Research paper : Relationship between Renal function status with infected of chronic Hepatitis B in Ramadi Teaching Hospital

Raed Obaid Saleh Al-Sabhany, Anas Shaker Latif, Entissar Mohammed Mosleh, Ansam Jassim Hamoudi, Anmar Anees Mohi Medical Laboratory Techniques department, College of Health and medical technology, University of Al Maarif , Anbar, Iraq *Corresponding AuthorEmail: Dr.raed.obaid@uoa.edu.iq ; https://orcid.org/0000-0003-3873-3181 Received 17/12/2025 Accepted 27/12/2025

Abstract
Renal failure can be described as a condition resulting from the kidneys’ failure of excretory functions, leading to blood retention of waste products of nitrogen excretion. Acute renal failure is acute and may be reversed, while chronic renal failure is slow and, most of the time, is perpetually present. Moreover, its growing rate can be ascribed to the growing number of diabetic and hypertensive people, considered two of the primary risk factors of chronic renal failure. Thus, this present study was done, namely Detection of Hepatitis B Virus from renal failure patients and examines its relationship and levels of urea, creatinine, phosphorus, Sodium, potassium, chloride, calcium, and albumin. Meanwhile, ALT, AST, TSB, and ALP are also examined.
Results of this study revealed that low blood urea and serum creatinine levels existed in chronic hepatitis B cases, when compared to that of the control group. There were no significant differences in LFTs between the patient and control groups, except for AST, which decreased significantly in the patient group (24.85±2.81 IU/L) compared to the control group (30.96±3.62 IU/L). There were no significant differences in any of the serum electrolytes in this study, as the p-values were greater than 0.05.
Keywords: Renal function , Hepatitis B , Ramadi .

Introduction

The Hepatitis B virus (HBV) remains a substantial global public health concern and poses a health danger to numerous individuals worldwide. More than 240 million individuals are chronic carriers of this virus. Hepatitis B virus (HBV) infection causes several clinical manifestations, such as acute and/or fulminant hepatitis, as well as several forms of chronic hepatitis, including asymptomatic carriers, cirrhosis,chronic hepatitis,  and hepatocellular carcinoma.

Every year, about 786,000 people die because of the hepatitis B virus (Kim and Kim,2015). Among all these routes of transmission, transfusion is the route that should be avoided. But due to hepatitis B surface antigen (HBs Ag), a screening tool of blood, transfused since the early 1970s, transfusion-associated hepatitis B has significantly improved (Kim and Kim,2015). Despite this improvement, the transfusion of hepatitis B has continued and has significantly decreased over the four decades following transfusions of blood components that are HBs Ag negative (Kim and Kim,2015). But research has continued, and it has confirmed that the HBV transmission via blood components, negatively testing for HBs Ag can occur, and it is concluded that HBV transmission is the most common viral transfusion-borne infection and that the hepatitis B virus can occur, and thus, this phenomenon is called occult hepatitis B virus (OBI). Additionally, this condition is defined by co-existence of positive HBV DNA and negative HBsAg (Kim &Kim,2015). Moreover, this is currently considered as a risk of hepatitis B virus transmission through blood transfusion, hemodialysis, and live-liver transplant and a cause of development of cirrhosis and hepatocellular carcinoma (Kim &Kim,2015). Moreover, a condition of HBV infection is called OBI and this is defined as presence of positive HBV DNA in serum and/or plasma and absent HbAg (Kim &Kim,2015).

identifiable in clinical settings (Almeida et al., 2017). There was a case report of HBV transmission by blood transfusion through an antibody to hepatitis B core antigen (anti-HBc) only positive blood donor, and this was documented for the first time nearly 30 years ago. Occult transmission risk of HBV through blood transfusion is due to blood donations that test negative.

for HBsAg that have been collected either during the pre-seroconversion window period (WP), defined as the time between infection and detection of a viral antigen or antibody marker, or during late stages of infection (Said, 2011.) OBI was identified in several clinical settings, such as Recovery from previous infection, indicated by the presence of hepatitis B surface antibody (antiHBs), chronic hepatitis due to surface gene escape mutants that are not detected by present tests, chronic carrier without any serologic sign of HBV infection, except HBV DNA, (so-called “seronegative”), most often observed in an endemic setting, chronic carrier stage with HBsAg concentrations below the threshold of detectability and identified only by the presence of anti- HBc as the only serologic marker, (so-called “anti-HBc alone” or “isolated anti-HBc”) (Allain, 2006). Conventionally, HBV infection is identified by serologic tests aiming at detecting viral antigens or antibodies. Among these, HBsAg is generally used as a tool for diagnosis because it is generally regarded as a marker of infection itself. Simultaneously, anti-HBc (both IgM and IgG, at first, persisting only IgG during chronic phase of infections)) appear 1-2 weeks following HBsAg appearance, while IgG antibodies persist during the chronic phase of hepatitis B virus (HBV), whereas its appearance indicates immunity against HBV infections (Kafi-Abad Sa et al., 2009). Following the development of molecular biologic tests, it has been observed that some persons may possess HBV DNA at low titers, and possibly, within their hepatocytes as well as blood, despite lack of HBsAg, as indicated by present tests (Gachara et al., 2017.(

Diagnoses of hepatitis B virus and other comorbid infections are made based on a number of clinical, biochemical, histologic, and serologic tests, and molecular diagnosis through serum antibodies that develop as a result of stimulation of the body’s immune system following an infection by the virus, and it is imperative that all other associated test results be interpreted (Liang, 2009).

HBV infection can influence biochemical function in human.

Functions of the Liver Can be Analyzed on the Basis of Certain Biochemical Tests, Including Total Bilirubin, Alanine Aminotransferase (ALT), Aspartate Aminotransferase

Alanine Amino Transferase that catalyzes the transfer of the amino group of alanine to alpha-ketoclotarite, resulting in pyruvite and glutamate (Harvey and Ferrier, 2011). The name of this enzyme was previously called (SGPT) serum glutamic pyruvate transaminase (Thapa and Walia, 2007). ALT is present in low concentrations in bone, muscle, and kidneys, and as such, ALT is more abundant in serum (Ali, 2008).

Aspartate Aminotransferase (AST)

AST is responsible for transferring an amine group of aspartate to oxaloacetate (Harvey and Ferrier, 2011). AST was previously known as serum glutamic oxaloacetic transaminase or

Liver disease, if it is due to acute or chronic damage, increases the concentration of serum amine vectors. AST is widely present in the cardiac muscles, muscles, skeleton, kidneys, brain, and red blood cells. In the case of the liver, ALT is present solely in the cytosol, whereas AST is present in the mitochondria as well as the cytosol (in 80% and 20% of total AST, respectively) (Ali, 2008).

Among these enzymes is alkaline phosphatase, responsible for transporting metabolites through cell membranes (Ali, 2008). It is present within the liver, as a histchemical substance on the microvilli of the bile duct and on the surface of sinusoidal liver cells (Thapa & Walia, 2007). ALP can be of other origins, such as placental, renal, intestinal, and leukocytic (Ali, 2008).

Biliverdin is produced from iron present as iron proteins, such as cytochrome P450 isoenzymes, myoglobin, and other iron proteins, whereas about 20% of its daily production comes from iron present as hemoglobin, iron released from aging red blood cells. Biliverdin is produced by phagocytic monocytes present in the spleen and bone marrow, and Coffer cells of the liver, and is released into the plasma. In a span of 24 hours, about 250-300 mg of natural bilirubin is produced, and a larger amount is secreted by neonates. More iron is used by bilirubin, opening up the heme ring at the alpha-carbon bridge (Harvey and Ferrier, 2011). Again, this is catalyzed by an enzyme called haem-oxygenase, resulting in the formation of more iron, carbon monoxide, and biliverdin. Biliverdin is then reduced by cytosol, reducing biliverdin to bilirubin. Since indirect bilirubin is relatively insoluble in water, it is present as tightly bound complexes of bilirubin and albumin present in plasma (Fevery, 2008).

Kidneys may be affected by other infections and can lead to this condition through a slowly and steady loss of kidney function due to chronic renal failure. It is normally an effect of a serious medical condition that poses some troubles or challenges. Unlike acute renal failure, chronic renal failure develops over a period of weeks, months, and years as the kidneys stop functioning as they should, finally reaching end-stage renal disease (ESRD). There is a reduction in renal clearance or glomerular filtration rate (GFR), and this leads to a build-up of urea, creatinine, and other materials within one’s blood (Amin et al., 2014). This research seeks to investigate the relationship that may exist between hepatitis B infection and renal function. Also, it was measured for Urea, Creatinine, Albumin, ALT, AST, ALP, TSB, Electrolytes, and HBsAg.

Methods

Study Design

A case control study design was used for this study, samples collected from the Dialysis Center in Al-Ramadi city at the period from November 2023 to the December 2023

Patient Selection

Blood samples were taken from patients on dialysis. Ten CKD patients with Hepatitis B Virus and 10 patients with renal failure were sampled. All these groups were collected before forming the hemodialysis apparatus.The control group consisted of 10 cases that were randomly selected. There was no history of illness in the control group

Blood Samples Collection

Five mL of blood were drawn from non-fasting patients and the control group and divided into two plain tubes and one EDTA tube. The EDTA tube was used to determine the ABO blood group and Hb. The serum tubes were centrifuged at 3000 rpm for 10 minutes then separated into new clean plastic tubes. Then used for biochemical parameters.

Identification of Chemical Factors by Beckman Coulter AU480 Clinical Chemistry System

Analytical Principle Beckman Coulter AU480 System Spectrophotometry is a method for quantifying the absorption of light by a chemical compound by assessing the intensity of light transmitted through a sample solution. Each chemical absorbs or transmits light within a defined wavelength range, in accordance with fundamental principles. This technique can also ascertain the quantity of a known chemical component present. Spectrophotometry is one of the most successful methods of quantitative analysis in fields such as chemistry, physics, biology, materials science, chemical engineering, and therapeutic applications. Potentiometry is an electrochemical measuring technique developed by Drucker in 1943. Urea, creatinine, albumin, calcium, phosphorus, sodium, potassium, chloride, total bilirubin, AST, and ALT were quantified.

Identification of Hepatitis B Surface Antigen (HBsAg) in serum or plasma

Unidirectional Strip Design The HBsAg Test is a quick, direct binding assay for the visual identification of Hepatitis B Virus Surface Antigen (HBsAg) in serum and plasma. It serves as a tool in the identification of hepatitis B infection.
Statistics analysis
Data entry was conducted using SPSS 26 software. The findings presented in this study were articulated as mean ± standard error of the mean (SEM). Analysis of variance (ANOVA) and Chi-square tests were conducted for comparisons among scattered groups. Probability values below 0.05 were deemed biologically significant, whereas those below 0.01 were classified as extremely significant.

Results

The data below indicates that the Urea in HBV patients was lower (27±1.69 mg/dL) than in the control (32.6±8.72 mg/dL); nevertheless, this difference was nosignificant, with a p-value of 0.4. The reduction in serum creatinine levels in patients (0.81±0.06 mg/dL) compared to the control (1.43±0.66 mg/dL) was not statistically significant, with a p-value of 0.3(Table1 and Figure1)

 

Table 1: Statistical analysis of renal function tests (RFT)

 

Factors Group Number Mean St. Error F P value
Urea (mg/dL) Patients 13 27.00 1.69  

0.51

 

0.483

  Control 10 32.60 8.72    
  Total 23 29.43 3.84    
Creatinine (mg/dL) Patients 13 0.81 0.06  

1.108

 

0.305

 

 

Figure 1. The mean levels of RFT

As presented in the table below, there were no differences in LFTs between the patients and control , except for AST, which decreased significantly in patients (24.85±2.81) compared to the control group (30.96±3.62 IU/L)(Table2 and Figure2).

 Table 2 : Statistical analysis of liver function tests (LFT)

Factors Group Number Mean St. Error F P value
TSB

(mg/dL)

Patients 3 4.89 0.32  

0.1

 

0.755

  Control 0 5.25 0.57    
  Total 23 1.15 0.32    
ALT (IU/L) Patients 13 32.88 3.10  

2.735

 

0.113

  Control 10 40.91 3.80    
  Total 23 36.37 2.50    
AST (IU/L) Patients 13 24.85 2.81  

4.26

 

0.052

  Control 10 38.90 6.89    
  Total 23 30.96 3.62    
Albumin (g/dL) Patients 13 4.13 0.08  

0.09

 

0.767

  Control 10 4.09 0.11    
  Total 23 4.11 0.07    

 

 

 

 

Figure 2 The mean levels of LFT.

As presented in Table 6, there were no differences in all serum electrolytes in this study, with p-values greater than 0.05(Table3).

Table 3 : statistical analysis of serum electrolytes.

 

Factors Group Number Mean St. Error F P value
K+(mmol/L) Patients 13 1.24 0.54 0.1 0.755
  Control 10 1.03 0.27    
  Total 3 5.05 0.30    
Na+(mmol/L) Patients 3 136.85 0.96 0.803 0.38
  Control 0 138.50 1.70    
  Total 3 137.57 0.91    
Cl- (mmol/L) Patients 3 106.08 0.78 0.052 0.821
  Control 0 106.40 1.26    
  Total 3 106.22 0.69    
P(mg\L) Patients 3 3.55 0.15 1.897 0.183
  Control 0 3.90 0.22    
  Total   3.70 0.13    

 

Figure 3 The mean levels of Electrolytes.

As presented in the table below, there was significant positive correlation between the ALT and AST (r=0.896, P=0.000) and significant moderate positive with ALB (0.46, P=0.027). While AST was related significantly and moderate positive with K (r=0.553, P=0.006). Then, Albumin (ALB) level was correlated negatively and moderated with B. Urea and S. Creatinine (r=-0.469, and r=-0.534, respectively), and these correlations were significant with p- values (0.024, and 0.009, respectively). Urea level was correlated strongly and positively with S. Cr (r=0.913), and it was significantly (r=0.913, P=0.000). Also, urea correlated moderately and positively with S. Cl and S. P with (r=0.446, and 0.526, respectively), and these correlations were significant with p-values (0.033, and 0.01, respectively). Serum creatinine level was correlated moderately and positively with S. Cl and S. P with (r=0.413, and 0.582, respectively), and these correlations were significant with p-value less than 0.05 .Serum sodium (Na) level was correlated moderately and positively with S. Cl, and significantly (r=0.634, P=0.001)

 

Table 7 The correlation among  the study’s variables

 

Variables   TSB ALT AST ALB Urea S. Cr K Na Cl P
 

TSB

r    

0.201

 

0.094

 

0.159

 

0.216

 

0.129

 

0.059

 

0.331

 

0.181

 

.275

P   .359 .668 .468 .321 .559 .789 .123 .408 .204
 

ALT

r 0.201   .896 .46 0.136 0.186 .263 .244 0.036 0.171
P .359   .000 .027 .535 .395 .225 .262 .869 .436
 

AST

r 0.094 .896   .339 0.1 0.136 .553 .092 0.161 0.062
P .668 .000   .113 .651 .536 .006 .678 .464 .778
 

ALB

r 0.159 .46 .339   0.469 0.534 0.088 .277 0.169 0.23
P .468 .027 .113   .024 .009 .688 .201 .442 .290
 

Urea

r 0.216 0.136 0.1 0.469   .913 .293 .284 .446 .526
P .321 .535 .651 .024   .000 .175 .189 .033 .010
 

S. Cr

r 0.129 0.186 0.136 0.534 .913   .145 .228 .413 .582
P .559 .395 .536 .009 .000   .508 .296 .050 .004
 

K

r 0.059 .263 .553 0.088 .293 .145   0.037 .004 .003
P .789 .225 .006 .688 .175 .508   .868 .984 .991
 

Na

r 0.331 .244 .092 .277 .284 .228 0.037   .634 0.028
P .123 .262 .678 .201 .189 .296 .868    

.001

.898
 

Cl

r 0.181 0.036 0.161 0.169 .446 .413 .004 .634   .009
P .408 .869 .464 .442 .033 .050 .984 .001   .968
 

P

r .275 0.171 0.062 0.23 .526 .582 .003 0.028 .009  
P .204 .436 .778 .290 .010 .004 .991 .898 .968  

 

 

Discussion

Viral hepatitis constitutes a significant global health issue. Chronic viral hepatitis C infection, more prevalent in developing nations with low to limited per capita income (Liaw, Yun-Fan, 2009), induces recurrent inflammation and tissue repair, leading to extracellular matrix deposition, scarring, progressive fibrosis, and ultimately liver cirrhosis. Iredale et al., 2007 Chronic hepatitis B virus infection

Hepatitis B virus (HBV) infection is a primary contributor to liver cirrhosis and hepatocellular cancer globally. Lozano et al. (2012) Besides liver damage, HBV infection is linked to extra-hepatic consequences. (Hong et al., 2018) This study aims to investigate the effects of chronic inflammatory disease on individuals with chronic hepatitis B and the functionality of several organs, particularly renal function. The Hepatitis B virus (HBV) is prevalent in the liver, although it has also been observed to induce chronic infections in various other human organs. We must examine the evidence for a potential link between HBV and other organs. The liver was previously the only focus of research on the hepatitis B virus. Clinicians and scientists were more interested in understanding the genotypes, the variations in biological characteristics, and the distribution of hepatitis B virus mutants in various geographical areas, together with to the clinical consequences and outcome of antiviral therapies in various demographic categories. (Baig, et al., 2007)

The Urea level in this study was lower in HBV patients (27±1.69 mg/dL) compared to those considered as the control group (32.6±8.72 mg/dL), but it was not significant, with a p-value of 0.4. Also, the decrease in S. creatinine in patients (0.81±0.06 mg/dL) compared to control group (1.43±0.66 mg/dL) was not significantly, with a p-value of 0.3. When renal outcomes were compared between controls and patients with CHB who had not been treated for cirrhosis in the study by Vu, Vinh, et al. (2019), the mean eGFR of the untreated CHB patients was significantly lower than the mean eGFR of the matched control patients at the end of the follow-up period. This suggests that CHB itself is linked to a small drop in renal function. These results are in line with others who have reported that CHB is the most common cause of viral nephropathy worldwide and that CHB is associated with a higher risk for chronic kidney disease in population-based claims data studies from Taiwan. (Chen, et al., 2015 a, b) Meanwhile, CHB treatment lasts a long time, so keeping an eye on renal function over time is an important part of caring for CHB patients.

There were no significant differences in LFTs in this study between the patients and control groups, except for AST, which decreased significantly in patients (24.85±2.81) compared to the control group (30.96±3.62 IU/L). Another study by Zaidan, et al., (2019) have shown serum transaminase enzymes (AST and ALT) revealed a significant increase in activity among patients with chronic hepatitis B. Another study by Saod, et al., (2019) revealed low serum albumin and higher serum S. ALT and S. AST in patients with chronic hepatitis B compared to those of healthy individuals. AST elevations are frequently prevalent in patients with cirrhosis, as well as in liver diseases that typically have an increased ALT. (Panteghini et al., 1983).A significant reduction in serum albumin levels in patients with chronic hepatitis B compared to healthy groups in another study by Zaidan, et al., (2019) may suggest decreased hepatic production due to decreased liver function following hepatocellular disease. However, a low serum albumin concentration is a recent finding in liver disease. When it is present, it suggests chronic disease. (D’Agata, et al., 1999).Liver failure typically progresses steadily over the years. Electrolyte abnormalities are among the most dreaded consequences of cirrhosis. This investigation revealed no significant changes in serum electrolytes, with p-values exceeding 0.05. Kim et al. (2008) demonstrated that 3.9% of hyponatremic patients were predisposed to developing hepatorenal syndrome and its related consequences, which represent some of the most lethal outcomes in cirrhotic patients. Cirrhotic patients have dilutional hyponatremia. Restricting fluid intake to half or less than the output can rectify fake hyponatremia. The severity of liver illness also leads to hypokalemia. Another study by Zaidan et al. (2019) demonstrated an elevation in mean levels of potassium in the blood in patients with chronic hepatitis B relative to healthy individuals. Saod et al. (2019) found that patients with chronic hepatitis B exhibited elevated mean serum potassium concentrations compared to healthy individuals. The serum potassium level may rise, accompanied by declining renal function. Consequently, the increased potassium concentration may independently provoke potassium excretion. Consequently, a new equilibrium is established devoid of medical issues. Gennari and Segal (2002) A reduction in glomerular filtration capacity will occur as a renal consequence of hepatitis B virus infection. The adjacent renal tubules, responsible for urine concentration, also harbor the DNA of the hepatitis B virus. (Lai, 1991) The notable reduction in serum sodium content relative to healthy persons may be attributed to compromised renal function and its incapacity to eliminate solute-free water. Agrawal et al. (2008) Hyponatremia and hypernatremia are disorders of water balance resulting from poor renal elimination of water and antidiuretic hormone dysfunction (El-Zawhry et al., 2013(.Hypokalemia was noted in 14.8% of instances in the study conducted by Akhter et al. (2021). Ahmad et al. (2006) obtained analogous results of 14%, while Alam et al. (2005) documented 18%. Diet, gastrointestinal loss, and diuretic therapy can alter potassium levels. Cirrhotic patients devoid of edema or ascites may exhibit a diminished total potassium in the body level despite having normal serum potassium levels. Potassium supplements should be administered orally or intravenously. Akhter et al. (2021) and Borroni et al. (2000) reported hyponatremia prevalence rates of 29.6% and 29.8%, respectively, with higher rates seen. The hyponatremia levels reported by Mamun et al. (2013), Angeli et al. (2006), and Kim et al. (2008), which are 35%, 49.4%, and 47.9% respectively, may be attributable to varying demographics and a substantial study population. The predominant electrolyte disturbance linked to cirrhosis is sodium concentration, with hyponatremia frequently reported in over 57% of hospitalized cirrhotic patients. Kumar et al. (2020) Chronic hyponatremia is characterized by sodium levels below 130 mEq/L and occurs in around 22% of individuals with cirrhosis. Ginés et al., 1998 Hyponatremia occurs due to increased water retention relative to sodium and other solutes. Consequently, reduced water excretion in urine relative to water intake results in dilutional hyponatremia. Patients with hyponatremia exhibit reduced survival rates compared to those without hyponatremia) Akhter et al,. (2021.The study by Saod, et al., (2019) showed that the serum sodium concentration dropped significantly compared to healthy people. This drop may be because the kidneys aren’t working as well and can’t get rid of solute-free water. (Agrawal et al., 2008). Vinay, et al. (2005) found that hyponatremia and hypernatremia represented disorders of water balance or impaired renal water excretion and antidiuretics, then portal hypertension commonly accompanies hyponatremia resulting from the impairment of solute-free water excretion (Adrogué et al., 2000). In recent years, hyponatremia has attracted interest as a possible prognostic factor for liver cirrhosis. Many ongoing studies are currently examining the pathophysiology of hyponatremia associated with liver cirrhosis, with dilutional hyponatremia being considered the most plausible pathophysiology (Gines et al., 1998).The association among several biochemical indicators tested in HBV was assessed using Pearson product-moment correlation analysis. A positive connection and a negative correlation were identified among several factors. The current work, along with several others, including those by Ayelagbe et al. (2012) and Zaidan et al. (2019), suggests that the virus replicates within the renal tubules. Akhter et al. (2021) identified a moderate to high correlation between certain electrolyte imbalances and the MELD score, the Child-Pugh score, and the Child-Pugh class in individuals with hepatitis C-induced liver cirrhosis. Numerous studies conducted by Borroni et al. (2000), Ahmad et al. (2006), and Alam et al. (2005) have elucidated the prevalence of hyponatremia and the emergence of numerous problems resulting from cirrhosis and its related electrolyte imbalances. We also advocate for the regulation of other confounding variables concerning various electrolytes. Hepatic dysfunction induces potassium depletion, hence requiring potassium supplementation. Electrolyte abnormalities may arise at any stage of liver disease, with cirrhosis being the primary instigator. Consequently, simultaneously monitoring their electrolytes to prevent associated complications such as arrhythmias, hypotension, peripheral edema, and CVS complications.

 

Conclusions:

This study shows that the Renal failure patient without HBs Ag and Renal failure patients with HBs.Ag aged 23 years old and above.A significant difference was observed in AST between renal failure with HBs.Ag and Renal failure without HBs.Ag while Alb, urea , creatinine, electrolytes and HB showed no difference between the two renal failure groups when compared with the control healthy group.

Acknowledgment

Non

Conflicts Interest

Non

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