Key Features:
- No of Pages: 76
Abstract:
There are several interactions between thyroid and kidney functions in health and disease states. Thyroid hormones affect renal development and physiology. Thyroid hormones have pre-renal and intrinsic renal effects by which they increase the renal blood flow and the glomerular filtration rate (GFR). Hyperthyroidism results in increase GFR as well as increased renin-angiotensin-aldosterone activation. This study was carried out to investigate changes in renal tissue and serum immunoglobulin G of hyperthyroid rats.
Twenty male Wistar rats weighing between 180-200g were divided into two groups: control rats and hyperthyroid rats. Animals in group A were given feed and distilled water while animals in group B were treated with 5ug/100g body weight of levothyroxine mixed with distilled water and feed , the administration lasted for 30 days. After the administration, the animals were sacrificed using cervical dislocation, blood and kidneys samples were collected. Serum level and kidney tissue level of thyroid stimulating hormone and immunoglobulin G were measured using enzyme link immunoabsorbent assay (ELISA) method. Serum protein, Lipid profile, Urea and Creatinine level were measured using Spectrophotometry method. Measurement of oxidative stress markers like MDA, SOD and CAT level in blood serum and kidney tissues homogenate were measured using Spectrophotometry and histopathology of the kidney tissue were also studied using H and E staining.
The results obtained re-establish the fact that thyroid dysfunctions have significant effect on the renal functions and serum immunoglobulins (especially IgG) as hyperthyroid groups have lower levels of serum immunoglobulin G (25.00±1.71ng/ml) when compared to control groups (45.00±2.33ng/ml) and the level of IgG in kidney is increased in control (175.27±55.85ng/ml) when compared to the hyperthyroid group (601.25±232.25ng/ml) which was significant. The level of TSH is decreased in hyperthyroid group (25.44±2.12mIU/ml) compared to the control group (49.04±7.62mIU/ml) in serum) which was significant (p˂0.05) while the level of TSH is increased in control group (76.00±1.34mIU/ml) compared to the hyperthyroid group (20.20±0.20mIU/ml) in kidney tissue homogenate which was significant (p˂0.05). MDA was significantly increased in hyperthyroid rats in comparison with the control. Histological study revealed lysis of renal cells in hyperthyroid rats.
In Conclusion, the response of the immune system is important in maintaining the intergrity of the renal system during hyperthyroidism.
KEYWORDS: Hyperthyroid, Immunoglobulin G, Creatinine, Urea.
Table of Content:
TITLE PAGE i
CERTIFICATION ii
DEDICATION iii
ACKNOWLEDGEMENT iv
ABSTRACT v
TABLE OF CONTENT vii
LIST OF TABLES xii
LIST OF FIGURES xiii
LIST OF PLATES xiv
LIST OF ABBREVIATIONS xv
CHAPTER ONE
1.0 INTRODUCTION 1
1.1 JUSTIFICATION 2
1.2 AIM AND OBJECTIVES 2
1.2.1 AIM 2
1.2.2 OBJECTIVES 2
CHAPTER TWO
2.0 LITERATURE REVIEW 3
2.1 THYROID GLAND 3
2.1.1 THYROID HORMONE SYNTHESIS 4
2.1.2 SECRETION AND TRANSPORT 4
2.1.3 THYROID HORMONE METABOLISM 5
2.1.4 PHYSIOLOGICAL EFFECT OF THYROID HORMONE 7
2.2 HYPERTHYROIDISM 9
2.2.1 HYPERTHYRODISM CAUSES 10
2.2.2 HYPERTHYRODISM RISK FACTORS 12
2.2.3 HYPERTHYRODISM SYMPTOMS 13
2.3 TREATMENT OF OVERACTIVE THYROID 13
2.3.1 ANTI THYROID DRUGS 13
2.3.2 RADIOACTIVE IODINE 14
2.3.3 SURGICAL REMOVAL OF THE GLAND OR NODULES 15
2.4 PHYSIOLOGY OF THE KIDNEY 15
2.4.1 FUNCTION OF THE KIDNEY 16
2.4.2 EFFECTS OF THYROID HORMONES ON RENAL DEVELOPMENT 17
2.4.3 EFFECTS OF THYROID HORMONES ON RENAL PHYSIOLOGY 18
2.4.4 HYPERTHYROIDISM AND RENAL FUNCTION 19
2.5 OXIDATIVE STRESS AND KIDNEY 21
2.6 UREA AND CREATININE 22
2.6.1 UREA 22
2.6.2 CREATININE 23
CHAPTER THREE
3.0 MATERIALS AND METHOD 25
3.1 SITE OF THE EXPERIMENT 25
3.2 EXPERIMENTAL ANIMALS 26
3.3 EXPERIMENTAL DESIGN AND PROTOCOL 26
3.4 DETERMINATION OF BODY WEIGHT 28
3.5 BLOOD AND ORGAN COLLECTION 28
3.6 THYROID FUNCTION TEST 28
3.6.1 SERUM COLLECTION AND PREPARATION 28
3.6.2 TEST FOR THYROID STIMULATION HORMONE 28
3.6.3 THYROXINE (T4) AND TRIIODOTHYRONINE (T3) 29
3.7 BIOCHEMICAL ANALYSIS 30
3.7.1 ESTIMATION OF SERUM LIPID PROFILE 30
3.7.2 ESTIMATION OF OXIDATIVE STRESS BIOMAKERS 30
3.7.3 ESTIMATION OF UREA AND CREATININE 31
3.8 HISTOLOGICAL EXAMINATION 32
3.9 STATISTICAL ANALYSIS 32
CHAPTER FOUR
4.0 RESULTS 33
4.1 INDUCTION OF HYPERTHYROIDISM AND EVALUATION OF THYROID 33 STIMULATING HORMONE LEVEL
4.1.1 EVALUATION OF THYROID STIMULATING HORMONE LEVEL IN CONTROL33 AND HYPERTHYROID RAT
4.1.2 EVALUATION OF IMMUNOGLOBULINS G LEVEL IN THE CONTROL AND 36 HYPERTHYROID RAT
4.1.3 EVALUATION OF LIPID PROFILE AND PROTEIN PROFILE IN CONTROL AND39 HYPERTHYROID RAT
4.1.4 EVALUATION OF UREA AND CREATININE LEVEL IN THE CONTROL AND 42 HYPERTHYROID RAT
4.1.5 EVALUATION OF OXIDATIVE STRESS MARKER POST-INDUCTION OF 44 HYPERTHYROID IN KIDNEY TISSUE
4.2 HISTOPATHOLOGICAL EXAMINATION OF KIDNEY OF HYPERTHYROID 47 RATS
4.3 HISTOPATHOLOGICAL EXAMINATION OF KIDNEY OF CONTROL RATS 48
CHAPTER FIVE
5.0 DISCUSSION, CONCLUSSION AND RECOMMENDATION 49
5.1 DISCUSSION 49
5.2 CONCLUSION 52
5.3 RECOMMENDATION 52
REFERENCES 53-60
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