Evaluating The Concentration Of Electrolytes, Urea And Creatinine In The Blood Samples Of Pregnant Women

ABSTRACT   

Background: This paper looks at the low concentration of urea, electrolytes and creatinine in pregnant women and argues that the causes may be due to physiological changes in the metabolism of these serum markers of kidney function. During pregnancy, physiological and anatomical changes occur resulting in increased renal workload. As a result of these changes, comparison of plasma levels of these biochemical markers to non-pregnant levels is inappropriate hence this study was aimed at evaluating the changes in the metabolism of these serum markers among pregnant women in the Ho municipality and to compare their reference intervals in both pregnant and non-pregnant women. Methodology: This case – control study involved 90 pregnant women and 90 aged-matched non-pregnant women who served as controls. Five milliliters of venous blood was obtained from each participant from which sera were obtained and concentrations of creatinine, urea and electrolytes determined across the trimester intervals, using SELECTRA PRO S chemistry analyzer. Results: Creatinine and urea (p<0.0001) were significantly lower in the cases than the controls and electrolytes was also significantly lower in the cases than the control (p<0.0185). Furthermore, electrolytes concentration increased from the second to the third trimester, though the increase was not statistically significant. Conclusion: There is progressive decrease in the concentration of urea, creatinine and electrolytes during normal pregnancy with a slight increase in the concentration of electrolytes during the third trimester.

 

CHAPTER ONE

 

INTRODUCTION

Human pregnancy takes about 40 weeks to complete starting from the last menstrual cycle to the time of delivery of the baby and comprises three time intervals known as first, second, and third trimesters. The first trimester starts from first day of conception up to 13th week and miscarriages are most likely to occur at this stage. Second trimester is from the 13th week to the 26th week, where the movement of the fetus may also be felt by monitoring and assessment by ultra sound. The third trimester starts from the 26th week to the end of pregnancy which is usually around the 40th week and marks the beginning of viability [1, 2]. At the time of pregnancy, the pregnant woman’s body undergoes substantial physiological and anatomical alterations making it possible to nurture and accommodate the developing fetus and these alterations which commence after conception affects every organ system [3].

This physiological phenomenon with many biochemical alterations (ranging from alterations in fluid and electrolyte concentrations to more complex modifications in cortisol and calcium metabolism), help in the nurturing and survival of the developing fetus [4]. During the first half of pregnancy, there is increase in cardiac output, accompanied by marked increase in intravascular and extracellular volume [5]. This is accompanied by enlargement of the kidneys due to fluid retention and failure of urine to properly drain from the kidney to the bladder, which is attributable to proliferation in kidney’s interstitial fluid volume and vascular system rather than proliferation in the number of nephrons [6].

This hydronephrosis which may be observed in pregnancy may be due to increased levels of progesterone and sudden changes in hormonal and hemodynamic environment during pregnancy [7]. This enlargement of the kidneys is prominent in the right kidney as a result of the angle at which it crosses the iliac and ovarian vessels at the point of  its entry to the pelvis [8, 9], and becomes more pronounced as the pregnancy advances through the trimesters due to fluid retention which predisposes the woman to urinary stasis, culminating in the increased risk of urinary tract infections [10]. Structural changes in the kidneys during pregnancy is also influenced by both hormonal and mechanical factors where elevated progesterone concentration in plasma creates force of contraction on the uterus leading to a compression effect exerted by the weight of the uterus as the pregnancy advances [4]. Hormonal and mechanical forces are thought to be responsible for ureteral dilation as early as 6 weeks of gestation [11].

Even before the onset of conception, hormonal changes influence renal function during the menstrual cycle especially in midluteal phase where there is increase in renal plasma flow (RPF) and glomerular filtration rate (GFR) as a result of increase cardiac output [8]. There is elevation in GFR and RPF due to marked vasodilation which is a characteristic of renal physiologic changes [11]. Subsequently, as a result of renal vasodilation, RPF and GFR both increase, compared to non-pregnant levels, by 40–65% and 50–85%, respectively [3, 6]. There is an increase in renal blood flow of 50% resulting in an increase in the size of the kidneys and eventually a raised GFR from 100 to 150 ml/min by the second trimester  leading to the increase in the clearance of creatinine, urea and drugs [12].

Glomerular filtration rate is good in assessing renal disease by estimating urine or plasma clearance of substances [13]. The GFR may increase by up to 50% in pregnancy above non-pregnant levels, primarily due to elevations in cardiac output and RPF [2, 6]. Notwithstanding the increase in RPF, the pressure within the glomerulus remains unchanged due to compensatory effects on the afferent and efferent arterioles, but this only occurs in a normal kidney. Any preexisting disease in the kidney will be accelerated, and usually accompanied by worsening in renal function [9]. In most women without complicated pregnancy, these changes resolve after delivery with minimal residual effects [3].

Furthermore, the handling of water and electrolytes by the renal tubules are altered, leading to lower serum osmolality, decline in serum sodium levelsand mild increases in glucosuria and proteinuria [6]. Physiologically, there will be increase in protein excretion during pregnancy because of increase GFR and increase in the permeability of the glomerular basement membrane and when this proteinuria becomes severe de novo or as a result of worsening of preexisting hypertension, then this will be pointing to underlying glomerular disease or preeclampsia [14]. The increased vascularity of the kidneys makes a renal biopsy beyond 32 weeks of pregnancy risky [9]. However, Renal biopsy is preferred in cases where accurate histological diagnosis will significantly change clinical management during pregnancy [15].

 

In a situation of suspected renal impairment, biochemical means of assessing renal function is the preferred method, especially in Nigeria where these methods are readily available in our health facilities. Factors such as nutrition, genetics and mother’s lifestyle influence the imbalance of metabolites in pregnant women [4]. Renal impairment is a common complication of pregnancy [8]. Biochemical parameters reflect these changes and are clearly distinct from the non-pregnant state [4]. Assessment of renal function during pregnancy should therefore take into consideration of these changes. Urea, Electrolytes and creatinine are part of panel of biochemical parameters usually employed in the assessment of renal function.

Urea is the major nitrogen containing metabolic product of protein catabolism in humans. It is synthesized in the liver from ammonia and formed as a result of deamination of amino acid and excreted by the kidneys [2, 16]. The factors that can influence the uptake of urate by the kidneys are: plasma concentrations, volemia and RPF modulators [17].

Many organs in the body including the kidneys are able to synthesize creatinine compound endogenously from the amino acids methionine, arginine and glycine by two enzymatically mediated reactions. This begins in the kidney with L-arginine: glycine aminotransferase (AGAT), an enzyme which initiate the transamination of arginine and glycine to form guanidinoacetic acid and ornithine. The second enzyme glycine N-methyltransferase (GAMT) causes methylation of guanidinoacetic acid which occurs with S-adenosylmethionine as the methyl donor [18]. Creatine is then transported in blood to the muscles, brain and other organs where it is phosphorylated to phosphocreatine. Inter conversion of phosphocreatine and creatine occurs in the muscle following muscular contraction. A fraction ( between 1% and 2% ) of free creatine in muscles spontaneously and irreversibly converts to creatinine, the  anhydride waste product [16]. The creatinine then diffuses passively into the bloodstream where it is excreted through the urine [2].

Electrolytes is the main product of catabolism of the purine nucleosides; adenosine and guanosine[16]. Plasma concentrations of electrolytes increase with age with relatively smaller concentrations in women [17]. It is transported in the blood from the liver to the kidney, where it is filtered. Reabsorption of about 98% of the electrolytes from the glomerular filtrate occurs in the proximal tubules while small amounts are secreted by the distal tubules into the urine. About 70% of electrolytes is excreted through kidney and the remainder sent to the gastrointestinal tract where it is degraded by bacterial enzymes [19]. Conditions such as dilutional effect of an expanding plasma volume, decreased production, and increased renal excretion due to pregnancy induced increase in the GFR causes a reduction in the concentration of serum electrolytes, creatinine and urea [20].

 

1.3 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.

 

1.4 Justification of study

Concentration of electrolytes, Urea and creatine have been postulated as a cause of preeclampsia in developing countries. This association has however, been found to have regional variation (Adam, Malatyalioglu, Alvur, & Talu, 2001; Cunningham et al., 2005; Joshi, Sapre, & Govilla, 2003). Altered NO production has also been postulated to be associated with preeclampsia even though the results are conflicting. Confirmation of these findings will be necessary in developing strategies for managing preeclampsia as there are no reliable cost effective screening tests and well established primary prevention measures.

Currently in Nigeria clinicians use magnesium to treat pregnancy related complications such as preterm labour, severe preeclampsia and eclampsia without monitoring the serum magnesium levels of these patients. This could be deleterious because both hypomagnesaemia and hypermagnesaemia has its antecedent complications. It would therefore be helpful to study the levels of these markers during pregnancy and in preeclamptics in Nigeria to guide clinical practice. The estimation of serum electrolytes in preeclampsia provides a very useful index for the study of physiological and pathological changes during pregnancy.

This study will therefore serve as an informed basis for identification of avenues and strategies for a more effective approach aimed at reducing some of the cardiovascular complications in pregnancy related to these biochemical indices.

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