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Study of Lipoprotein (a) in Chronic Renal Failure

Journal of Research in Medical and Dental Science
eISSN No. 2347-2367 pISSN No. 2347-2545

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Research - (2021) Volume 9, Issue 6

Study of Lipoprotein (a) in Chronic Renal Failure

Vasanthan M and SV Mythili*

*Correspondence: SV Mythili, Department of Biochemistry, Sree Balaji Medical College, India, Email:

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Abstract

To compare the Lipoprotein (a) levels between non- diabetics and diabetics and compare the Lipoprotein (a) levels between diabetics with normal kidney function and diabetic CRF patients. To compare the Lipoprotein (a) levels between non-diabetic and diabetic CRF patients. This study was undertaken to study the level of Lipoprotein (a) levels in Chronic renal failure patients and to compare the levels of Lipoprotein(a)in three study groups. The mean Lp (a) level was high in diabetics with normal renal function and even more in diabetic Chronic renal failure patients compared to the controls with normal FBS, HbAlc, Urea and Creatinine. The same was compared between the three study groups using One-way ANOV A test and Tukey's HSD test. The difference in Lp (a) levels among the three diabetic groups was significant (P<0.01). This suggests that the Lp (a) levels.

Keywords

Hyperglycaemia, Diabetes mellitus, Antioxidant, Lipoproteins

Introduction

Diabetes mellitus is a systemic metabolic disorder caused by various reasons like impaired insulin secretion, insulin action, or both. The disease is characterized by the hyperglycaemic status and complications due to the same. Diabetes mellitus (DM) is associated with oxidative stress which occurs as a result of imbalance between prooxidants and antioxidants. Chronic hyperglycaemia and high fatty acid concentrations can cause damage in different types of cells by a variety of mechanisms collectively known as glucolipotoxicity, and oxidative stress is considered to be the common link [1,2]. Lipid peroxidation of the cellular structures, a consequence of increased oxygen free radicals, is thought to play an important role in atherosclerosis and micro vascular complications of DM [3].

Acute uncontrolled diabetes results in hyperglycaemia with ketoacidosis or the nonketotic hyperosmolar syndrome. The long-term complications of diabetes are micro-vascular (retinopathy, peripheral neuropathy) and macro-vascular (cardiovascular, peripheral arterial, and cerebra-vascular disease) complications. The two broad categories of diabetes are type 1 and type 2. In type 1 diabetes there is an absolute deficiency of insulin secretion. In type 2 diabetes, which is the more prevalent category there is a combination of resistance to insulin action and an inadequate compensatory insulin secretory response. Type 2 diabetes (accounting for 90-95% of those with diabetes), previously referred to as noninsulin- dependent diabetes or adult onset diabetes, encompasses individuals from dominantly insulin resistance with relative insulin deficiency to predominantly an insulin secretory defect with insulin resistance [4,5].

Chronic renal failure (CRF) or chronic kidney disease (CKD) is a progressive loss in renal function over a period of months or years. It is differentiated from acute kidney disease in that the reduction in kidney function must be present for over 3 months. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes. Chronic renal failure may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia. It is important to identify these risks early to reduce the development of diabetes and CRF , since CRF greatly amplifies the risk of cardiovascular events in the diabetic patient. The common causes of chronic renal failure are diabetes, hypertension and glomerulonephritis, among which diabetes is responsible for almost 30% of all CRF. Therefore, diabetes is the most common cause of CRF [6,7].

Chronic renal failure (CRF) 1s characterized by progressive loss of renal function. These patients are at risk for adverse cardiovascular outcomes. Cardiovascular disease is the leading cause for morbidity and mortality in these patients. Lipoprotein (a) (also called Lp (a)) is a lipoprotein subclass. Genetic studies and numerous epidemiologic studies have identified Lp (a) as a risk factor for atherosclerotic diseases such as coronary heart disease and stroke. Lipoprotein(a) (Lp (a)) is a cholesterol-rich particle existing in human plasma, first described by Berg in 19634. Lp (a) is made up of a lowdensity lipoprotein (LDL) cholesterol particle attached to Apo lipoprotein (a), which is a plasminogen like glycoprotein 5. The prevalence of hyperlipidaemia or dyslipidaemia in CRF is much higher compared to the general population [6]. However, in patients with CRF, the impact of dyslipidemia on cardiovascular disease is uncertain [7]. Previous studies have shown that there was positive correlation between increased Lp (a) levels and CRF patients [8].

Atherogenic lipid abnormalities are noticed m CRF patients. A study was done to show the impact of lipid abnormalities in patients with chronic renal failure, which revealed that there was increase in triglyceride, total cholesterol, and decrease in HDL-Cholesterol levels chronic renal failure patients compared to controls [9].

Material and Method

The study was conducted in 90 subjects attending Sree Balaji Medical College and Hospital totally.

Study individuals were divided into 3 groups

Group A-30 age, sex and Body mass index matched healthy controls.

Group B-Composes of 30 Type 2 diabetic patients with normal renal function, belonging to the age group between 40 and 50 years.

Group C-Composes of 30 diabetic Chronic renal failure patients, belonging to the age group between 40 and 50 years.

This study was conducted between December 2012 and May 2014. The Institutional Research and Ethical Committee approved the study protocol. Written informed consent was obtained from all the participants before enrolment in the study. Demographic data, age, gender, height, weight, DM duration, general history and medications, were recorded. (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL), serum urea and creatinine were measured.

Inclusion criteria

2 diabetics and diabetic CRF patients as Groups B and C respectively in the age group 40 - 50.

Exclusion criteria

Estrogen depletion.

Severe hypothyroidism.

Sample collection

The blood samples were collected by venepuncture under aseptic precautions.

Results

The study population comprised of a total of 90 individuals and of these, Group-A were 30 healthy controls, Group-B were 30 Diabetic study individuals with J:?Ormal renal functions and Group-C were 30 diabetics with Chronic renal failure. All the biochemical study parameters were analysed with the help of Statistical Product and Service Solutions (SPSS) 17 software (Table 1 and Table 2). Statistical tests used were Descriptives, ANOVA & TUKEY'S HSD test. The results of the various biochemical parameters for Group-A are as follows. Lp(a) concentration was 10.29 ± l.2888mg/dl (Mean and Standard deviation).The Mean and Standard of Urea, Creatinine, FBS,HbAlc,TC, HDL,TG,VLDL,LDL are 28.1 ± 8.3lmg/ dl, 0.877 ± 0.339 mg/dl,88.9 ± 11.598 mg/dl, 4.39 ± 0.5592%, 159.1 ± 21.796 mg/dl, 44 ± 10.072 mg/dl, 155.43 ± 19.611 mg/dl, 31.07 ± 3.859 mg/dl and 84.03 ± 26.538 mg/dl respectively (Table 3).

Group Lp(a) mg/di Urea mg/di Creatinine mg/di FBS mg/di HbAlc % TC mg/di HDL mg/di TG mg/di VLDL mg/di LDL mg/di
A 9.6 18 0.9 108 5.2 180 34 172 34 112
A 10.2 27 1 98 4.4 165 42 145 29 94
A 8.9 35 0.3 81 4.8 146 33 128 26 87
A 11.8 21 0.6 105 5.4 167 56 155 31 80
A 10.6 17 1.3 93 4.7 189 32 134 27 130
A 12.1 26 0.4 83 3.5 133 30 162 32 71
A 9.8 38 0.6 72 4.3 146 48 118 24 74
A 10.9 20 0.9 101 3.9 129 51 155 31 47
A 8.1 28 1.4 95 4.6 186 34 177 35 117
A 10.5 16 0.5 73 5.2 157 56 132 26 75
A 12.4 25 1.3 84 3.6 154 39 166 33 82
A 9.3 37 0.4 109 4.9 130 36 146 29 65
A 11.4 23 1.1 74 4.1 176 59 155 31 86
A -8.7 19 0.9 97 4.6 190 34 148 30 126
A 10.3 29 0.7 86 5.1 153 60 174 35 58
A 9.4 15 1.2 93 3.7 161 44 179 36 81
A 8.8 30 0.8 79 4.1 127 57 167 33 37
A 10.4 24 0.5 99 5.4 146 33 188 38 75
A 9.9 33 1.1 75 4.2 173 45 154 31 97
A 12.3 40 1.3 87 3.8 188 45 165 33 110
A 11.9 22 1 100 4.5 139 32 116 23 84
A 8.4 36 0.7 76 3.9 122 60 177 35 27
A 10.7 32 1.3 89 4.3 190 54 149 30 106
A 12.6 25 1.4 103 4.7 168 56 157 31 81
A 9.5 41 0.8 71 4.2 173 40 165 33 100
A 8.5 34 0.6 89 3.7 168 41 143 29 98
A 10.1 39 1.2 77 4 133 56 178 36 41
A 11.5 18 0.6 101 4.4 172 36 177 35 101
A 9.3 31 1.1 78 4.9 130 42 162 32 56
A 10.8 44 0.4 91 3.6 182 35 119 24 123
B 16.8 41 1.2 189 7.9 210 30 184 37 143
B 22.1 20 0.8 142 8.4 208 55 230 46 107
B 27.CJ 27 1.4 129 7.4 247 33 243 49 165
B 15.5 31 1.2 169 8.6 238 50 223 45 143
B 18.3 42 0.7 139 7.5 233 31 184 37 165
B 20.7 36 1.1 150 8.7 226 49 190 38 139
B 19.2 16 0.4 144 7.3 283 51 194 39 193
B 26.9 28 0.6 174 8.1 249 32 211 42 175
B 21.5 35 1.4 125 7.7 209 54 186 37 118
B 16.7 21 0.9 154 8.1 271 48 251 50 173
B 28.6 30 0.5 140 7.6 283 33 234 47 203
B 19.2 18 0.8 132 7.1 213 44 180 36 133
B 27.3 44 1 171 8.5 215 40 188 38 137
B ..... 19.4 29 0.9 152 7.2 243 36 194 39 168
B 26.5 22 0.4 137 7.5 223 31 222 44 14 8
B 20.9 34 1 160 8.4 273 29 193 39 205
B 28.1 19 1.3 127 7.2 219 23 205 41 155
B 23.1 38 0.6 156 8.8 230 38 231 46 146
B 19.7 25 0.4 143 7.9 220 27 192 38 155
B 16.1 32 1.1 178 8.3 263 39 255 51 173
B 21.3 40 0.9 135 7.6 288 25 200 40 223
B 14.9 23 1.1 129 8.8 240 22 195 39 179
B 25.7 17 0.3 163 8 222 26 206 41 155
B 27.4 37 1.3 176 7.3 256 18 205 41 197
B 23.6 26 0.9 131 7.8 268 28 199 40 200
B 19.5 19 0.8 157 8.9 287 33 282 56 198
B 18.9 24 1.2 146 7.4 265 31 203 41 193
B 22.8 39 0.4 168 8.2 244 27 186 37 180
B 8.3 33 0.9 133 9 236 30 222 44 162
B 6.7 18 1.4 159 7.1 221 38 201 40 143
C 19.5 92 3.4 214 7.9 289 22 289 58 209
C 15.8 110 4.1 135 8.9 290 19 303 61 210
C 2.3 67 3.2 189 8.3 302 33 189 38 231
C 17.6 125 5.3 139 7 322 30 289 58 234
C 4.8 78 2.7 145 7.5 319 28 321 64 227
C 9.3 94 4.9 194 7.8 249 23 209 42 184
C 8.7 108 4.1 127 8.2 302 22 287 57 223
C 7.4 62 2.7 150 7.4 344 27 193 39 278
C l6.8 90 2.4 127 7.6 340 30 321 64 246
C 8.5 76 3.8 204 8.7 311 33 198 40 238
C 9.4 97 5.2 155 8.1 372 25 276 55 292
C 1.6 114 6.5 210 7.9 342 23 253 51 268
C 3.8 88 5.9 125 7.7 302 28 298 60 214
C 8.9 65 3.6 175 8.5 293 30 254 51 212
C 1.5 105 6 129 8 255 26 336 67 162
C 5.7 75 2.7 140 7.2 290 24 300 60 206
C 5.1 99 4.3 201 8.4 302 17 274 55 230
C 39.8 116 7.1 130 7.5 250 22 260 52 176
C 44.6 68 2 150 8.7 283 28 312 62 193
C 36.9 86 4.8 168 8.6 321 30 219 44 247
C 65.4 101 5.4 194 7.1 202 18 204 41 143
C 43.9 72 3.6 165 7.9 235 29 288 58 148
C 69.2 118 6.4 139 8.8 301 20 198 40 241
C 45.1 127 7.3 135 8.5 283 22 200 40 221
C 52.3 81 2.9 197 7.1 244 38 273 55 151
C 61.2 103 4.1 160 7.3 239 33 300 60 146
C 56.3 69 3.2 149 8.9 220 18 304 61 141
C 47.5 123 6 179 8.6 306 31 291 58 217
C 3S.4 85 3.7 187 7.4 221 27 322 64 130
C 6 5.6 70 2.8 170 8.1 264 23 364 73 168

Table 1: Master chat.

Group Frequency Percent Valid Percent Cumulative Percent
Group A 30 33.3 33.3 33.3
Group B 30 33.3 33.3 66.7
Group C 30 33.3 33.3 100
Total 90 100 100  

Table 2: Groups.

  N Minimum Maximum Mean Std. Deviation
Lipoprotein (a) 30 8.1 12.6 10.29 1.2888
Urea 111g/dl 30 15 44 28.1 8.31
Creatinine mg/dl 30 0.3 1.4 0.877 0.339
FBSmg/dl 30 71 109 88.9 11.598
HbAl c¾ 30 3.5 5.4 4.39 0.5592
TC mg /dl 30 122 190 159.1 21.796
HDLm g/dl 30 30 60 44 10.072
TG mf /dl 30 116 188 155.43 19.611
VLDLn1g/dl 30 23 38 31.07 3.859
LDLm g/dl Valid N (listwi se) 30 27 130 84.03 26.538

Table 3: Descriptive statistics-Group A.

The results of the various biochemical parameters for Group-B are as follows. Lp(a) concentration was 22.12 ± 4.32 mg/dl (Mean and Standard dev i at io n ). The Mean and Standard of Urea , Creatinine, FBS, HbAlc, TC, HDL, TG,. VLDL, LDL are 28.8 ± 8.48 mg/dl, 0.897 ± 0.334 mg/dl, 150.27 ± 17.54 mg/dl, 7.94 ± 0.59 %, 242.77 ± 25.46 mg/dl, 35.03 ± 9.94 mg/dl, 209.63 ± 24.85 mg/dl, 41.93 ± 4.91 mg/dl and 165.8 ± 27.81 mg/dl respectively (Table 4). The results of the various biochemical parameters for Group-C are as follows. Lp(a) concentration was 51. l:!:11.26 mg/dl (Mean and Standard deviation). The Mean and Standard of Urea, Creatinine, FBS, HbA1c, TC, HDL, TG, VLDL, LDL are 92.1 ± 19.695 mg/dl, 4.34 ± 1.49 mg/dl, 162.73 ± 28.29 mg/dl, 7.99 ± 0.59 %, 286.43 ± 41.16 mg/dl, 25.97 ± 5.23 mg/dl, 270.83 ± 48.63 mg/dl, 54.27 ± 9.61 mg/dl and 206.2 ± 43.16 mg/dl respectively (Table 5).

    Minimum Maximum Mean Std.Deviation
Lipoprotein (a) mg/di 30 14.9 28.6 22.12 4.3154
Urea mg/di 30 16 44 28.8 8.475
Creatinine mg/dl 30 0.3 1.4 0.897 0.3347
FBS mg/dl 30 125 189 150.27 17.544
HbAlc % 30 7.1 9 7.943 0.5911
TCmg/dl 30 208 288 242.77 25.461
HDL mg/di 30 18 55 35.03 9.936
TG mg/dl 30 180 282 209.63 24.848
VLDL mg/di 30 36 56 41.93 4.913
LDL mg/di 30 107 223 165.8 27.805
Valid N (listwise) 30  

Table 4: Descriptive statistics-Group B.

  N Minimum Maximum Mean Std.Deviation
Lp(a) mg/dl 30 31.6 69.3 51.097 11.2604
Urea mg/dl 30 62 127 92.13 19.695
Creatinine mg/dl 30 2 7.3 4.337 1.4827
FBS mg/dl 30 125 214 162.73 28.285
HbAlc % 30 7 8.9 7.987 0.5888
TC mg/dl 30 202 372 286.43 41.155
HDL mg/dl 30 17 38 25.97 5.229
TG mg/di 30 189 364 270.83 48.632
VLDL mg/dl 30 38 73 54.27 9.609
LDL mg/dl 30 130 292 206.2 43.164
Valid N (listwise) 30  

Table 5: Descriptive Statistics-Group C

The Means of different groups of patients, namely A,B & C are unequal. The ONE-WAY ANOV A test was used to calculate the Means of each and every independent variable of the group. The Means of individual variable was compare d between and within the groups. It also indicates that the P value is significant (P<0.01) between the groups and insignificant within the same group (Table 6).

  Sum of Squares Df Mean Square F Significance
Lp(a) Between Groups 26447.802 2 13223.901 269.73 0
Within Groups 4265.305 87 49.026
Total 30713.106 89  
Urea Between Groups 81118.689 2 40559.344 230.106 0
Within Groups 15334 .967 87 176.264
Total 96453.656 89  
lLe Between Groups 238.056 2 119.028 147.234 0
Within Groups 70.333 87 0.808
Total 308.389 89  
FBS Between Groups 93726.467 2 46863.233 113.163 0
Within Groups 36028.433 87 414.12
Total 129754 .900 89  
HbAl Between Groups 255.641 2 127.82 380.114 0
Within Groups 29.255 87 0.336
 Total 284.896 -89  
Total Choles Between Groups 251206.667 2 125603 .333 133.759 0
Within Groups 81695.433 87 939.028
 Total 332902.1 89  

Table 6: One-way analysis of variance (One-way anova).

Discussion

The study was done on Type 2 Diabetic patients with normal renal function and Diabetic Chronic renal failure patients. Age, Sex and BMI matched healthy individuals were taken as controls. Between the two study groups and the control group, the routine biochemical parameters, fasting blood sugar (FB S), glycated haemoglobin (HbA1C), serum urea, serum creatinine and lipid profile differed significantly [10].

Serum Lipoprotein (a) was also estimated in patients under, all the three groups to show the significance of athe rosclerotic pathogenic effect of the same. The fasting plasma sugar was done to assess the short term glycaemic control. The difference in short term glyclemic control (FBS) values between the two study groups was statistically significant (P< .001). To assess the long term glycaemic control HbA 1C levels were measured. The difference in mean values between two study groups was also statistically significant (P<0.001). This shows that long term glycaemic control was significantly proportional to the Lp(a) levels in controls of Group A, Group B-diabetics with normal renal function and Group C-diabetics with CRF [11]. This suggests that long term glycaemic control is directly related to the complications of diabetes . This study also observed that there is significant elevation of total cholesterol, LDL, VLDL, triglycerides and significant lowering of HDL in diabetics with normal renal function when compared to healthy controls. The levels of Lp (a) were significantly increased in Group C Diabetic CRF patients which is evident from the Mean and Standard Deviation of 51.097 ± 11.26. The Lp (a) levels were 10.29 ± 1.29 and 22.12 ± 4.32 among Group A and B respectively. The significance is also shown by the One- way ANOVA test and TUKEY'S HSD test with P<0.001 [12-15].

The studies conducted shows the genetically importance of apoA isoforms and the level of Lp(a) depending on the apoA isoform. There are also other studies based on the genetic relationship between apoA and Lp (a), the isoforms and the gene polymorphism [16-21]. These studies suggest that despite significant correlation between APOA kringle 4 size polymorphism and Lp (a) levels, there sequence variations either in the APOA gene or closely linked genes may account for relatively higher Lp (a) levels. Various other studies conducted showed the decreased levels of Lp (a) among the patients using atorvastatin [22,23]. There are also other studies based on the treatment modalities for increased Lp (a). Unlike the above mentioned studies, our study shows significantly increased levels among the patients on statin therapy. These unique features of Lp (a) justifies the elevation in the level of Lp (a) in Diabetics and Diabetic CRF causing generation of clots and atherosclerosis [24-27].

Conclusion

The results of this study and previous studies provide ample evidence that the levels of Lp (a) are increased in patients with type 2 diabetes mellitus and also in patients with diabetic CRF. The present study observed that there is positive correlation of Lp (a) levels with the duration of diabetes and is progressive with the diabetic complications. As in the general population, Lp (a) is a risk factor for cardiovascular events in CRF patients.

Funding

No funding sources.

Ethical Approval

The study was approved by the Institutional Ethics Committee.

Conflict of Interest

The authors declare no conflict of interest.

Acknowledgement

The encouragement and support from Bharath University, Chennai, is gratefully acknowledged. For provided the laboratory facilities to carry out the research work.

References

Author Info

Vasanthan M and SV Mythili*

Department of Biochemistry, Sree Balaji Medical College, India
Department of Biochemistry, Sree Balaji Medical College, India
 

Citation: Vasanthan M, SV Mythili, Study of Lipoprotein (a) in Chronic Renal Failure, J Res Med Dent Sci, 2021, 9(6): 367-374

Received Date: May 06, 2021 / Accepted Date: Jun 23, 2021 / Published Date: Jun 30, 2021

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