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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 27  |  Issue : 2  |  Page : 363-371

Prevalence of proteinuria among type 2 diabetic patients in Menoufia governorate, Egypt


1 Department of Family Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department ofClinical Pathology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Endocrinology and Obesity Unit, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Date of Submission18-Jun-2013
Date of Acceptance13-Oct-2013
Date of Web Publication26-Sep-2014

Correspondence Address:
Tamer Ibrahim Elsayed
MBBCh, Tanta, Gharbia Governorate
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.141710

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  Abstract 

Objective
The aim of the study was to determine the prevalence and risk factors of proteinuria among type 2 diabetic patients in Menoufia governorate.
Background
Type 2 diabetes is the leading cause of end-stage renal disease worldwide. Microalbuminuria or incipient diabetic nephropathy is one of the initial clinical manifestations of early diabetic nephropathy.
Patients and methods
A total of 234 type 2 diabetic patients were included in this study; they attended the outpatient clinics of the Family Health Center of 'Kafr Tanbedy' and Internal Medicine Department of Faculty of Medicine, Menoufia University, for routine follow-up.
Patients were classified according to their urinary albumin-to-creatinine ratio (ACR) as having normoalbuminuria (ACR < 30 mg/g creatinine), microalbuminuria (ACR = 30 to <300 mg/g creatinine), or macroalbuminuria (ACR≥300 mg/g creatinine). The three groups were compared to analyze the association between albuminuria and its risk factors. In addition, independent predictors of albuminuria were determined using multivariate logistic regression and presented as an odds ratio.
Results
Prevalence of microalbuminuria (incipient diabetic nephropathy) was 34.2% and that of macroalbuminuria (overt diabetic nephropathy) was 12.8% in the studied group.
Conclusion
The overall prevalence rate of albuminuria was considerably high (47.01%) among the studied diabetic patients. Therefore, regular screening for microalbuminuria is recommended for all diabetic patients, as early treatment is critical for reducing cardiovascular risks and slowing the progression to late stages of diabetic nephropathy (overt proteinuria and end-stage renal disease).

Keywords: Diabetic nephropathy, proteinuria, type 2 diabetes mellitus


How to cite this article:
Farahat TM, Elsaeed GK, Gazareen SS, Elsayed TI. Prevalence of proteinuria among type 2 diabetic patients in Menoufia governorate, Egypt. Menoufia Med J 2014;27:363-71

How to cite this URL:
Farahat TM, Elsaeed GK, Gazareen SS, Elsayed TI. Prevalence of proteinuria among type 2 diabetic patients in Menoufia governorate, Egypt. Menoufia Med J [serial online] 2014 [cited 2020 Jul 12];27:363-71. Available from: http://www.mmj.eg.net/text.asp?2014/27/2/363/141710


  Introduction Top


Type 2 diabetes mellitus (DM) is a public health concern worldwide and an important cause of morbidity and mortality. Through lifelong vascular complications, DM leads to excessive rates of myocardial infarction, stroke, renal failure, blindness, and amputations. The projections of its future impact are alarming. According to the WHO, DM affects more than 170 million people worldwide, and this number will increase to 370 million by 2030 [1].

Type 2 DM results from dysfunction in insulin action and insulin secretion, either of which may be the predominant feature and both of which are usually present when the disease becomes clinically manifest [2].

By definition, specific causes are not known and autoimmune destruction of the pancreas does not occur. Type 2 DM is preceded by insulin resistance and impaired glucose tolerance. Once insulin resistance is pronounced, the likelihood of type 2 DM development depends on the ability of the b cells to compensate adequately by increasing insulin secretion. Thus, the disease is of insidious onset and may remain asymptomatic for many years. The true duration of the disease is often not known. It has been reported that the duration of DM for more than 6 years may have existed before diagnosis [3].

About one-third of type 2 DM patients will eventually have progressive deterioration of renal function [4].

Diabetic nephropathy is a public health concern of increasing proportions. It has become the most common single cause of end-stage renal disease worldwide [5].

The prevalence of diabetic nephropathy as a cause of end-stage renal disease in the Egyptian renal data system was evaluated during the period 1996-2001 for the prevalence of diabetic nephropathy, which gradually increased from 8.9% in 1996 to 14.5% in 2001 [6].

The first clinical sign of renal dysfunction in patients with DM is generally microalbuminuria (a sign of endothelial dysfunction that is not necessarily confined to the kidney). The degree of microalbuminuria determines the progression of diabetic nephropathy. It may reflect the renal manifestation of a global vascular dysfunction [7].

It refers to the excretion of albumin in the urine at a rate that exceeds normal limits, but is less than the detection level for traditional dipstick methods [8].

Microalbuminuria is also a marker of inflammation and an independent risk factor for cardiovascular mortality [9]. It develops in 2-5% of patients with type 2 DM every year [10].

Microalbuminuria is often present at the time of diagnosis, either because of its insidious nature and asymptomatic initial years of type 2 DM or because of its positive association with insulin resistance, even in nondiabetic people [11].

The normal rate of albumin excretion is less than 20 mg/day (15 mg/min); persistent albumin excretion between 30 and 300 mg/day (20-200 mg/min) is called microalbuminuria. Values above 300 mg/day (200 mg/min) are considered to represent overt proteinuria. Although the 24-h urine collection was previously considered as the gold standard for the detection of microalbuminuria [12], it has been suggested that screening can be more simply achieved by a timed urine collection or an early morning specimen to minimize changes in urine volume that occur during the day [13]. The effect of volume can be avoided entirely by calculating the albumin-to-creatinine ratio (ACR) in an untimed urine specimen. A value above 30 mg/g (or 0.03 mg/mg) suggests that albumin excretion is above 30 mg/day and therefore that microalbuminuria is probably present. With standard units, the comparable value is 3.4 mg of albumin/mmol of creatinine [14].


  Aim Top


The main goal of the study was to improve the outcomes of type 2 DM and prevent its complications through handling of risk factors, as well as determine the prevalence and risk factors of proteinuria among type 2 DM patients.


  Patients and methods Top


We evaluated 234 participants in a cross-sectional study, conducted during the period from the beginning of February 2011 to the end of August 2012.

The participants included in the study were above 25 years of age, had a known history of type 2 DM, and attended the Family Health Center of Kafr Tanbedy and Internal Medicine Department of Menoufia University Hospital for routine follow-up. The exclusion criteria were any evidence of nondiabetic renal disease, obstructive uropathy, severe renal disease [serum creatinine >177 mmol/l (2.0 mg/dl)], severe heart failure, liver disease, cancer, autoimmune disease, urinary tract infection, pregnant women, and patients using drugs that could alter insulin sensitivity such as hormone replacement therapy, steroids, or antituberculosis drugs, except antidiabetic drugs.

A complete history was taken, including the known duration of disease, smoking status, and medications used, as well as a complete physical examination including measurements of height, weight, and blood pressure.

Albuminuria was assessed by collecting a morning urine sample to calculate the ACR. Patients were classified according to ACR as having microalbuminuria (ACR = 30 to <300 mg/g creatinine) and macroalbuminuria (ACR ≥ 300 mg/g creatinine). Patients with normoalbuminuria were compared with those with microalbuminuria and macroalbuminuria.

Urinary albumin

It was measured using RA 50 analyzer, wave length 560, using BioSystems Kit.

Principle of the method

Albumin in the urine sample causes agglutination of the latex particles coated with antihuman albumin. The agglutination of the particles is proportional to the albumin concentration and can be measured by turbidimetry [15-18].

Urinary creatinine

It was measured using RA 50 analyzer, wave length 505, using BioSystems Kit.

Principle of the method

Creatinine in the sample reacts with picrate in alkaline medium forming a colored complex. The complex formation rate is measured in a short period to avoid interferences [19],[20].

Patients were considered hypertensive if they were already administered antihypertensive medications, or if they were found in the clinic to have elevated blood pressure (systolic blood pressure≥140 mmHg, diastolic blood pressure≥90 mmHg), and mean arterial pressure was calculated for each patient.

Fasting venous blood was sampled in all patients from the antecubital vein for the measurement of glycated hemoglobin (HbA1c) and serum glucose.

Fasting blood glucose

It was measured using RA 50 analyzer, wave length 505, using Spinreact Kit.

Principle of the method

Glucose oxidase (GOD) catalyzes the oxidation of glucose to gluconic acid. The formed hydrogen peroxide (H 2 O 2 ) is detected by a chromogenic oxygen acceptor, phenol, 4-aminophenazone (4-AP), in the presence of peroxidase (POD):

D-Glucose + O 2 + H 2 O gluconic acid + H 2 O 2 GOD.

H 2 O 2 + phenol + 4-AP quinone + H 2 O POD.

The intensity of the color formed is proportional to the glucose concentration in the sample [21],[22].

HbA1c

It was measured by RA 50 analyzer, wave length 405, using BioSystems Kit.

Principle of the method

After preparing the hemolysate using tetradecyltrimethylammonium bromide as the detergent, the hemoglobin A1c (HbA1c) concentration is quantified by a turbidimetric inhibition immunoassay. By adding the sample to a reagent with antibodies against a specific site of HbA1c, soluble complexes formed by the union of two molecules appear. After adding a second reagent formed by polyhaptens to the reaction mixture, the excess anti-HbA1c antibodies form an insoluble complex, antibody-polyhapten, which can be determined turbidimetrically. The estimation of the HbA1c in percent is made by the measurement of total hemoglobin concentration by spectrometry [23].

Statistical analysis

The collected data were statistically analyzed using the statistical package for the social sciences (SPSS Software, version 17; SPSS Inc., Chicago, Illinois, USA). Quantitative data were expressed as mean and SD, and qualitative data were expressed as number, percent, and tested by F-test (analysis of variance) and c2 -test, using the 5% level of significance.


  Results Top


A total of 234 patients were included in the study; the overall prevalence of nephropathy (proteinuria) in type 2 DM patients was 47.01% [Table 1].
Table 1: Prevalence of diabetic nephropathy among the studied groups

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On the basis of their urinary albumin : creatinine ratio, participants were divided into three groups: normoalbuminuria, microalbuminuria, and macroalbuminuria, with prevalence rate of 53, 34.2, and 12.8%, respectively [Table 2].
Table 2: Distribution of albuminuria among the studied groups

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The age of patients at diagnosis ranged between 25 and 70 years. The mean age at onset of DM in microalbuminuric patients was 45.55 ± 8.565 years, in macroalbuminuric patients it was 44.099 ± 6.580 years, and in normoalbuminuric patients it was 43.912 ± 5.288 years [Table 3].
Table 3: Clinical characteristic of the studied type 2 diabetic group (n = 234)

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This study found that of the type 2 DM patients included, 149 were women and 85 were men. Of the patients with microalbuminuria, 15 (18.75%) were men and 65 (81.25%) were women. Of the patients with macroalbuminuria, eight (26.67%) were men and 22 (73.33%) were women. The differences in the sex distribution were significant (P0 < 0.001) [Table 3].

The number of patients who were currently smoking amounted to 63 (26.9%). Of them, 15 (12.10%) patients had normoalbuminuria, 40 (50%) had microalbuminuria, and eight (26.67%) had macroalbuminuria. It was also found that smoking correlated significantly with microalbuminuria (P < 0.001) [Table 3].

Patients who had hypertension equal to or greater than 140/90 had the risk of microalbuminuria occurrence. There were 86 (69.4%) patients with normoalbuminuria, 66 (82.5%) with microalbuminuria, and 27 (90%) with macroalbuminuria (P = 0.037, significant) [Table 3].

BMI of the patients was 27.554 ± 3.155 (mean ± SD) in the microalbuminuria group, 30.155 ± 4.215 in the microalbuminuria group, and 32.780 ± 5.827 in the macroalbuminuria group, which was statistically significant with a P-value of less than 0.001 [Table 3].

HbA1c was 6.845 ± 0.114 (mean ± SD) in the normoalbuminuria group, 11.540 ± 2.488 in the microalbuminuria group, and 9.550 ± 1.119 in the macroalbuminuria group, which was statistically significant with a P-value of less than 0.001 [Table 4].
Table 4: Laboratory tests as determinants of microalbuminuria in the studied group

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Fasting blood sugar (FBS) level was 147.6 ± 64.8 (mean ± SD) in the normoalbuminuria group, 183.6 ± 70.2 in the microalbuminuria group, and 226.8 ± 77.4 in the macroalbuminuria group, which was statistically significant with a P-value of less than 0.001 [Table 4].

The risk of microalbuminuria occurrence tended to increase with the duration of DM, which was also statistically with a P-value of less than 0.001 [Table 5] and [Figure 1],[Figure 2],[Figure 3],[Figure 4] and [Figure 5].
Figure 1:

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Figure 2:

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Figure 3:

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Figure 4:

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Figure 5:

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Table 5: Duration of diabetes mellitus as a determinant of microalbuminuria in the studied group

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  Discussion Top


This is a cross-sectional study that represents data on prevalence and determinant risk factors of microalbuminuria as an early predictor of diabetic nephropathy.

The study was conducted in a rural area represented by Kafr Tanbedy Family Health Center, and in an urban area represented by Menoufia University Hospital. All diabetic patients attended selected Family Health Center and Internal Medicine Department for routine follow-up of type 2 DM (calculated sample size was 220 cases, which was increased to 234 cases to avoid any dropping out during the study).

The present study showed that the prevalence of microalbuminuria (incipient diabetic nephropathy) was 34.2% and that of macroalbuminuria (overt diabetic nephropathy) was 12.8% [Table 2].

This rate is higher than that reported for the UK Prospective Diabetes Study (UKPDS) population, wherein the prevalence was 25 and 5% for microalbuminuria and macroalbuminuria, respectively [24]. It is noteworthy that a higher ACR range (50-299 mg/g creatinine) for defining microalbuminuria and a slightly higher mean duration of disease were reported in the UKPDS group than in patients recruited in this study.

However, the prevalence rates of albuminuria in this study were also higher than those reported for a diabetic population from Chennai, India, where, as in this study, the diagnosis of albuminuria was based on a single ACR of greater than 30 mg/g creatinine; in that study, the prevalence of overt nephropathy was 2.2% and that of microalbuminuria was 26.9% [25].

A study in Tanzania showed that the percentage of microalbuminuria in type 2 DM is 9.8% [26], and studies on the white UK populations revealed prevalence of microalbuminuria to be 7-9% [27],[28].

Higher prevalence in the present study may be because most of the patients were on irregular treatment with poor glycemic control. The level of glycemic control seems to be the strongest factor influencing transition from normoalbuminuria to microalbuminuria [29].

This prevalence was slightly lower when compared with the study conducted by Chowta et al. [30]; in their study on 100 type 2 Indian diabetic patients attending outpatient clinics the prevalence of microalbuminuria was reported to be 37%.

Al-Maskari et al. [31], in their study on diabetic nephropathy in the United Arab Emirates, stated that the prevalence of microalbuminuria was 60% and that of macroalbuminuria was 12.5%.

Thakkar et al. [32] reported 50% prevalence of microalbuminuria among type 2 diabetic patients.

Maharjan et al. [33] reported 35.89% prevalence for microalbuminuria and 20.75% for macroalbuminuria. Another study by Wu et al. [34] reported 39.8% prevalence for microalbuminuria and 18.8% prevalence for macroalbuminuria among type 2 diabetic patients.

The variation in the prevalence rates is most probably because of the differences in diagnostic criteria, the stage of the disease, and the method of assessment.

Parving et al. [35] and Taneja et al. [36] reported that in type 2 DM the prevalence of microalbuminuria ranges from 8 to 47%, which is in agreement with the results of this study.

The sociodemographic characteristics of the studied group were classified into high, middle, and low socioeconomic status, which was represented by 21.4, 41, and 37.6% of the studied groups, respectively [Table 3].

There was no significant effect of socioeconomic status on microalbumin in urine.

This study revealed that microalbuminuria was significantly increased with the age of patients [Table 3]. This may be attributed to the long duration of DM as the patient age. Mean age in the microalbuminuric and macroalbuminuric groups was 45.55 ± 8.565 and 44.099 ± 6.580, respectively.

This result agreed with those of Thakkar et al. [32] and Chowta et al. [30], who reported that there was a statistically significant linear relationship between degree of albuminuria and age, although Thakkar et al. [32] in their study on type 2 Indian diabetic patients reported mean age of 61.91 ± 9.16 in the microalbuminuric group and 48.61 ± 7.6 in the normoalbuminuric group. The difference in the values of the mean did not affect the significant linear relationship. Sheikh et al. [37] reported that there was a high prevalence of microalbuminuria with increasing age in type 2 diabetic patients. Moreover, Ruilope et al. [38] have shown a positive correlation of microalbuminuria with age of the patients.

This study showed that the participation of women was more than men (63.7% were women as shown in [Table 2]). This could be explained by high compliance among women compared with men.

This study found that there was a significant relation between the sex of patients and level of microalbumin in urine [Table 3], which is in agreement with the results of study conducted by Vimalkumar et al. [39]. However, many studies reported that the male sex is still a risk factor for the development of renal disease in DM [40],[41],[42],[43]. In contrast, Orchard et al. [44] reported that the female sex appears to accelerate the renal disease progression in DM.

This study showed significant relation between BMI and the level of microalbumin in urine [Table 3], which agreed with the results of Mokdad et al. [45] and Sheikh et al. [37] but disagreed with the results of Chowta et al. [30], who reported that there was no effect of BMI on the prevalence of microalbuminuria among type 2 diabetic patients.

This study showed that hypertension was significantly more frequent among the incipient diabetic nephropathy group and overt diabetic nephropathy group [Table 3], which agreed with the study conducted on type 2 diabetic patients by Stratton et al. [40], who found that systolic blood pressure was significantly higher in those who progressed to incipient and overt diabetic nephropathy.

This study found a significant relation between smoking and microalbuminuria [Table 3], which agreed with the findings of Hertzel C et al. [46] but disagreed with those of Vimalkumar et al. [39].

This study found that there was a significant relation between family history of DM and microalbuminuria [Table 3], which agreed with a study conducted by Tagle et al. [47] and Shaukat et al. [48], who reported that type 2 DM has a strong genetic component, and parental history of DM is significantly associated with microalbuminuria; however, disagreed with the study conducted by Ahmedani et al. [49] and Agarwal et al. [50].

There is a high significant effect of family history of hypertension on microalbuminuria and this agreed with a study by Valensi et al. [51], who reported that urinary albumin excretion rate was significantly higher in patients with positive family history of hypertension, but disagreed with the study conducted by Ahmedani et al. [49].

This study revealed that diabetic nephropathy groups significantly had uncontrolled blood glucose [Table 4].

The data were confirmed in a study by Stratton et al. [40], who found that poor long-term glycemic control was an important predictor of the development of abnormally increased urinary albumin excretion. Another confirmation in a study by Sheikh et al. [37] reported that microalbuminuria has highly significant correlation with HbA1c. Kassab et al. [52] reported the same significant correlation of microalbuminuria with HbA1c.

FBS and HbA1c concentrations were significantly higher in the microalbuminuric and macroalbuminuric groups compared with the normoalbuminuric participants (P < 0.001) [Table 4]. Similar observations have been made by Unnikrishnan et al. [25].

This study showed that the level of microalbumin in urine increased with an increase in the duration of DM [Table 5], which agreed with study by Cowta et al. [30], who reported that the mean duration of DM in the microalbuminuric patients was 10.7 ± 5.0 years, whereas in the normoalbuminuric patients it was 3.2 ± 2.0 years, which was statistically highly significant. The same finding by Sheikh et al.
[37] and Naz et al. [53] stated that microalbuminuria had a highly significant correlation with the duration of DM. However, this result disagrees with the study by Krolewski et al. [54], who reported that the occurrence of nephropathy has no relation with the duration of DM because of the predominant effect of uncontrolled blood glucose.

This study shows multiple regressions between the patient groups and independent variables. There is significant effect for HbA1c, smoking, FBS, duration, BMI, sex, and hypertension [Table 6].{Table 6}


  Conclusion Top


This study has found that the prevalence of microalbuminuria was 34.2% and that of macroalbuminuria was 12.8%. The presence of microalbuminuria, which is the predictor of later development of diabetic nephropathy, increases with age, female sex, duration of DM, smoking, BMI, and uncontrolled blood pressure and blood glucose.

The presence of microalbuminuria is an indication to the physician to take steps to prevent further renal damage by correction of risk factors. Urinary excretion of microalbumin should be monitored routinely in patients with DM.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.World Health Organization. The diabetes program; 2004. Available at: http//www.who.int/diabetes/en/. [Accessed 21 September 2004].  Back to cited text no. 1
    
2. Haring HU. Pathogenesis of type II diabetes: are there common causes for insulin resistance and secretion failure? Exp Clin Endocrinol Diabetes 1999; 107:S17-S23.  Back to cited text no. 2
    
3. Harris M, Klein R, Welborn T, Knuiman M. Onset of NIDDM occurs at least 4-7 years before clinical diagnosis. Diabetes Care 1992; 15:815-819.  Back to cited text no. 3
    
4. Remuzzi G, Schieppati A, Ruggenenti P. Nephropathy in patients with type 2 diabetes. N Engl J Med 2002; 346:1145-1151.  Back to cited text no. 4
    
5. Molitch ME, DeFronzo RA, Franz MJ, Keane WF, Mogensen CE, Parving HH, Steffes MW. the American Diabetes Association. Nephropathy in diabetes (position statement). Diabetes Care 2004; 27:S79-S83.  Back to cited text no. 5
    
6. Afifi A, El Setouhy M, El Sharkawy M, Ali M, Ahmed H, El-Menshawy O, Masoud W. Diabetic nephropathy as a cause of end-stage renal disease in Egypt: a six-year study. East Mediterr Health J 2004; 10:620-626.  Back to cited text no. 6
    
7. Asselbergs FW, Diercks GF, Hillege HL, van Boven AJ, Janssen WM. The Prevention of Renal and Vascular Endstage Disease Intervention Trial (PREVEND IT) Investigators: effects of fosinopril and pravastatin on cardiovascular events in subjects with microalbuminuria. Circulation 2004; 110:2809-2816.  Back to cited text no. 7
    
8. American Diabetes Association. Diabetic nephropathy. Diabetes Care 2003; 26:S94-S98.  Back to cited text no. 8
    
9. Agewall S, Wilkstrand J, Ljungman S, Fagerbaerg B. Usefulness of microalbuminuria in predicting cardiovascular mortality in treated hypertensive men with and without diabetes mellitus. Am J Cardiol 1997; 80:164-169.  Back to cited text no. 9
    
10.Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull C. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int 2003; 63:225-232.  Back to cited text no. 10
    
11.Mykkanen L, Zaccaro DJ, Wagenknecht LE, Robbins DC, Gabriel M, Haffner SM. Microalbuminuria is associated with insulin resistance in nondiabetic subjects: the Insulin Resistance Atherosclerosis Study. Diabetes 1998; 47:793-800.  Back to cited text no. 11
    
12.Consensus development conference on the diagnosis and management of nephropathy in patients with diabetes mellitus. American Diabetes Association and the National Kidney Foundation. Diabetes Care 1994; 17:1357.  Back to cited text no. 12
    
13.Zelmanovitz T, Gross JL, Oliveira JR, et al. The receiver operating characteristics curve in the evaluation of a random urine specimen as a screening test for diabetic nephropathy. Diabetes Care 1997; 20:516-519.  Back to cited text no. 13
    
14.Nakamura Y, Myers BD. Charge selectivity of proteinuria in diabetic glomerulopathy. Diabetes 1988; 37:1202-1211.  Back to cited text no. 14
    
15.Cambiaso CL, Collet-Cassart D, Lievens M. Immunoassay of low concentrations of albumin in urine by latex particle counting. Clin Chem 1988; 34:416-418.  Back to cited text no. 15
    
16.Medcalf EA, Newman DJ, Gorman EG, Price CP. Rapid, robust method for measuring low concentrations of albumin in urine. Clin Chem 1990; 36:446-449.  Back to cited text no. 16
    
17.Harmoinen A, Ala-Houhala I, Vuorinen P. Rapid and sensitive immunoassay for albumin determination in urine. Clin Chim Acta 1985; 149:269-274.  Back to cited text no. 17
    
18.Bernard A, Lauwerys R. Latex immunoassay of urinary albumin. J Clin Chem Clin Biochem 1983; 21:25-30.  Back to cited text no. 18
    
19.Bartels H, Böhmer M. Eine mikromethode zur kreatininbestimmung. Clin Chim Acta 1971; 32:81-85.  Back to cited text no. 19
    
20.Fabiny DL, Ertingshausen G. Automated reaction-rate method for determination of serum creatinine with CentrifiChem. Clin Chem 1971; 17:696-700.  Back to cited text no. 20
    
21.Kaplan LA, Glucose, Kaplan A et al. Clin Chem The C.V. Mosby Co. St Louis. Toronto. Princeton (1984); 1032-1036.  Back to cited text no. 21
    
22.Trinder P. Ann Clin Biochem 1969; 6:24-33.  Back to cited text no. 22
    
23.Karl J, et al. Development and standardization of a new immunoturbidimetric HbA1C assay. Klin Lab 1993; 39:991-996.  Back to cited text no. 23
    
24.Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull CA, Holman RR, UKPDS Group. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int 2003; 63:225-232.  Back to cited text no. 24
    
25.Unnikrishnan RI, Rema M, Pradeepa R, Deepa M, Shanthirani CS, Deepa R, et al. Prevalence and risk factors of diabetic nephropathy in an urban South Indian population: the Chennai Urban Rural Epidemiology Study (CURES 45) Diabetes Care 2007; 30:2019-2024.  Back to cited text no. 25
    
26.Lutale JJK, Thordarson H, Abbas ZG, Vetvik K. Microalbuminuria among Type 1 and Type 2 diabetic patients of African origin in Dar Es Salaam, Tanzania. BMC Nephrol 2007; 8:1471-2369.  Back to cited text no. 26
    
27.Gatling W, Knight C, Mullee MA, et al. Microalbuminuria in diabetes: a population study of the prevalence and an assessment of three screening tests. Diabet Med 1988; 5:343-347.  Back to cited text no. 27
    
28.Marshall SM, Alberti KG. Comparison of the prevalence and associated features of abnormal albumin excretion in insulin-dependent and non-insulin-dependent diabetes. Q J Med 1989; 70:61-71.  Back to cited text no. 28
    
29.Ismail-Beigi F, Craven T, Banerji MA, Basile J, Calles J, Cohen RM, et al. Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial. Lancet 2010; 376:419-430.  Back to cited text no. 29
    
30.Chowta NK, Pant P, Chowta MNP. Microalbuminuria in diabetes mellitus: association with age, sex, weight, and creatinine clearance. Indian J Nephrol 2009; 19:53-56.  Back to cited text no. 30
[PUBMED]  Medknow Journal  
31.Al-Maskari F, El-Sadig M, Obineche E. Prevalence and determinants of microalbuminuria among diabetic patients in the United Arab Emirates. BMC Nephrol 2008; 9:1.  Back to cited text no. 31
    
32.Thakkar B, Arora K, Vekariya R, Lulania M. Prevalence of microalbuminuria in newly diagnosed type 2 diabetes mellitus. Natl J Integr Res Med 2011; 2:22-25.  Back to cited text no. 32
    
33.Maharjan BR, Bhandary S, et al. Microalbuminuria and macroalbuminuria in type 2 diabetes. J Nepal Health Res Counc 2010; 8:110-115.  Back to cited text no. 33
    
34.Wu A, Kong N, de Leon F, Pan C, Tai T, Yeung V, et al. An alarmingly high prevalence of diabetic nephropathy in Asian type 2 diabetic patients: the MicroAlbuminuria Prevalence (MAP) Study. Diabetologia 2005; 48:17-26.  Back to cited text no. 34
    
35.Parving HH, Gall MA, Skott P. Prevalence and causes of microalbuminuria in patients with non-insulin dependent diabetic patients. Kidney Int 1992; 41:758-762.  Back to cited text no. 35
    
36.Taneja V, Sircar S, Kansra U, Lamba IMS. Microalbuminuria in normotensive non-insulin dependent diabetic subjects - associations and predictions J Diab Assoc India 1997; 37:30-36.  Back to cited text no. 36
    
37.Sheikh SA, Baig JA, Iqbal T, Kazmi T, Baig M, Husain SS. Prevalence of microalbuminuria with relation to glycemic control in type-2 diabetic patients in Karachi. J Ayub Med Coll Abbottabad 2009; 21:60-67.  Back to cited text no. 37
    
38.Ruilope LM, Segura J. Predictors of the evolution of microalbuminuria. Hypertension 2006; 48:832-833.  Back to cited text no. 38
    
39.Vimalkumar VK, Anand Moses CR, Padmanaban S. Prevalence & risk factors of nephropathy in type 2 diabetic patients. Int J Collab Res Intern Med Public Health 2011; 3:598-615.  Back to cited text no. 39
    
40.Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000; 321:405-412.  Back to cited text no. 40
    
41.Sibley SD, Thomas W, de Boer I, Brunzell JD, Steffes MW. Gender and elevated albumin excretion in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) cohort: role of central obesity. Am J Kidney Dis 2006; 47:223-232.  Back to cited text no. 41
    
42.Jones CA, Krolewski AS, Rogus J, Xue JL, Collins A, Warram JH. Epidemic of end-stage renal disease in people with diabetes in the United States population: do we know the cause? Kidney Int 2005; 67:1684-1691.  Back to cited text no. 42
    
43.Hovind P, Tarnow L, Parving HH. Remission and regression of diabetic nephropathy. Curr Hypertens Rep 2004; 6:377-382.  Back to cited text no. 43
    
44.Orchard TJ, Dorman JS, Maser RE, Becker DJ, Drash AL, Ellis D, et al. Prevalence of complications in IDDM by sex and duration. Pittsburgh Epidemiology of Diabetes Complications Study II. Diabetes 1990; 39:1116-1124.  Back to cited text no. 44
    
45.Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, Marks JS. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA 2003; 289:76-79.  Back to cited text no. 45
    
46.Hertzel C, et al. Epidemiologic analysis of risk factors, risk indicators, risk markers, and causal factors. Endocrinol Metab Clin North Am 2002; 31:537-551.  Back to cited text no. 46
    
47.Tagle R, Acevedo M, Vidt DG. Microalbuminuria: is it a valid predictor of cardiovascular risk? Cleve Clin J Med 2003; 70:255-261.  Back to cited text no. 47
    
48.Shaukat A, Arian TM, Shahid A. Microalbuminuria: incidence in patience of diabetes at Bhawalpur. Pak J Pathol 2005; 16:17-21.  Back to cited text no. 48
    
49.Ahmedani MY, Hydrie MZ, Iqbal A, Gul A, Mirza WB, Basit A. Prevalence of microalbuminuria in type 2 diabetic patients in Karachi: Pakistan: a multi-center study. J Pak Med Assoc 2005; 55:382-386.  Back to cited text no. 49
    
50.Agarwal N, Sengar NS, Jain PK, Khare R. Nephropathy in newly diagnosed type 2 diabetics with special stress on the role of hypertension. J Assoc Physicians India 2011; 59:145-147.  Back to cited text no. 50
    
51.Valensi P, Busby M, Combes ME, Attali JR. Microalbuminuria and hypertension in obese patients: Arch Mal Coeur Vaiss 1992; 85: 1193-1195.  Back to cited text no. 51
    
52.Kassab A, Ajmi T, Issaoui M, Chaeib L, Miled A, Hammami M. Homocysteine enhances LDL fatty acid peroxidation, promoting microalbuminuria in type 2 diabetes. Ann Clin Biochem 2008; 45:476-480.  Back to cited text no. 52
    
53.Naz S, Sadaruddin A, Khannum A, Osmani R. Frequency of microalbuminuria in diabetic patients of Islamabad and Rawalpindi. Pak J Med Res 2007; 46:70-74.  Back to cited text no. 53
    
54.Krolewski, AS, Poznik, GD, Placha, G, Canani, L, Dunn, J, Walker, W et al. A genome-wide linkage scan for genes controlling variation in urinary albumin excretion in type II diabetes. Kidney Int 2006; 69:129-136.  Back to cited text no. 54
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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Abstract
Introduction
Aim
Patients and methods
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