonparametric or categorical data. For analysis of ordinal scale data, Student's t-test was used. Karl–Pearson correlation coefficient was calculated to observe correlation between variables. P < 0.05 was taken as significant and <0.01 as highly significant. All the data were computed on Microsoft® Office 2007 database (Microsoft Corporation USA), and statistical analysis was done using SPSS Windows version 12.0 (SPSS in Chicago, IL, USA).

  Results Top

Demographic profile

A total of fifty patients including 28 males and 22 females were studied. The mean age of the patients was 51.82 ± 10.17 years.


In our study, MA was present in 44% of patients (n = 22), which included 10 males (35.71%) and 12 females (54.54%) (P = 0.253). MA was present in the highest number of patients in 60–70 years age group [Figure 1]. Correlation of MA with various parameters is summarized in stromal cell-derived factor (SDF)-1.
Figure 1: Relation between microalbuminuria and age distribution

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Relation of microalbuminuria with age

The mean age of patients with MA was 57.18 ± 9.59 years while that of patient without MA was 46.46 ± 10.74 years (P = 0.001). Thus, age showed a significant positive correlation with MA in the study.

Relation of microalbuminuria with blood pressure

Patients with MA had significantly higher mean systolic blood pressure (SBP) (153.91 ± 5.571 mmHg) than those without MA who had mean SBP (149.8 ± 6.6 mmHg, P = 0.025). However, the mean diastolic blood pressure (DBP) of patients with MA was similar in both groups (95.64 ± 3.6 mmHg vs. 96.8 ± 4.6 mmHg, P = 0.279).

Relation of microalbuminuria with the left ventricular hypertrophy

Based on echocardiography, LVH prevalence was found to be present in 22 (44%) patients which included 10 males and 12 females. Among the 22 patients with MA, 15 patients had LVH (68.18% n = 22) and 7 did not have LVH. Among 28 patients without MA, only 7 patients had LVH. Thus, it showed a significant positive relation between MA and LVH (P value 0.004) [Figure 2].
Figure 2: Relation between microalbuminuria and left ventricular hypertrophy

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Relation of left ventricular hypertrophy with blood pressure

Patients with LVH had a higher mean SBP (153.09 vs. 150.50 P value = 0.0.477) and higher mean DBP (97.00 vs. 95.57 P value = 0.440) although this is not statistically significant.

Increased common carotid intima-media thickness

In the present study, twenty patients of essential hypertension had increased CCIMT and thirty patients had normal CCIMT. Thus, the prevalence of increased CCIMT was 40%. Out of the 22 patients with MA, 18 (81.81%) patients had increased CCIMT while 4 patients had normal CCIMT which shows a significant association between MA and increased CCIMT (P < 0.001). Patients with increased CCIMT were significantly older (58.80 ± 9.80 years) compared to those patients with normal CCIMT (46.10 ± 9.66 years, P < 0.001). Mean value of MA in patients with increased CCIMT was significantly higher than those with normal CCIMT (183.25 ± 80.36 vs. 42.80 ± 62.49, P < 0.001) [[Figure 3] and SDF-2]. However, there was no difference with respect to serum total cholesterol levels (174.65 ± 32.23 mg/dl vs. 173.03 ± 36.28 mg/dl, P = 0.874), serum triglycerides levels (143.23 ± 38.43 mg/dl vs. 134.15 ± 26.17 mg/dl, P = 0.361), mean low-density lipoprotein levels (123.97 ± 31.32 mg/dl vs. 122.00 ± 29.43 mg/dl, P = 0.825), mean SBP levels (153.6 ± 5.2 mmHg vs. 150.4 ± 6.8 mmHg, P = 0.061), and mean DBP (96.40 ± 4.8 mmHg vs. 96.2 ± 3.6 mm Hg, P = 0.333) in patients with increased CCIMT versus those with normal CCIMT.
Figure 3: Correlation between urinary albumin excretion and increased common carotid intima-media thickness

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The mean LVMI of patients with increased CCIMT was 132.48 ± 32.10 g/m2 while the mean value of LVMI with normal CCIMT was 94.27 ± 29.527 g/m2 (P = < 0.001) [Figure 4] and SDF-3]. Fourteen of the twenty patients with increased CCIMT had raised LVH whereas only 8 of 22 patients with LVH did not have increased CCIMT. On doing t-tests, exact significant (two-sided) was 0.0001, which is statistically highly significant.
Figure 4: Correlation between increased common carotid intima-media thickness and left ventricular mass index

Click here to view

  Discussion Top

Hypertension is one of the major public health problems. Worldwide prevalence of hypertension is as much as 1 billion while 7.1 million deaths may be attributable to hypertension.[12] The JNC 7 report states that high blood pressure is the number one attributable risk for death in the world.[8] Uncontrolled hypertension is directly associated with end organ damages including CHD, CHF, LVH, stroke, and peripheral vascular disease.[13] Despite dangers of uncontrolled hypertension being widely recognized, the disease remains inadequately recognized and treated in most of the patients. The WHO report shows that suboptimal blood pressure control is responsible for 62% of cardiovascular disease and 49% of ischemic heart disease with little variation with sex.[12]

MA is an early sign of renal damage and it foretells the development of nephropathy and other complications of hypertension like LVH and stroke. MA is defined as UAE in the range of:

  • 30–300 mg/24 h
  • 20–200 mg/L in the first morning sample
  • 20–200 μg/min in a timed overnight 24 h sample
  • Urinary albumin to creatinine ratio of >30 mg/g (30–300 mg/g) in a first morning midstream sample.[14]

Any urinary albumin value below these limits is normal urinary excretion and above these limits reflects the presence of macroalbuminuria or clinical proteinuria. Measurement of albumin in a 24 h urine collection has been the “gold standard“ for the quantitative evaluation of MA. Exact pathogenesis of MA in patients with essential hypertension has not been established, putative mechanisms include:

  1. Increased glomerular hydrostatic pressure due to defect in autoregulation
  2. Increased permeability of glomerular basement membrane
  3. Endothelial dysfunction
  4. Inflammation.

Parving et al. in 1974 were the first to report MA in hypertensive patients without diabetes since then several studies have found an overall prevalence of around 6%–42%.[15] Bigazzi et al. measured UAE in 123 patients of essential hypertension and 110 normal individuals. In their study, 40% of patients of essential hypertension showed UAE in microalbuminuric range while none of normal individuals had MA.[16] Mimran et al. examined 106 lean patients of essential hypertension and found 24.5% prevalence of MA in their study.[17] Indian study by Hitha et al. has found a prevalence of 26% and Jalal et al. have shown a prevalence of 37.5% of MA in patients of hypertension.[7],[18] Gatzka et al. found MA in 42% of patients with hypertension.[19] In our study, MA was detected in 22 patients (44%) out of which 10 were male and 12 were female.

The present study did not find difference in prevalence of MA in males and females. However, the mean age of patients with MA was higher than those without MA and this was statistically significant (P = 0.001). In study by Hitha et al., also, it was found that the prevalence of MA increased steadily in patients of hypertension with advancing age.[7] In another large study of 11,343 nondiabetic hypertensive patients with a mean age of 57 years, MA was present in 32% of men and 28% of women and prevalence increased with age, severity, and duration of hypertension.[20]

In the present study, patients with MA had higher value of mean SBP and DBP in comparison with patients without MA. SBP, but not DBP, had statistically significant positive correlation with MA (P = 0.001). Opsahl et al. also observed a significant correlation between average 24 h systolic but not DBP and UAE.[21] Mimran et al. assessed 60 lean patients of essential hypertension and observed higher values of systemic arterial pressure in patients with MA than those without MA.[17] Jalal et al. noticed increasing trends in UAE in normal, mild, and moderately hypertensive patients.[18]

Hypertension doubles the risk for symptomatic CAD, including acute myocardial infarction and sudden death and more than triples the risk for CHF.[15] Hypertension places increased tension on the left ventricular myocardium that is manifested as stiffness and hypertrophy, which accelerates the development of atherosclerosis within coronary vessels. The combination of increased demand and lessened supply increases the likelihood of myocardial ischemia and thereby leading to a higher incidence of myocardial infarction, sudden death, arrhythmias, and congestive failure in hypertensive patients. Endothelial dysfunction and chronic inflammation have been suggested as possible causes to explain the association between MA and cardiovascular disease. Brantsma et al. observed MA to be a sensitive marker for detecting onset of cardiovascular risk factors such as hypertension and type II diabetes.[22],[23] The LIFE study showed that more the angiotensin-II antagonist losartan lowers albuminuria the more the patient was cardio-protected.[24] In this regard, monitoring of UAE and LVH rate has ultimately been useful as surrogate for efficiency of blood pressure control and cardiovascular risk reduction. Failure of MA and LVH to regress may indicate inadequacy of the interventions. A study by Stein et al. shows that MA is associated with increased cardiovascular mortality with relative risk of 3.2 (95% confidential limit).[26] Plavnik et al. in their study of relationship between MA and cardiac structural change in mild hypertensive patients found significant correlation between UAE and cardiac structural parameters such as IVS (r = 0.71), PSVT (r = 0.64), and LVM (r = 0.65).[4] Those who had MA presented higher values of all cardiac parameters. These data indicate that MA in essential hypertension represents an early marker of cardiac structural abnormalities.

In the present study, LVH was present in significant number of patients with MA as compared to those without MA (68.2% vs. 33.3%, P = 0.004). Gatzka et al.studied 704 patients of essential hypertension and observed higher LVM in microalbuminuric patients than nonmicroalbuminuric patients.[19] In a large study by Agrawal et al. of 11343 nondiabetic hypertensive patients, those with MA had a higher prevalence of LVH and other cardiovascular events as compared to those without MA.[20] Wachtell et al. observed that in patients with moderately severe hypertension and LVH on two consecutive electrocardiographies had increased prevalence of MA as compared to patients without LVH.[24] High albumin excretion was related to LVH independent of age, blood pressure, diabetes mellitus, race and serum creatinine, and smoking. In a study done by Hitha et al., they also found significant association between MA and LVH, and thus, both are early markers of target organ damage in hypertensive patients.[7]

In the present study, patients with LVH were found to have higher mean SBP (P < 0.477) and mean DBP than those without LVH (P < 0.413) though this was not statistically significant. This finding in our study is in conformity with a study done by Kozàkovàet al.[25]

CCIMT represents a marker of subclinical atherosclerosis and helps in early detection of atherosclerosis in presymptomatic individuals.[26] Several previous studies have demonstrated relationship between CCIMT and CAD or CAD risk factors in Indian patients,[27],[28],[29],[30] and a recent study has also provided normative data for CCIMT among Indians.[31]

Pontremoli et al. have shown that UAE is associated with signs of subclinical organ damage such as LVH and increased CCIMT.[32] In a study by Mykkanen et al., patients with MA had greater CCIMT than those without MA.[33] Similarly, in an Indian study by Jadhav et al., it was concluded that MA had a strong association with increased CCIMT and CAD in diabetics.[34] The association of MA and CCIMT was independent of age, sex, ethnicity, smoking, and lipoprotein levels. MA may be a marker of generalized vascular disease and also MA per se could be a risk factor of atherosclerosis. The study by Bigazzi R et al. showed that hypertensive patients with MA have an increase thickness of the carotid intima and media layers, suggesting a greater degree of atherosclerosis.[35] In the present study, the mean SBP and DBP of patients with increased CCIMT were higher than mean SBP (P = 0.061) and DBP (P = 0.333) of patients without increased CCIMT. Bots et al. in the Rotterdam study found a positive association of CCIMT with age, male, sex, BMI, SBP, and hypertension.[36] They concluded that increased CCIMT was associated with future cerebrovascular and cardiovascular events. In the study by Bigazzi et al., it was found that thickness of carotid artery was significantly correlated with MA, blood pressure, and serum lipids.[35] Thus, our study is in conformity with above study and has shown a very significant correlation between the two. CCIMT was increased in 18 of 22 patients with MA (81.8%, P < 0.001), showing positive correlation between them. Henareh et al. found that UAE was significantly and positively associated with calculated intima-media area in both brachial and common carotid arteries as well as with age and interventricular septum thickness.[37] Mykkänen et al. in their study found a positive association of MA with CCIMT. This association was independent of age, sex, ethnicity, smoking, and lipoproteins and was partly mediated by hypertension.[33] Thus, our study is in conformity with the above studies and has shown a positive correlation between the two. The study by Kramer et al. showed a positive correlation of MA and LVMI but no significant difference between mean CCIMT of those with or without MA.[38]

In the present study, out of 22 patients with LVH, 18 had increased CCIMT (P = 0.000). In a study done by Henareh L et al., in 2005, MA was found to be associated with calculated intima-media area.[37] Leoncini et al. in their study of treatment-naive patients of primary hypertension found an overall prevalence of MA, LVH, and carotid plaque as 13%, 51%, and 24%, respectively. MA was found to be significantly correlated with LVMI (P < 0.0001), IMT (P < 0.0001) and several metabolic and nonmetabolic risk factors. The authors concluded that MA is an integrated marker of subclinical target organ damage in patients with primary hypertension.[39]

Despite limitations of our study like a limited number of patients, the use of single cutoff value for measurement of variables such as CCIMT irrespective of sex, age, and ethnicity of the patients, the results are in accordance with many of the published studies, and hence, important conclusions can be drawn from it.

  Conclusions Top

Our study demonstrated the presence of MA in a significant number of newly detected and untreated patients of essential hypertension. Further, MA had a statistically significant relationship with LVH and CCIMT. There was a positive correlation between MA and LVH and between MA and CCIMT. These findings imply an underlying vascular relationship between MA, LVH, and CCIMT. Therefore, screening of all recently diagnosed patients of essential hypertension for MA may be a reasonable strategy to predict the presence of ongoing vascular damage, cardiac geometric adaptation, and the future risk for cardiovascular events.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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