Annals of African Medicine

: 2010  |  Volume : 9  |  Issue : 2  |  Page : 62--67

Microalbuminuria and its relations with serum lipid abnormalities in adult Nigerians with newly diagnosed hypertension

OA Busari, OG Opadijo, OT Olarewaju 
 Department of Internal Medicine, Federal Medical Center, Ido-Ekiti, Ladoke Akintola University of Technology, Ogbomoso, University of Ilorin Teaching Hospital, Ilorin, Nigeria

Correspondence Address:
O A Busari
Department of Internal Medicine, Federal Medical Centre, PMB 201, Ido-Ekiti


Background: Microalbuminuria (MA) has been associated with increased risk of adverse cardiovascular events in nondiabetic hypertensive patients. This may be partly due to increased serum lipid abnormalities in these patients. The objective was to evaluate the association between MA and serum lipid abnormalities in nondiabetic adult Nigerians with hypertension. Materials and Methods: A prospective study which recruited 96 consecutive newly diagnosed adult Nigerian hypertensive met the study criteria. These patients were compared with the same number of age- and sex-matched healthy normotensive individuals. Results: 52 (54.2%) and 44 (45.8%) of patients were males and females, respectively. Mean ± SD ages were 51.2 ± 10.1 and 48.2 ± 8.8 years for male and female patients, respectively. Microalbuminuria was more than five times more prevalent in the patients than in the controls. The means ± SD serum total cholesterol (5.0 ± 0.56 vs. 4.05 ± 0.50 mmol/L, P = 0.04) and low-density lipoprotein cholesterol (3.99 ± 0.49 vs. 2.84 ± 0.58 mmol/L, P = 0.001) were significantly higher, while the mean ± SD for high-density lipoprotein cholesterol was (0.91 ± 0.16 vs. 1.04 ± 0.13 mmol/L, P = 0.03) significantly lower in microalbuminuric patients than in non-microalbuminuric patients. Conclusion: This study has shown that adult nondiabetic Nigerians with MA are significantly more likely to have dyslipidemia than patients without MA. Hence, this subset of hypertensive patients constitutes a high risk group. Screening for MA, and early recognition and prompt treatment of serum lipid abnormalities in these patients may reduce the risk of adverse cardiovascular events.

How to cite this article:
Busari O A, Opadijo O G, Olarewaju O T. Microalbuminuria and its relations with serum lipid abnormalities in adult Nigerians with newly diagnosed hypertension.Ann Afr Med 2010;9:62-67

How to cite this URL:
Busari O A, Opadijo O G, Olarewaju O T. Microalbuminuria and its relations with serum lipid abnormalities in adult Nigerians with newly diagnosed hypertension. Ann Afr Med [serial online] 2010 [cited 2021 Oct 19 ];9:62-67
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Full Text


Microalbuminuria (MA) is a condition in which albumin excretion in the urine is above the 'normal' range but below the clinically detectable level, by standard screening tests i.e. urine dipsticks. It is defined as the presence of 20-200 ΅g/min or 30-300 mg/day of albumin excretion in the urine. [1] Microalbuminuria occurs in nondiabetic hypertensive populations [2],[3],[4],[5] and it has prognostic implication in these patients as it has been associated with increased cardiovascular morbidity and mortality. [6],[7]

The excess cardiovascular morbidity and mortality associated with MA in nondiabetic hypertensive patients may partly be related to their serum lipid abnormalities, particularly, reductions in high-density lipoprotein cholesterol (HDL-c) and elevations in low-density lipoprotein cholesterol (LDL-c) and lipoprotein(a). Some lipid components can directly injure the kidneys. [8] Thus adverse lipid profile may contribute not only to the development of MA in hypertension (HT) but also to its ultimate correlate, cardiovascular morbidity and mortality. [9] The objective of the study was to determine the prevalence of MA in nondiabetic adult Nigerians with essential HT and to evaluate its association with serum lipid abnormalities

 Materials and Methods

Ninety-six adult Nigerians with newly diagnosed HT were compared with age- and sex-matched healthy normotensive controls. The study was done at the Cardiology Unit of the University of Ilorin Teaching Hospital, Ilorin, Nigeria. Both oral and written consent was obtained from all the participants. Patients with previous use of antihypertensives, diabetes mellitus, obesity, overt proteinuria or congestive heart failure were excluded from the study. The study protocol was approved by the Ethical and Research Committee of the University of Ilorin Teaching Hospital, Ilorin, Nigeria.

Clinical evaluation, definitions and measurements

All participants had a detailed history and a thorough physical examination, including anthropometry. Blood pressure was measured using mercury column sphygmomanometer and a cuff of appropriate size. A standardized protocol was followed, in which systolic (SBP) and diastolic blood pressure (DBP) was measured on the left arm after participants had been seated for at least 5 min. The phase I Korotkoff's sounds were taken as SBP. The disappearance of these sounds (phase V) was the criterion for DBP. Three measurements were done at least 2 min apart and the mean value used for the study. Hypertension was defined as SBP ≥140 mmHg and/or DBP ≥90 mmHg, or use of antihypertensive drugs. [10],[11],[12] Pulse pressure (PP) was calculated as the difference between SBP and DBP while the mean arterial pressure (MAP) was derived with the formula:

MAP (mmHg) = DBP (mmHg) + (1/3 PP) mmHg

Microalbuminuria testing

Microalbuminuria was determined using the Micra Test strips (Boehringer Mannheim, Germany) urine dipstick. This dipstick has been found to be a rapid, accurate and cheap mean to screen the presence of MA. [13] There are four colour blocks corresponding to negative (or 0), 20, 50 and 100 mg/L of albumin. The test was done on three consecutive first morning voided urine samples of both patients and controls. Microalbuminuria was considered to be present when two of the three urine samples tested produce a reaction color corresponding to 20 mg/L or more. The mean value of the MA was recorded for each participant.

Laboratory evaluation

Blood samples were collected and analyzed in the laboratory for electrolytes, urea (BUN), creatinine (Cr) and fasting plasma glucose (FPG). Blood samples were also analyzed for fasting lipid profile; serum TC and triglyceride (TG) were determined using the standard colorimetric enzymatic methods, while serum LDL-c and HDL-c were precipitated by the polyvinyl sulfate and phosphotungstic acid method, respectively. Atherogenic index (AI) was calculated from the formula:

AI = LDL-c (mmol/L)/HDL-c (mmol/L)

Estimated glomerular filtration rate (eGFR) was derived using Cockcroft Gault formula: [14] eGFR = (140-age [years]) / serum creatinine (΅mol/L) Χ 0.85 (if female) Χ BSA/1.732 m 2 (where BSA is the body surface area estimated with the formula: [15] BSA (m 2 ) = 0.20247 Χ height (m) 0.725 Χ weight (kg) 0.425 . Some previous studies in Africa have showed a good correlation between eGFR derived from Cockcroft Gault formula and GFR measured using endogenous creatinine clearance and Cr-ethylenediaminetetra-acetic acid (Cr-EDTA) [16],[17]

Data analysis

Statistical analysis was performed using SPSS version 9. Descriptive data were presented as mean ± standard deviation. Continuous variables were compared using t test. P value P = 0.054). Twenty seven (27.1%) were petty traders, 33 (34.4%) were civil servants and 11 (11.5%) pensioners. Others were 3 (3.1%) students, 8 (8.3%) farmers, 8 (8.3%) artisans and 7 (7.3%) business persons.

MAL was more than five times more prevalent in hypertensive patients than in the normotensive controls. Thus, the proportion of MA positivity in the patients was significantly more than in the controls (32.3 vs 6.25%, P P = 0.04). The mean ± SD serum LDL-c was also significantly higher in the MA hypertensive patients (3.99 ± 0.49 vs. 2.84 ± 0.58 mmol/L, P = 0.001). On the other hand, the mean ± SD serum HDL-c in patients with MA was lower than in patients without MA (0.91 ± 0.16 vs. 1.04 ± 0.13 mmol/L). The difference was statistically significant (P = 0.001). There was no statistically significant difference in the mean ± SD of serum TG between these subgroups of hypertensive patients. Also, the mean ± SD of LDL-c/HDL-c ratio was higher in MA than in non-MA subgroups (4.38 ± 0.31 vs. 2.43 ± 0.42, P = 0.02).

[Table 3] and [Table 4] compare patients with MA and those without MA with the control group. The pattern of dyslipidemia in the hypertensive patients with and without MA is shown in [Table 5]. Dyslipidemia was more common in patients with MA than in those without MA (67.7 vs. 23.1%, P = 0.002). Low HDL-c and high TC were the most common types of dyslipidemia in hypertensive patients with MA.


This study shows that MA is a common finding in newly diagnosed adult Nigerians with HT. Although the reported prevalence of MA in 32.3% of the patients is higher than what Akinsola et al.[4] found in their study, it is still within the range of 4.7-40% documented in some other previous studies. [18],[19],[20],[21],[22] The variability in prevalence may be due to factors such as patient selection procedures, duration of hypertension, existence of prior antihypertensive treatment and method of estimation or detection of MA. [23],[24]

The study also reveals that MA is a coronary risk factor in adult Nigerian with HT, compatible with previous documentation. [4],[6],[25],[26] This is due to the fact that hypertensive patients with MA were more likely to have serum lipid abnormalities when compared with the hypertensives without MA and with the normotensive controls. The hypertensive patients with MA had significantly higher mean serum TC, LDL cholesterol and AI and significantly lower mean serum HDL than their counterparts without MA. Microalbuminuria was also significantly and positively correlated with serum TC and LDL cholesterol and significantly and negatively correlated with serum HDL. This is consistent with the report of other studies that have been done before. [26],[27],[28] Bigazzi et al. [26],[29] reported that dyslipidemia was associated with MAL and adds to the cardiovascular risk in HBP.

The reason for the association between MA and serum lipid abnormalities has not been established. Lundman et al. [30] demonstrated an association between mild-to-moderate HBP and endothelial dysfunction and increased plasma asymmetric dimethylarginine. Microalbuminuria has been well recognized as a marker of endothelial dysfunction in HBP. [7],[31] However, the serum lipid abnormalities may precede and possibly be responsible for the development of MA. [26] It is known that cholesterol-rich diet may cause albuminuria and glomerulosclerosis, and pharmacological agents that lower serum lipids may ameliorate renal injury in different animal species. [8],[9],[32],[33] On the other hand, MA may be an early manifestation or even precede the development of HBP and be responsible for serum lipid abnormalities. Fauvel [34] and Grunfeld [35] have shown that MA could be found in normotensive offspring of hypertensive parents. Proteinuria or MA may increase serum levels of TC, LDL-cholesterol and lipoprotein(a). [36],[37]

Limitations of the study

There is no doubt that this study has some limitations. Fasting plasma glucose alone is not enough to classify individuals as not having cardiovascular risk associated with glucose intolerance. This is because some form of glucose intolerance such as impaired glucose intolerance is also associated with increased cardiovascular risk as in diabetes mellitus. Also, the presence of MA was detected using a semi-quantitative method in a setting where a quantitative measurement would have been more appropriate. However, a number of previous studies have documented a close correlation between this albumin measurement for overnight or 24-hour urine collections. [38],[39] In addition this study was designed to assess association between MA and lipid abnormalities and not to elucidate information on the possible mechanism(s) of this association


This study has shown that adult Nigerian hypertensive patients with MA are significantly more likely to have dyslipidemia than patients without MA. This study provides evidence that in nondiabetic patients with HBP, MA signals presence of serum lipid abnormalities with atherogenic potential. Hence this subset of adult Nigerian hypertensive with MA constitutes a high risk group. We suggest that screening of MA be made part of routine investigation and follow-up assessment for all patients with HT. Early recognition and prompt treatment of serum lipid abnormalities in this subset of patients may reduce the risk of adverse cardiovascular events.


1Kilaru P, Bakris GL. Microalbuminuria and progressive renal disease. J Hum Hypertens 1994;8:809-17.
2Erley CM, Haefele U, Heyne N, Braun N, Risler T. Microalbuminuria in essential hypertension: Reduction by different antihypertensive drugs. Hypertension 1993;21:810-5.
3Gerber LM, Shmukler C, Alderman MH. Differences in urinary excretion rate between normotensive and hypertensive white and nonwhite subjects. Arch Intern Med 1992;152:373-7.
4Akinsola A, Balogun MO, Arogundade FA, Olatunde LO. Microalbuminuria and its clinical correlates in essential hypertension. Nig J Health Sci 2002;2:25-9.
5Busari OA. Correlation between electrocardiographic left ventricular hypertrophy and microalbuminuria in newly diagnosed adult Nigerian hypertensive patients. Fellowship Dissertation of National Postgraduate Medical College of Nigeria, 2004
6Jensen JS, Feig DI, Johnson RJ. Microalbuminuria and its relationship with cardiovascular disease and risk factors. A population based study of 1254 hypertensive individuals. J Human Hypertens 1997;11:727-37.
7Yudkin JS, Forrest RD, Jackson CA. Microalbuminuria as a predictor of vascular disease in non-diabetic subjects. Islington Diabetes Survey. Lancet 1988;2:530-3.
8Kasiski BL. Lipids and the kidney. Hypertension 1990;15:443-50.
9Keana WF. Hyperlipidaemia and progressive renal disease. Kidney Int 1991;39:41-8.
10The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Arch Int Med 1997;157:2413-46.
11Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: JNC 7 Report. JAMA 2003;289:2560-72.
12World Health Organization (WHO)/ International Society of Hypertension (ISH) statement on management of hypertension. J Hypertens 2003;32:1983-92.
13Tiu SC, Lee SS, Cheng MW. Comparison of six commercial techniques in the measurement of microalbuminuria in diabetic patients. Diabetes Care 1993;16:616-20.
14Cockcroft DW, Gault MH.Prediction of creatinine clearance from serum creatinine. Nephron 1976;16:31-41
15Du Bois D, Du Bois EF. A formula to estimate the approximate surface area if height and weight are known. 1916. Nutrition 1989;5:303-11.
16McLigeyo SO. Calculation of creatinine clearance from plasma creatinine. East Afr Med J 1993;70:3-5.
17Sanusi AA, Akinsola A, Ajayi AA. Creatinine clearance estimation from serum creatnine values: Estimation and comparison of five prediction formulae in Nigerians patients. Afr J Med Med Sci 2000;29:7-11.
18Gould FG. Microalbuminuria: Association with height and sex in non-diabetic subjects. Br Med J 1993;306:240-2.
19Derhaschnig U, Kittler H, Woisetschlδger C, Bur A, Herkner H, Hirschl MM. Microalbuminuria measurement alone or calculation of albumin/creatinine ratio for the screening of hypertensive patients? Nephrol Dial Transplant 2002;1:81-5.
20Losito A, Fortunati F, Zampi I, Del Favero A. Impaired renal functional reserve and albuminuria in essential hypertension. Br Med J (Clin Res Ed) 1988;296:1562-4.
21Pedersen EB, Mogensen CE. Effects of antihypertensive treatment on urinary albumin excretion, glomerular filtration rate and renal plasma flow in patients with essential hypertension. Scand J Clin Lab Invest 1976;36:231-7.
22Bigazzi R, Bianchi S, Campese VM, Baldari G. Prevalence of microalbuminuria in a large population of patients with mild to moderate essential hypertension. Nephron 1992;61:94-7.
23Rosa TT, Palatini P. Clinical value of microalbuminuria in hypertension. J Hypertens 2000;18:645-54.
24Bianchi S, Bigazzi R, Baldari G, Campese VM. Microalbuminuria in patients with essential hypertension: Effects of several antihypertensive drugs. Am J Med 1992;93:525-8.
25Biensenbach G, Zazgornik J. High prevalence of hypertensive retinopathy and coronary artery disease in patients with persistent microalbuminuria. J Hum Hypertens 1995;9:827-33.
26Bigazzi R, Bianchi S, Nenci R, Baldari D, Baldari G, Campese VM. Increased thickness of carotid artery in patients with essential hypertension and microalbuminuria. J Hum Hypertens 1995;9:827-33
27Jensen JS. Microalbuminuria and the risk of atherosclerosis. Clinical epidemiology and physiological investigation. Dan Med Bull 2000;47:63-78.
28Biesenbach G, Zazgornik J. High prevalence of hypertensive retinopathy and coronary artery disease in patients with persistent microalbuminuria under short intensive antihypertensive therapy. Clin Nephrol 1994;41:211-8.
29Bigazzi R, Bianchi S, Baldari D, Sgherri G, Baldari G, Campese VM. Microalbuminuria in salt sensitive patients: Marker for renal and cardiovascular disease. Hypertension 1994;23:195-9.
30Lundman P, Eriksson MJ, Stόhlinger M, Cooke JP, Hamsten A, Tornvall P. Mild to moderate hypertriglyceridaemia in young men is associated with endothelial dysfunction and increased plasma asymmetric dimethlyarginine. J Am Coll Cardiol 2001;38:111-6.
31Mimran A, Ribstein J, DuCailar G. Is microalbuminuria a marker of early intrarenal vascular dysfunction in essential hypertension? Hypertension 1994;23:1018-21.
32Ridker PM, Hennekens CH, Stampfer MJ. A prospective study of lipoprotein (a) and the risk of myocardial infarction. JAMA 1993;270:2195-9.
33Klahr S, Schreiner G, Ichikawa I. The progression of renal disease. N Engl J Med 1988;318:1656-7.
34Fauvel JP, Hadj-Aοssa A, Laville M, Fadat G, Labeeuw M, Zech P, et al. Microalbuminuria in normotensives with genetic risk of hypertension. Nephron 1991;57:371-6.
35Grunfeld B, Perelstein E, Simsolo R, Gimenez M, Romero JC. Renal functional reserve and microalbuminuria in offspring of hypertensive parents. Hypertension 1990;3:257-61.
36Keane WF, Peter JV, Kasiske BL. Is the aggressive management of hyperlipidaemia in nephritic syndrome mandatory? Kidney Int 1992;42:S134-41.
37Thomas ME. Raised lipoprotein (a) [Lp (a)] levels in proteinuric patients. J Am Soc Nephrol 1990;1:344-7.
38Eshψj O, Feldt-Rasmussen B, Larsen ML, Mogensen EF. Comparison of overnight morning and 24-hour urine collections in the assessment of diabetic microalbuminuria. Diabet Med 1987;4:531-3.
39Jensen JS, Clausen P, Borch-Johnsen K, Jensen G, Feldt-Rasmussen B. Detecting microalbuminuria by urinary/creatinine excretion ratio. Nephrol Dial Transplant 1997;12:6-9.