122 Original ISSN 2413-0516 J Contemp Med Sci | Vol. 7, No. 2, March-April 2021: 122 – 127 Introduction Metabolic syndrome is associated with an increased risk of type 2 diabetes mellitus (DM) and cardiovascular disease (CVD).1-4 Metabolic syndrome is the coincidence in a person of interrelated risk factors for CVD and diabetes. These factors include hyperglycemia, raised blood pressure, elevated tri- glyceride level, reduced HDL-C, and obesity (particularly cen- tral adiposity).5 Various reports indicate that the individual of the metabolic syndrome is associated with increased risk for both CVD and type 2 diabetes.6,7 Higher blood pressure, the shorter life expectancy, people with high blood pressure run a higher risk of having a stroke (which damages the brain) or a heart attack. If left untreated for a long time, high blood pressure can lead to kidney failure and even damage the eye. It can also make the heart abnor- mally large and less efficient (a condition called ‘left ventricu- lar hypertrophy’). This can lead to heart failure, which is when the pumping action of the heart becomes less effective. It also known as hypertension – rarely makes people feel ill. It is sometimes called a ‘silent threat’ because there are usually no symptoms, and it very often goes undiagnosed.8 Blood pres- sure is regulated by renin–angiotensin system (RAS). DM is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, activation, or action.9 The effects of DM include long-term damage, dysfunction, and failure of various organs. DM may present with characteristic symptoms such as thirst, polyuria, blurring of vision, and weight loss. Most cases of DM fall into three general broad catego- ries: type 1 DM (T1DM), type 2 DM (T2DM), and gestational DM (GDM) and another type is a specific type of diabetes.10 Blood pressure is the force of blood against the walls of arter- ies. Blood pressure rises and falls throughout the day. When blood pressure stays elevated over time, it’s called high blood pressure.11 The myosin heavy chain 9 (MYH9) gene, which is located on chromosome 22 q12.3-13.2, has 40 exons that encode a pro- tein of approximately 224,000 kDa. The protein is a non-muscle myosin heavy chain that dimerizes to form the motor domain of non-muscle myosin IIA, an important motor protein found in most cells of the body.12 The MYH9 gene is expressed in fibroblasts, erythroblasts, and kidney cells.13 Abnormal MYH9 expression, positioning, or function change leads to cytoskel- eton damage, causing proteinuria, hematuria, or renal failure in some cases.14 MYH9 has also been shown to be a major sus- ceptibility gene for nephropathy, and hypertension. This asso- ciation has also been demonstrated in various populations, ranging from African-Americans and Hispanic Americans to Europeans.15–18 Freedman et al. found that mutations in MYH9 Association between microalbuminuria and MYH9 gene polymorphisms in hypertensive Iraqi patients with metabolic syndrome Alaa Fahem Jasim1, Fadhil Jawad Al-Tu’ma1*, Dhafir Abdul-Mahdi Faisal2 1 Department of Chemistry and Biochemistry, College of Medicine, University of Kerbala, Kerbala, Iraq. 2 College of Pharmacy, University of Kufa, Najaf, Iraq. *Correspondence to: Fadhil Jawad Al-Tu’ma (E-mail: fadhil.jawad@uokerbala.edu.iq) (Submitted: 21 December 2020 – Revised version received: 09 January 2021 – Accepted: 19 February 2021 – Published online: 26 April 2021) Abstract Objective The presented work aimed to study the correlation between microalbuminuria and MYH9 (T>C) (rs3752462) gene polymorphisms in metabolic syndrome of Iraqi patients. Methods This study was a cross-sectional study. Sample size was 140 persons of both gender selected randomly between April 1, 2019 and Aug. 15, 2020. They are divided into two groups, 80 with metabolic syndrome patients and 60 with control groups subdivided into another two groups: 30 persons with obese and 30 persons without obese. The distribution of sample according to the gender, the number of males had metabolic syndrome were 47 and female 33, but in obese healthy control the number of males were 19 and female 11, while in non-obese healthy control the number of males were 15 and female 15. The age groups were ranged between 40 and 60 years. Typing of MYH9 was performed by refractory mutation system-polymerase chain reaction (ARMS-PCR). The current study was performed to investigate the SNPs that affected MYH9 gene which was (T>C) (rs3752462). Results There was a significant difference between blood sugar, HbA1c, total cholesterol, TG, VLDL-C, LDL-C, blood urea, microalbuminuria, BMI, and HOMA-IR in metabolic syndrome patients as compared with healthy control groups (P ≤ 0.01). The significant result (P ≤ 0.01) were appeared between TT for MYH9 genotype patients and obese control with biochemical parameters (Blood glucose, HbA1c, TC, TG, VLDL-C, and LDL-C). The correlation between TT SNP for MYH9 genotype patients and non-obese control with biochemical parameters is significant result (P ≤ 0.01 and P ≤ 0.05) (Blood glucose, HbA1c, insulin, TC, TG, VLDL-C, LDL-C, urea, and microalbuminuria). The significant result (P ≤ 0.01 and P ≤ 0.05) appeared between CT for MYH9 genotype patients and obese control with biochemical parameters (Blood glucose, HbA1c, TC, TG, and VLDL-C) respectively. Conclusions There is a significant difference between blood glucose, HbA1c, total cholesterol, TG, VLDL-C, LDL-C, blood urea, microalbuminuria, BMI, and HOMA-IR in metabolic syndrome patients and healthy control groups (P ≤ 0.01). Also, a significant result (P ≤ 0.01) obtained between TT for MYH9 genotype patients and obese and non-obese control with some biochemical parameters. (P ≤ 0.01 and P ≤ 0.05). The significant results (P ≤ 0.01 and P ≤ 0.05) appear between CT for MYH9 genotype patients and obese control with some biochemical parameters. Keywords Metabolic syndrome, Albumins, MYH9, genotype, ARMS-PCR http://en.wikipedia.org/wiki/Diabetes_mellitus_type_1 http://en.wikipedia.org/wiki/Diabetes_mellitus_type_2 123 Original Association between microalbuminuria and MYH9 gene polymorphismsFadhil Jawad Al-Tu’ma et al. J Contemp Med Sci | Vol. 7, No. 2, March-April 2021: 122 – 127 associated with African-American proteinuria caused by high blood pressure were associated with end-stage renal disease (ESRD).19 Other investigator show that the rs3752462 was associated with chronic kidney disease (CKD).20 The present study was aimed to investigate the correlation between microalbuminuria and MYH9 (T>C) (rs3752462) gene polymorphisms in metabolic syndrome of Iraqi patients and its correlation with various biochemical markers. Materials and Methods This work was designed as a cross-sectional study, 140 subjects were recruited, about 80 of them with metabolic syndrome and the other 60 of apparently healthy individuals randomly with age ranged between 40 and 50 years between April 1, 2019 and Aug. 15, 2020. The patients were diagnosed by a specialist phy- sician at Al-Hassan Medical Center for Endocrinology, in the Al-Hussein Medical City / Kerbala Health Directorate - Iraq. It should be noted that Kerbala is a holy city and one of the biggest cities in Iraq. The study protocol was approved by the Medical Ethics committee of College of Medicine/ University of Kerbala and the Kerbala Health Directorate. The glycated hemoglobin (HbA1c) level was assessed, using the COBAS HbA1c kit (Roche, Germany), by COBAS INTEGRA® 400 (Roche, Germany); the turbidity measure- ment was made with a spectrophotometer to determine the light absorbance. The amount of light blocked by particle sus- pension depends not only on concentration, but also on the particle size, because particles tend to aggregate and settle out of suspension, consequently sample handling becomes crit- ical. Blood samples were collected from T2DM patients and the control group in EDTA tubes. Total genomic DNA was extracted from the peripheral blood sample (1 ml), using the kit ReliaPrep™ Blood gDNA Miniprep System obtained from (Promega USA). The protocol was followed according to the manufacturers’ recommendations. DNA concentration and purity were measured, using a BioDrop (UK). Genotyping of MYH9 (T>C) (rs3752462) polymorphism was performed by tetra-primer amplification refractory muta- tion system-polymerase chain reaction technique (T-ARMS- PCR) with the use of thermocycler (Cleaver/UK). Outer forward: 5ʹ-AGCTGCAGCCCAGAGCATCTCCTCTA- AT-3ʹ; Outer reverse: 5ʹ-TCGTTTGAGCAGCTGTG- CATCAATTACA-3ʹ; Inner forward: 5ʹ-CAGGTGTG AGGTCAAAGCAAGCCTTGT-3ʹ. Inner reverse: 5ʹ-ATC- GACC TCATTGAGA AGCCAGTGAGGAG-3ʹ. The ampli- fication was performed in a total volume of 25 μl consisted of 12.5 μl of Taq green master mix (Promega, USA) 1, 1, 1 and 1 μl of outer forward, reverse forward, inner forward and inner reverse primers, respectively and 5 μl genomic DNA as a template. The PCR reaction program protocol was 94 °C for 5 min followed by 35 cycles of 94 °C for 35 s, 55 °C for 45 s, 72 °C for 55 s and a final cycle 72 °C for 5 min. The amplifi- cation products were 381 bp for control band. The product of amplification was analyzed by 2% agarose gel electrophoresis. Results In the present study that is shown in Table 1, there was a sig- nificant difference between blood glucose, HbA1c, total cho- lesterol, TG, VLDL-C, LDL-C, blood urea, microalbuminuria, BMI, and HOMA-IR in metabolic syndrome patients and Table 1. Correlation between biochemical parameters with metabolic syndrome and compared with healthy control. P value Mean ± SD Parameters Control Groups Patients Non-ObeseObese ≤ 0.01110.87 ± 17.31112.33 ± 27.22244.31 ± 98.28Blood glucose, mg/dl ≤ 0.015.64 ± 0.486.08 ± 0.739.30 ± 2.15HbA1c% 0.1313.13 ± 2.3014.37 ± 3.2314.8 ± 4.48Insulin, µU/ml ≤ 0.01120.00 ± 22.57124.07 ± 23.71178.28 ± 47.32TC, mg/dl ≤ 0.01107.50 ± 20.89114.30 ± 25.09254.29 ± 101.50TG, mg/dl 0.6835.47 ± 6.7833.60 ± 5.7434.95 ± 9.96HDL-C, mg/dl ≤ 0.0120.40 ± 4.2322.83 ± 4.5650.81 ± 20.76VLDL-C, mg/dl ≤ 0.0161.97 ± 27.2463.93 ± 25.59100.70 ± 43.28LDL-C, mg/dl ≤ 0.0126.40 ± 7.0829.93 ± 6.7635.09 ± 12.97Urea, mg/dl 0.500.87 ± 0.180.90 ± 0.220.95 ± 0.426Creatinine, mg/dl ≤ 0.0113.40 ± 5.3313.83 ± 20.8550.08 ± 77.95Microalbuminuria ≤ 0.0123.78 ± 1.0037.01 ± 1.8237.48 ± 1.98BMI, kg/m2 ≤ 0.013.66 ± 1.14.05 ± 1.58.4 ± 3.02HOMA-IR (HbA1c) glycated hemoglobin A1c, (TG) triglycerides, (TC) total cholesterol, (HDL-C) high-density lipoprotein- cholesterol, (VLDL-C) very low density lipoprotein-cholesterol, (LDL-C) low density lipoprotein-cholesterol, (BMI) body mass index, (HOMA-IR) homeostatic model assessment of insulin resistance. https://www.mayoclinic.org/diseases-conditions/chronic-kidney-disease/symptoms-causes/syc-20354521 http://www.webmd.com/cholesterol-management/default.htm 124 Original Association between microalbuminuria and MYH9 gene polymorphisms Fadhil Jawad Al-Tu’ma et al. J Contemp Med Sci | Vol. 7, No. 2, March-April 2021: 122 – 127 healthy control groups (P ≤ 0.01). While a non-significant differences between metabolic syndrome patients and healthy control groups regarding insulin (P = 0.13), HDL-C (P = 0.68), and serum creatinine (P = 0.50). The amplification of MYH9 (T>C) gene polymorphism was observed in 381 bp as shown in Fig. 1. Lane 1: Represented DNA marker 100 - 1000 bp. Lane 4, 8 and 9: Represented heterozygote (CT) and internal control of (T>C) SNP of MYH9 gene were showed in (381 bp, 234 bp and 201 bp). Lane 2 and 6: Represented mutant type (CC) and internal control of (T>C) SNP of MYH9 gene were showed in (381 bp and 201 bp). Lane 3 : Represented wild type (TT) and internal control of (T>C) SNP of MYH9 gene were showed in (381 bp and 234 bp). Lane 5 and 7: Represented internal control of (CC) of MYH9 gene were showed in (382 bp). Fig. 1 Amplification of SNP of MYH9 (T>C) was showed in this figure Table 2. Correlation between SNP (T>C) for MYH9 genotype and biochemical parameters in patients with MetS. MYH9 (T>C)Patients Group Mean of Parameters CCCTTT 54233No. of patients 185.25256.67239.78Blood glucose, mg/dl 9.429.3959.236HbA1c% 1614.315.42Insulin, µU/ml 172.75173.97182.09TC, mg/dl 146.75268.82245.57TG, mg/dl 4032.8537.12HDL-C, mg/dl 27.2553.4550.03VLDL-C, mg/dl 113.2595.42103.57LDL-C, mg/dl 36.534.9535.06Urea, mg/dl 0.880.940.97Creatinine, mg/dl 1755.8750.30Microalbuminuria 36.5737.6337.28BMI, kg/m2 (HbA1c) glycated hemoglobin A1c, (TG) triglycerides, (TC) total cholesterol, (HDL-C) high-density lipoprotein-cholesterol, (VLDL-C) very low density lipoprotein-cholesterol, (LDL-C) low density lipoprotein-cholesterol, (BMI) body mass index. Table 3. Correlation between control group had SNP (T>C) for MYH9 genotype and biochemical parameters. MYH9 (T>C) Control Groups Mean of Parameters Non obese controlObese Control CCCTTTCCCTTT 00301821No. of subjects //110.8691117.12111.52Blood glucose, mg/dl //5.635.76.236.03HbA1c, % //13.131113.514.85Insulin, µU/ml //120123130.75121.57TC, mg/dl //107.5119116.37113.28TG, mg/dl //35.463135.2533.09HDL-C, mg/dl //20.4212322.85VLDL-C, mg/dl //61.966870.8761.09LDL-C, mg/dl //26.42029.2530.66Urea, mg/dl //0.870.80.950.88Creatinine, mg/dl //13.4611.515.09Microalbuminuria //23.7836.337.6536.80BMI, kg/m2 (HbA1c) glycated hemoglobin A1c, (TG) triglycerides, (TC) total cholesterol, (HDL-C) high-density lipoprotein- cholesterol, (VLDL-C) very low density lipoprotein-cholesterol, (LDL-C) low density lipoprotein-cholesterol, (BMI) body mass index. http://www.webmd.com/cholesterol-management/default.htm http://www.webmd.com/cholesterol-management/default.htm 125 Original Association between microalbuminuria and MYH9 gene polymorphismsFadhil Jawad Al-Tu’ma et al. J Contemp Med Sci | Vol. 7, No. 2, March-April 2021: 122 – 127 Discussion Metabolic syndrome and hypertension verified the convinc- ing association with microalbuminuria in both females OR = 3.34; 95% (CI 2.45- 4.55) and males OR = 2.51; 95% (CI 1.63- 3.86)21(Table 3). The most common component of meta- bolic syndrome in our sample was shown to be central obesity and DM followed by hypertriglyceridemia and hypertension; this disagrees with the Indian study, which showed that the main component was hypertension (98.37%), followed by dyslipidemia (77.05%), hyperglycemia (75.41%), and obesity (59.02%).22 Most of the obese who showed metabolic syndrome were not exercising, but no significant association was found between metabolic syndrome and practicing exercises. The heritage family study in the United States showed that exercise training resulted in improvement in the metabolic profile of the participants; the prevalence of metabolic syndrome was decreased from 16.9% before training to 11.8% after training.23 The higher prevalence of high TG in our country relative to most of the studies elsewhere might be due to higher intake simple carbohydrates and higher ratio of simple to com- plex carbohydrate consumption by the Persian people.24 We observed higher prevalence of hypertriglyceridemia in Iranian males similar to findings in most other countries.25 Older adults are highly susceptible to overweight and obesity due to reduced mobility.26 Kuchak and colleagues, as well as Simoes and colleagues, reported that a lack of physical activity program and movement in older adults can intensify the growth of body mass and obesity.27,28 Dyslipidemia is one of the major risk factors for cor- onary heart disease besides age, family history, cigarette smoking, hyperglycemia, and hypertension. The prevalence of dyslipidemia varies widely according to the ethnic, socio- economic, and cultural characteristics of distinct population groups.29 Hypertriglyceridemia was independently associated with DM. A similar association between hypertriglyceridemia and HbA1c was reported in a Russian study.30 The present study showed the independent risk factors of the different types of dyslipidemia by multivariate analysis. DM and hyperten- sion were independent risk factors for hypercholesterolemia. A study from Saudi Arabia also reported same association between DM, hypertension, and hypercholesterolemia.31 The mean value of HOMA-IR was significantly higher in adult male with essential hypertension when compared with that of controls. Systolic blood pressure and diastolic blood pressure show positive correlation with HOMA-IR but was sig- nificant only with systolic blood pressure. This finding is con- sistent with the findings of some other investigators of other countries.32,33 PA Sarafidis and AN Lasaridis was designed to determine the validity and the reproducibility of HOMA-IR, 1/HOMA-IR, QUICKI and McAuley’s index in a population of patients that have developed hypertension before type II diabetes.34 An elevated serum creatinine level is also a late sign of renal damage in essential hypertension with frankly elevated serum creatinine values predict a poor prognosis in patients with hypertension.35 A study by Wachtell et al in 2002 showed an association with raised microalbuminuria and increased risk of heart attacks and stroke. Among the patients with hypertension.36 The prevalence of microalbuminuria was also higher among those with hypertensive retinopathy in our study and it was statistically significant. Microalbuminuria is more prevalent in essential hypertensive with target organ dysfunction.36 Table 4. The correlation between SNP (T>C) for MYH9 genotype and biochemical parameters MYH9 (T>C) CCCTTT Patients vs. Non-Obese control Patients vs. Obese control Patients vs. Non-Obese control Patients vs. Obese control Patients vs. Non-Obese control Patients vs. Obese control Biochemical parameters -0.3-≤ 0.01≤ 0.01≤ 0.01Blood sugar, mg/dl -0.097-≤ 0.01≤ 0.01≤ 0.01HbA1c% -0.6-0.7≤ 0.010.6Insulin, µu/ml -0.6-≤ 0.01≤ 0.01≤ 0.01TC, mg/dl -0.5-≤ 0.01≤ 0.01≤ 0.01TG, mg/dl -0.2-0.40.50.2HDL-C, mg/dl -0.4-≤ 0.01≤ 0.01≤ 0.01VLDL-C, mg/dl -0.7-0.1≤ 0.01≤ 0.01LDL-C, mg/dl -0.6-0.16≤ 0.010.24Urea, mg/dl -0.7-0.90.30.5Creatinine, mg/dl 0.6-0.13≤ 0.050.07Microalbuminuria (HbA1c) glycated hemoglobin A1c, (TG) triglycerides, (TC) total cholesterol, (HDL-C) high-density lipoprotein-cholesterol, (VLDL-C) very low density lipoprotein- cholesterol, (LDL-C) low density lipoprotein-cholesterol. http://www.webmd.com/cholesterol-management/default.htm 126 Original Association between microalbuminuria and MYH9 gene polymorphisms Fadhil Jawad Al-Tu’ma et al. J Contemp Med Sci | Vol. 7, No. 2, March-April 2021: 122 – 127 The amplification of SNP of MYH9 (T>C) was showed in 381 bp as in Fig 3. Association between MYH9 (T>C) SNP and biochemical parameters The results in current study are shown in Tables 2-4. The cor- relation between metabolic syndrome patients and control groups have MYH9 (T>C) SNP with biochemical parameters (Blood glucose, HbA1c, Insulin, TC, TG, HDL-C, VLDL-C, LDL-C, urea, creatinine, microalbuminuria, and BMI). The significant results (P ≤ 0.01) appear between TT for MYH9 genotype patients and obese control with biochemical parameters (Blood glucose, HbA1c, TC, TG, VLDL-C, and LDL-C). The correlation between TT SNP for MYH9 genotype patients and non-obese control with biochemical parameters is significant result (P value ≤ 0.01 and P ≤ 0.05) (Blood glu- cose, HbA1c, insulin, TC, TG, VLDL-C, LDL-C, Bl. urea, and microalbuminuria). The significant results (P ≤ 0.01 and P ≤ 0.05) appear between CT for MYH9 genotype patients and obese control with biochemical parameters (Blood glucose, HbA1c, TC, TG, and VLDL-C). The non-significant results (P-value > 0.01) are appear between CC for MYH9 genotype patients and obese control with biochemical parameters (Blood glucose, HbA1c, insu- lin, TC, TG, HDL-C, VLDL-C, LDL-C, urea, creatinine, and microalbuminuria). The correlation between TT SNP for MYH9 genotype patients and obese control with biochemical parameters (insulin, HDL-C, urea, creatinine and microalbuminuria) is non-significant (P > 0.01). The non-significant results (P > 0.01) showed between TT SNP for MYH9 genotype patients and non-obese control with biochemical parameters (HDL-C and creatinine). The correlation between CT SNP for MYH9 genotype patients and obese control with biochemical parameters (Insulin, HDL-C, LDL-C, urea, creatinine, and microalbumin- uria) is non-significant (P > 0.01). The results in current study that are shown in the same tables that the correlation between metabolic syndrome patients and control groups have MYH9 (T>C) SNP with bio- chemical parameters (Blood glucose, HbA1c, insulin, TC, TG, HDL-C, VLDL-C, LDL-C, urea, creatinine, microalbumin- uria, and BMI). There is a difference in the distribution of the CC, CT, and TT genotypes at rs3752462 in patients with CKD with SBP ≥ 140 mmHg and SBP < 140 mmHg. The multivariate analysis showed that the CC genotype at rs3752462 was associated with a lower risk of concurrent higher SBP than the TT geno- type in CKD patients. This result provides evidence that there is a genetic link between MYH9 and hypertension in patients with CKD in China.37 It is found that MYH9 SNP rs3752462 is involved in the susceptibility of CKD patients to hypertension. Multivariate logistic regression analysis indicated that the CC genotype was a protective factor against higher SBP in patients with CKD. It also indicated that the mutation of a C allele to a T allele can lead to an SBP increase.38,39 The minor allele of SNP rs3752462 is associated with an increased risk of DKD. The results suggest that MYH9 rs3752462 might play an important role in the risk of DKD in the Chinese Han population.40 MYH9 rs3752462 was asso- ciated with cerebrovascular blood flow (CBF) in patients with type 2 diabetes.41 Albuminuria is highly associated with Indian blood quantum in this population suggesting a strong genetic susceptibility to CKD.42 Conclusion 1. There is a significant difference between blood glucose, HbA1c, total cholesterol, TG, VLDL-C, LDL-C, blood urea, microalbuminuria, BMI, and HOMA-IR in meta- bolic syndrome patients and healthy control groups (P ≤ 0.01). 2. Most of metabolic syndrome patients are found in age group of 40–49 years. 3. The significant result (P ≤ 0.01) appear between TT for MYH9 genotype patients and obese control with bio- chemical parameters (Blood glucose, HbA1c, TC, TG, VLDL-C, and LDL-C). 4. The correlation between TT SNP for MYH9 genotype patients and non-obese control with biochemical param- eters is significant result (P ≤ 0.01 and P-value ≤ 0.05) (Blood glucose, HbA1c, insulin, TC, TG, VLDL-C, LDL- C, urea, and microalbuminuria). 5. The significant result (P ≤ 0.01 and P ≤ 0.05) appear between CT for MYH9 genotype patients and obese con- trol with biochemical parameters (Blood sugar, HbA1c, TC, TG, and VLDL-C). Conflict of Interest None References 1. Grundy, SM. Metabolic syndrome: connecting and reconciling cardiovascular and diabetes worlds. J Am Coll Cardiol, 2006;47.6:1093-1100. 2. Grundy SM. Does a diagnosis of metabolic syndrome have value in clinical practice? June 2006;83(6). 3. Grundy, SM. Drug therapy of the metabolic syndrome: minimizing the emerging crisis in polypharmacy. Nat Rev Drug Discov, 2006;5.4:295-309. 4. 4. Moller, DE, Kaufman, K D. Metabolic syndrome: a clinical and molecular perspective. Annu Rev Med, 2005;56:45-62. 5. Eckel, RH., et al. The metabolic syndrome. The Lancet, 2010;375.9710: 181-183. 6. Lakka, H-M, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. Jama, 2002;288.21:2709-2716. 7. Hunt, Kelly, et al. NCEP versus WHO metabolic syndrome in relation to all cause and cardiovascular mortality in the San Antonio Heart Study (SAHS). Diabetes, 2003;52. 8. Hansen, ML, Gunn, PW, Kaelber, DC. Underdiagnosis of hypertension in children and adolescents. Jama, 2007;298.8:874-879. 9. American Diabetes Association, et al. Standards of medical care in diabetes—2010. Diabetes Care, 2010;33(1):S11-S61. 10. Baynes, HW. Classification, pathophysiology, diagnosis and management of diabetes mellitus. J Diabe Metab, 2015;6.5:1-9. 11. Chobanian, AV. National heart, lung, and blood institute joint national committee on prevention, detection, evaluation, and treatment of high blood pressure; national high blood pressure education program 127 Original Association between microalbuminuria and MYH9 gene polymorphismsFadhil Jawad Al-Tu’ma et al. J Contemp Med Sci | Vol. 7, No. 2, March-April 2021: 122 – 127 coordinating committee: the seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report. Jama, 2003;289:2560-2572. 12. Arrondel, Christelle, et al. Expression of the nonmuscle myosin heavy chain IIA in the human kidney and screening for MYH9 mutations in Epstein and Fechtner syndromes. J Am Soc Nephrol, 2002;13.1:65-74. 13. Marini MBM, Pecci A, Romagnoli R, Musante L, Candiano G, Ghiggeri GM, Balduini C, Seri M, Marini M, Bruschi M, Pecci A, Romagnoli R, Musante L, Candiano G, Ghiggeri GM, Balduini C, Seri M,Marini M, Bruschi M, Pecci A, Romagnoli R, Musante LC, Non-muscle myosin heavy chain iia and iib interact and co-localize in living cells: Relevance for myh9-related disease. 2016;41(6). 14. Cheng, Wenrong, et al. Polymorphisms in the nonmuscle myosin heavy chain 9 gene (MYH9) are associated with the progression of IgA nephropathy in Chinese. Nephrol Dial Transplant, 2011;26.8:2544-2549. 15. Behar, DM., et al. African ancestry allelic variation at the MYH9 gene contributes to increased susceptibility to non-diabetic end-stage kidney disease in Hispanic Americans. Human Mol Genet, 2010;19.9:1816-1827. 16. Pattaro, Cristian, et al. Genome-wide linkage analysis of serum creatinine in three isolated European populations. Kidney Int, 2009;76.3:297-306. 17. Kopp, Jeffrey B., et al. MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis. Nat Genet, 2008;40.10:1175-1184. 18. Liu, Liping, et al. Association of MYH9 polymorphisms with hypertension in patients with chronic kidney disease in China. Kidney Blood Press Res, 2016;41.6:956-965. 19. Freedman, BI., et al. The non-muscle Myosin heavy chain 9 gene (MYH9) is not associated with lupus nephritis in African Americans. Am J Nephrol, 2010;32.1:66-72. 20. Lipkowitz, MS, et al. Association analysis of the non-muscle myosin heavy chain 9 gene (MYH9) in hypertensive nephropathy: African American Study of Kidney Disease and Hypertension (AASK). J Am Soc Nephrol, 2009;20:56A. 21. Palaniappan, L, Carnethon, M, Fortmann, SP. Association between microalbuminuria and the metabolic syndrome: NHANES III. Am J Hypertension, 2003;16.11:952-958. 22. Kaur, J. Assessment and screening of the risk factors in metabolic syndrome. Med Sci, 2014;2.3:140-152. 23. Katzmarzyk, PT., et al. Targeting the metabolic syndrome with exercise: evidence from the HERITAGE Family Study. Med Sci Sports Exercise, 2003;35.10:1703-1709. 24. Bahreinian, Maryam, and Ahmad Esmaillzadeh. “Opinion: quantity and quality of carbohydrate intake in Iran: a target for nutritional intervention.” (2012): 648-649. 25. Tabatabaei-Malazy O, Qorbani M, Samavat T, Sharifi F, Larijani B, Fakhrzadeh H. Prevalence of dyslipidemia in Iran: a systematic review and meta-analysis study. Int J Prev Med. 2014;5(4):373. 26. Nelson ME, Rejeski WJ, Blair SN, Duncan PW, Judge JO, King AC, et al. Physical activity and public health in older adults: recommendation from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exercise. 2007;39(8):1435-45. 27. Koochek A, Johansson S, Kocturk T, Sundquist J, Sundquist K. Physical activity and body mass index in elderly Iranians in Sweden: a population- based study. Eur J Clin Nutr. 2008;62(11):1326-32. 28. Simoes EJ, Kobau R, Kapp J, Waterman B, Mokdad A, Anderson L. Associations of physical activity and body mass index with activities of daily living in older adults. J Commun Health. 2006;31(6):453-67. 29. Bayram F, Kocer D, Gundogan K, Kaya A, Demir O, Coskun R, et al. Prevalence of dyslipidemia and associated risk factors in Turkish adults. J Clin Lipidol. 2014;8(2):206-16. 30. Karpov Y, Khomitskaya Y. PROMETHEUS: an observational, cross-sectional, retrospective study of hypertriglyceridemia in Russia. Cardiovasc Diabetol. 2015;14(1):115. 31. Abujbara M, Batieha A, Khader Y, Jaddou H, El-Khateeb M, Ajlouni K. The prevalence of dyslipidemia among Jordanians. J Lipids. 2018;2018. 32. Penesova A, Cizmarova E, Belan V, Blazicek P, Imrich R, Vlcek M, et al. Insulin resistance in young, lean male subjects with essential hypertension. J Human Hypertension. 2011;25(6):391-400. 33. Sinha S, Qazi SA, Banik S, Islam MZ. Correlation study of insulin resistance and essential hypertension among Bangladeshi male volunteers. J Young Pharm. 2015;7(3):200. 34. Sarafidis P, Lasaridis A, Nilsson P, Pikilidou M, Stafilas P, Kanaki A, et al. Validity and reproducibility of HOMA-IR, 1/HOMA-IR, QUICKI and McAuley’s indices in patients with hypertension and type II diabetes. J Human Hypertension. 2007;21(9):709-16. 35. Schillaci G, Reboldi G, Verdecchia P. High-normal serum creatinine concentration is a predictor of cardiovascular risk in essential hypertension. Arch Intern Med. 2001;161(6):886-91. 36. Kumar A, Rekha N, Raghav ED. A Study of microalbuminuria in patients with essential hypertension. Int J Contemp Med Res. 2016. 37. Liu L, Wang C, Mi Y, Liu D, Li L, Fan J, et al. Association of myh9 polymorphisms with hypertension in patients with chronic kidney disease in china. Kidney Blood Pressure Res. 2016;41(6):956-65. 38. Masconi K. The occurance of genetic variations in the MYH9 gene and their association with CKD in a mixed South African population: Stellenbosch: Stellenbosch University; 2012. 39. Bondzie PA. New insights into the molecular regulation of kidney disease: contributions of APOL1 and MYH9: Boston University; 2014. 40. Zhao H, Ma L, Yan M, Wang Y, Zhao T, Zhang H, et al. Association between MYH9 and APOL1 gene polymorphisms and the risk of diabetic kidney disease in patients with Type 2 diabetes in a Chinese Han population. J Diab Res. 2018;2018. 41. Ling C, Cai C, Chang B, Shi W, Wei F, Yu P, et al. MYH9 gene polymorphisms may be associated with cerebrovascular blood flow in patients with type 2 diabetes. Genet Mol Res. 2015;14(1):1008-16. 42. Franceschini N, Voruganti VS, Haack K, Almasy L, Laston S, Göring HH, et al. The association of the MYH9 gene and kidney outcomes in American Indians: the Strong Heart Family Study. Human Genet. 2010;127(3):295-301. 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