Evaluating the Concentration of Electrolytes, Urea and Creatinine in the Blood Samples of Pregnant Women
Chapter One
Objective of study
The aim of this study was to determine the concentration of electrolyte, Urea and creatine in the blood cell of pregnant women.
CHAPTER TWO
LITERATURE REVIEW
Anatomy
The bean-shaped kidneys lie in a retroperitoneal position in the superior lumbar region. Extending approximately from T12 to L3, The right kidney is crowded by the liver and lies slightly lower than the left. An adult‟s kidney has a mass of about 150 g (5 ounces) and its average dimensions are 12 cm long, 6 cm wide, and 3 cm thick. Each kidney comprises an outer cortex and an inner medulla.The lateral surface is convex. The medial surface is concave and has a vertical cleft called the renal hilum that leads into an internal space within the kidney called the renal sinus. The ureter, renal blood vessels, lymphatics, and nerves all join each kidney at the hilum and occupy the sinus. The kidney is supplied with oxygenated blood via the renal artery and drained of deoxygenated blood by the renal vein. In addition, urine produced by the kidney as part of its excretory function, drains out via narrow “tubules” called ureters, which in turn connected to the bladder.Atop each kidney is an adrenal (or suprarenal) gland, an endocrine gland that is functionally unrelated to the kidney.(snell 2012 ).
Blood pressure regulation:
Although the kidney cannot directly sense blood, long-term regulation of blood pressure predominantly depends upon the kidney. This primarily occurs through maintenance of the extracellular fluid compartment, the size of which depends on the plasma sodium concentration. Renin is the first in a series of important chemical messengers that make up the renin-angiotensin system. Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but both increase the kidney’s absorption of sodium chloride, thereby expanding the extracellular fluid compartment and raising blood pressure. When renin levels are elevated, the concentrations of angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption, expansion of the extracellular fluid compartment, and an increase in blood pressure. Conversely, when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the extracellular fluid compartment, and decreasing blood pressure.(Elaine N. 2004 )
Hormone secretion:
The kidneys secrete a variety of hormones, including erythropoietin, and the enzyme renin. Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow. Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate. Part of the renin–angiotensin–aldosterone system, renin is an enzyme involved in the regulation of aldosterone levels. (Elaine N. 2004 )
Nephron:
The kidney consists of over a million individual filtering units called nephrons. Each nephron consists of a filtering bodytherenal corpuscle, and a urinecollecting and concentrating tube the renal tubule. (Elaine N. 2004 )
Renal Capsule:
The renal capsule is the part of the kidney nephron in which blood plasma is filtered.
The term “capsule” means “tiny” or “small” body. The renal capsule of each kidney nephron has two parts – they are the Glomerulus which is a network of small blood vessels called capillaries, and the Bowman’s Capsule (also known as the Glomerular Capsule), which is the double-walled epithelial cup within which the glomerulus is contained.
Within the glomerulus are glomerular capillaries that are located between the afferent arteriole bringing blood into the glomerulus and the efferent arteriole draining blood away from the glomerulus. The (outgoing) efferent arteriole has a smaller diameter than the (incoming) afferent arteriole. This difference in arteriole diameters helps to raise the blood pressure in the glomerulus.
The area between the double-walls of the Bowman’s Capsule is called the capsular space. The cells that form the outer edges of the glomerulus form close attachments to the cells of the inner surface of the Bowman’s Capsule. This combination of cells adhered to each other forms a filtration membrane that enables water and solutes (substances that are dissolved in the water/blood) to pass through the first wall of the Bowman’s Capsule into the capsular space. This filtration process is helped by the raised blood pressure in the glomerulus – due to the difference in diameter of the afferent and efferent arterioles. (Elaine N. 2004 ).
Renal Tubule:
The renal tubule is the part of the kidney nephron into which the glomerular filtrate passes after it has reached the Bowman’s capsule. The first part of the renal tubule is called the proximal convoluted tubule (PCT), The water and solutes that have passed through the proximal convoluted tubule (PCT) enter the Loop of Henle, which consists of two portions – first the descending limb of Henle, then the ascending limb of Henle. In order to pass through the Loop of Henle, the water (and substances dissolved in it) pass from the renal cortex into the renal medulla, then back to the renal cortex.
When this fluid returns to the renal cortex (via the ascending limb of Henle) it passes into the distal convoluted tubule (DCT) , The distal convoluted tubules of many individual kidney nephrons converge onto a single collecting duct.
The fluid that has passed through the distal convoluted tubules is drained into the collecting duct (far left-hand-side of the diagram above). Many collecting ducts join together to form several hundred papillary ducts. There are typically about 30 papillary ducts per renal papilla (the renal papillae being the tips of the renal pyramids – which point towards the Centre of the kidney). At each renal papilla the contents of the papillary ducts drain into the minor calces – the channels through which the fluid passes, via the major calyx, into the Centre of the kidney – called the renal pelvis.
CHAPTER THREE
MAATERIALS AND Methods
Study Design/Study Site
This hospital-based case-control study was carried out between October, 2015, and April, 2016, at the Koforidua Polyclinic. A total of 100 patients (50 with gestational malaria as cases and 50 healthy pregnant women as controls) were recruited for this study.
CHAPTER FOUR
RESULTS
CHAPTER FIVE
DISCUSSION OF FINDINGS AND CONCLUSION
DISCUSSION
The physiological state of pregnancy brings about a lot of with metabolism and excretion of biochemical markers of changes which affect the metabolism of various biochemical renal impairment. Furthermore, during pregnancy cardiac parameters. These changes are largely thought to provide output and renal blood flow are increased together with conducive environment for the growing fetus but may affect
The results of this study indicates lower reference interval for urea, creatinine and electrolytes as compared to the reference interval currently being used at the Awka Hospital physiological increase in GFR resulting increased clearance of creatinine [6], hence pregnant patients with serum creatinine level closer to the upper limit of reference interval for the “normal’’ population, should be examined further for possible renal impairment.
To this end, a slight rise in creatinine level during pregnancy may indicate progression of renal disease and thus serum creatinine has greater predictive ability compared with urea for the determination of the adverse outcomes of kidney disease [5, 10, 12].
The gradual decrease in the concentration of creatinine in plasma from the first to the third trimesters of pregnancy is likely to be as result of increase in GFR associated with pregnancy but not a reduction in its plasma concentration. The increase in GFR may be due partly to upsurge in the concentration of aldosterone which increases the blood volume, in some instances, up to 50% and increase renal blood flow [4] resulting in an increase in the rate at which creatinine is cleared from plasma.
In this study, creatinine concentration was significantly reduced among the pregnant women compared to the nonpregnant controls. This is in consonant with one study which reported significantly lower creatinine levels in the cases as against the control [2]. Some report indicated about 50% increase in glomerular filtration rate during pregnancy [3], and this could lead to increase in creatinine excretion. Creatinine is freely filtered and its level falls in normal pregnancy due partly to a pregnancy-induced increase in GFR on one hand and on the other hand due to hemodilution from plasma expansion culminating in the decrease in serum creatinine concentration [9].
Consequently, the reduction in serum creatinine is ancillary to plasma volume expansion, renal vasodilation, hyperfiltration, and increased glomerular basement membrane permeability [15].
In this study there was significant decrease in the urea concentration across the various trimesters. This is similar to a study which showed a general decrease in urea level between pregnant women and controls though the decrease was not statistically significant [2]. This decrease might be as a result of hydration, a rise in GFR, increase anabolic rate and increased demand of the fetus on the maternal protein [2]. The rise in glomerular filtration rate that normally occurs in pregnancy results in lower levels of urea [5]. As GFR increases without significant increase in urea synthesis, its concentration decreases in plasma [5]. In late pregnancy, there is alteration in protein metabolism suggesting that amino acids are preserved for tissue synthesis and evidence points to enhanced metabolic rate and increased placental uptake [2], consequently serum concentration of urea declines.
There was generally statistically significant decrease in electrolytes level between the controls and the pregnant women during the first trimester. This is in consonant with a study in which there was a decline in electrolytes level during the first trimester between the pregnant women and the controls [2]. Paradoxically, the electrolytes level in this study increased though not statistically significant as the pregnancy progressed to the third trimester. This is similar to a study which showed a general increase in electrolytes level as the pregnancy progressed from the second to the third trimester [21].
During the late stages of pregnancy more profoundly in the third trimester, tubular reabsorption of electrolytes increases dramatically which increases serum electrolytes concentration in addition to decrease in the clearance of electrolytes from the proximal and distal tubules [1]. The increase in concentration of electrolytes at the late stage of pregnancy may also be secondary to improved fetal production, reduced binding to albumin and elevated tubular re-absorption with decreasing renal clearance of the electrolytes [21]. There is a gradual decrease in serum electrolytes concentration in normal pregnancy up to 16 weeks of gestation. The electrolytes levels then tend to stabilize between 17 and 28 weeks of pregnancy and start increasing during the third trimester [21].
CONCLUSION
Normal pregnancy is associated with progressive decrease in urea and creatinine levels from the first trimester to the third trimester while electrolytes decreases in first half of pregnancy followed by increases from the second trimester to the third trimester. The upsurge in electrolytes concentration from the second to the third trimester of pregnancy may be attributable to the dramatic increase in tubular re-absorption and fetal production.
The absence of reliable data on reference intervals for urea, creatinine and electrolytes among pregnant women in Nigeria call for the establishment of these reference ranges using larger sample size and should cover all the ten regions of the country. This is because the physiological and anatomical changes that come with pregnancy especially those related to the kidney means that the laboratory reference intervals of non-pregnant women are not suitable for pregnant women.
REFERENCES
- 1.Das B, Chakma M, Mustafa A, Paul D, Dhar K: A study on serum urea, creatinine and uric acid levels in normal pregnancy (first and third trimester) in Rohilkhand Region, Uttar Prades. Scholars J of Applied Med Sci (SJAMS) 2016; 4 (9A):3236-3241.
- Patricia OO, Christiana BA, Raphael OJ: Evaluation of changes in renal functions of pregnant women attending ante-natal clinic in Vom Plateau State, North-Central Nigeria. Arch ApplSci Res 2013; 5:111-116.
- Soma-Pillay P, Nelson-Piercy C, Tolppanen H, Mebazaa A: Physiological changes in pregnancy: review articles. Cardiovas j of Africa 2016; 27(2):89-94.
- Damudi H, Bello B, Yahaya SI, Kurawa M, Musa S, Ibrahim ZU: Biochemical Assessment of Pregnancy-Related Physiological Changes in Renal Function. Am SciRes J for Engineering, Technology, and Sciences (ASRJETS) 2015; 14(3):264-271.
- Lindheimer MD, Taler SJ, Cunningham FG: Hypertension in pregnancy. J of the Am Society of Hypertension 2010; 4(2):68-78.
- Cheung KL, Lafayette RA: Renal physiology of pregnancy. Advances in chronic kidney disease 2013; 20(3):209-214.
- Kuper SG, Tita AT, Youngstrom ML, Allen SE, Tang Y, Biggio JR, Harper LM: Baseline Renal Function Tests and Adverse Outcomes in Patients With Chronic Hypertension. Obs andgyn 2016; 128(1):93.
- Hussein W, Lafayette RA: Renal function in normal and disordered pregnancy. Current opinion in nephrology and hypertension 2014; 23(1):46.
