Evaluation Of Some Minerals And Biochemical Parameters In Patients Undergoing Haemodialysis In Nnamdi Azikiwe University Teaching Hospital, Nnewi

 

LIST OF TABLES

Table 4.1 Urea and Creatinine in PRE-D, 0-HAD, 1-HAD and controls 45

Table 4.2 Sodium, Chloride, Potassium and Bicarbonate In

PRE-D, 0-HAD, 1-HAD and controls 47

Table 4.3 Zinc, Copper, Selenium, Cobalt in PRE-D,

0-HAD, 1-HAD and controls 49

Table 4.4 Calcium, Phosphate, Parathyroid Hormone

in PRE-D, 0-HAD, 1-HAD and controls 51

Table 4.5 Parathyroid Hormone Levels in Both Haemodialysis

and controls 53

Table 4.6 Urea, Creatinine and Electrolytes Levels in Male and Female

Subjects in PRE-D group 55

Table 4.7 Zinc, Copper, Selenium, Cobalt in Male and Female

Subjects in PRE-D group 57

Table 4.8 Calcium, Phosphate, Parathyroid Hormone

in Male and Female Subjects in PRE-D group 59

Table 4.9 Urea, Creatinine and Electrolytes Levels in Male and Female

Subjects in 0-HAD Group 61

Table 4.10 Zinc, Copper, Selenium, Cobalt in Male and Female

Subjects in 0-HAD Group 63

Table 4.11 Calcium, Phosphate, Parathyroid Hormone

in Male and Female Subjects in 0-HAD Group 65

Table 4.12 Urea, Creatinine and Electrolytes Levels in Male and Female

Subjects in 1-HAD Group 67

Table 4.13 Zinc, Copper, Selenium, Cobalt in Male and Female

Subjects in 1-HAD Group 69

Table 4.14 Calcium, Phosphate, Parathyroid Hormone

in Male and Female Subjects in 1-HAD Group 71

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ABBREVIATIONS

ROD Renal Osteodystrophy

CKD Chronic kidney disease

PTH Parathyroid hormone

Na+ Sodium

K+ Potassium

Cl- Chloride

HCO3- Bicarbonate

PO4

2- Phosphate

Ca2+ Calcium

Zn Zinc

Cu Copper

Se Selenium

Co Cobalt

OPG Osteoprotegerin

RANKL Receptor activator of NF-kappa B ligand

RANK Receptor for RANKL

PRE-D Predialysis

0-HAD 0-hour after dialysis

1-HAD 1-hour after dialysis

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TABLE OF CONTENTS

CHAPTER ONE

1.0 Introduction 1

1.1 Justification 4

1.2 Aims 4

1.3 Objectives 4

CHAPTER TWO

2.0 Literature Review 5

2.1 The Kidney 5

2.2 Pathophysiology 6

2.3 Chronic Kidney Diseases 7

2.4 Signs and Symptoms of Chronic Kidney Disease 8

2.5 Causes of Chronic Kidney Disease 9

2.6 Stages in Chronic Kidney Disease 10

2.7 Prevalence of Chronic Kidney Disease 12

2.8 Dialysis 14

2.9 Haemodialysis 14

2.10 Trace Element 15

2.11 Trace Elements Status in Haemodialysis Patients 20

2.12 Renal Osteodystrophy 22

2.13 Parathyroid Hormone 23

2.14 Calcium 26

2.15 Phosphorous 27

2.16 Bone and Mineral Metabolism In Chronic Kidney Diseases 27

2.17 Sodium 29

2.18 Potassium 30

2.19 Bicarbonate 31

2.20 Chloride 32

CHAPTER THREE

3.0 Subjects, Material and Methods 34

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3.1 Subjects 34

3.2 Materials 34

3.3 Methods of Analysis 35

Chapter Four

4.0 Results 45

CHAPTER FIVE

5.0 Discussion, Conclusion and Recommendations 73

5.1 Discussion 73

5.2 Conclusion 79

5.3 Recommendations 80

References 81

Appendix 89

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ABSTRACT

Haemodialysis is the most common form of treatments for end stage renal disease(ESRD), and is associated with considerable morbidity and mortality. This cross sectional study was conducted to determine the biochemical changes in haemodialysis patients by accessing their minerals and also to identify any biomarker that may lead to renal osteodystrophy in these patients. A total of 100 participants were used for this study. 50 haemodialysis subjects grouped into predialysis, 0-hour after dialysis and 1- hour after and 50 apparently normal subjects. They were age matched into 21-30, 31- 40, 41-50, 51-60, 61-70. The minerals assayed were Na+, K+, Cl-, HCO3-, Ca2+, PO4 2-, Se, Zn, Cu and Co. PTH was also analysed. Electrolytes were assayed by ion selective electrode, trace elements by atomic absorption spectroscopy, Ca2+ by colorimetric method, PO4 2+ by UV method and PTH by enzyme immunoassay method. The results were subjected to statistical analysis (SPSS ver.17) and comparison made using student’s t-test and ANOVA at P-value<0.05. The mean values of Na+, Cl-, HCO3- were significantly lower in haemodialysis patients (Na+:127.92+6.24mmol/l, P=0.00; Cl-: 88.84+6.14mmol/l,P=0.00; HCO3-:16.46+2.97mmol/l,P=0.00) compared with the controls (Na+: 141.28+2.51mmol/l; Cl- 100.32 + 2.28mmol/l;HCO3-24.64 +1.83mmol/l).

Also, the mean value of K+ was significantly higher in dialysis subjects (4.21±0.88mmol/l, P=0.041) when compared with the control subjects (3.92±0.34mmol/l). Calcium level was significantly low in dialysis subjects (8.41±0.72mg/dl, P=0.000) as compared with the controls (9.65±0.50mg/dl). Phosphate on the other hand was significantly higher in dialysis group (4.35±1.06mg/dl, P=0.00) when compared with the controls (3.58±0.47mg/dl). However, the mean value of PTH in dialysis subjects was (165.32±154.90ng/l) and it was significantly higher than the control (P=0.00) (38.2±12.18ng/l). Zn and Se mean levels were significantly lower in dialysis subjects (79.33±16.27μg/dl, P=0.02 and 6.67±1.43μg/dl, P=0.00) compared with the control (88.97±9.77μg/dl and 9.00±2.48μg/dl) respectively. Cu showed a significantly high mean value in the dialysis (117.54±14.69μg/dl, P=0.01) when compared with the control subjects (108.50±15.49μg/dl). There was no significant difference in the mean level of Co (0.03±0.01μg/dl, P=0.26) when compared with the controls (0.04±0.00). Comparison of the mean levels of these minerals between male and female counterparts among the different dialysis groups showed no significant differences. More so, no significant difference was observed when the mean levels of these minerals were compared between 1-hour after dialysis and immediately after dialysis group. In conclusion, this study showed that there is a marked reduction in the zinc and selenium status in haemodialysis patients. Also there appears to be prevalence of renal osteodystrophy (ROD) in our institution probably because of inadequate monitoring of these patients.

Decrease in these minerals may be the cause of high risk of infection and oxidative stress observed in these patients. The prevalence of ROD in these patients may result in cardiovascular death. Therefore, I recommend that these minerals should be assessed from time to time so as to monitor these biochemical changes observed in these patients.10

 

CHAPTER ONE

1.0 INTRODUCTION

Haemodialysis is the most common form of treatment for end stage renal disease (ESRD), and is associated with considerable morbidity and mortality due to accelerated cardiovascular disease and infection. Despite the well documented burden of disease much remains to be learned about how best to prevent these complications of haemodialysis. Haemodialysis removes uremic toxins primarily allowing equilibration of plasma and dialysate across a semi-permeable membrane. Dialysate is created by adding carefully regulated quantities of biologically essential ions such as potassium, sodium, bicarbonate and calcium to water that has been treated to reduce solutes to very low levels. The dialysate concentration of other substances such as trace elements is not routinely manipulated. Substances that have lower concentration in dialysate than in blood tend to be removed by dialysis. Although this is appropriate in the case of uremic toxins, it may lead to depletion of biologically essential substances. Besides the potential for ongoing removal of trace elements by dialysis, haemodialysis patients are at risk for low dietary intake of such substances due to uremia related anorexia and dietary restriction. Haemodialysis patients are exposed to very high volumes (> 300 litres/week) of dialysate therefore even minute levels of toxic substances in source water could lead to tiny concentration gradients between blood and dialysate which in turn could lead to clinically relevant toxicity. Substances present in dialysate but not in blood will tend to accumulate in the patient and the lack of renal clearance in haemodialysis patients might theoretically lead to toxicity of ingested trace elements even when they are not present in dialysate. Thus haemodialysis patients are at theoretical risk for both deficiency and accumulation of trace element depending on dietary intake removal by dialysis, the 11 composition of the source water used for haemodialysis, and residual kidney function (D’Hease et al., 1996; Zima et al., 1999).