European Journal of Cardiovascular Medicine

Chronic kidney disease (CKD), particularly in its end stage (ESRD), represents a significant public health challenge worldwide. Defined as abnormalities in kidney structure or function persisting for over three months, CKD is a progressive and irreversible condition that compromises renal excretory, endocrine, and metabolic functions. As the glomerular filtration rate (GFR) declines, patients increasingly develop metabolic complications and fluid and electrolyte imbalances, particularly sodium and potassium abnormalities, which are critical determinants of morbidity and mortality in CKD patients [1,2].

In the context of ESRD, hemodialysis becomes an essential renal therapy. It corrects fluid overload, removes toxins, and helps restore electrolyte balance. However, it may also cause abrupt shifts in sodium and potassium levels, leading to complications such as arrhythmias, muscle weakness, or neurological symptoms if not properly monitored [3]. Sodium and potassium, as primary extracellular and intracellular cations respectively, play vital roles in maintaining membrane potential, acid-base homeostasis, nerve impulse transmission, and muscle contraction [4].

Sodium homeostasis in CKD is affected by impaired tubular reabsorption, inadequate natriuretic responses, and altered hormonal control. Hyponatremia or hypernatremia may both develop, depending on the volume status and dialysis parameters [5]. Hypernatremia, though less common, may arise due to excessive sodium loading or insufficient water intake, while hyponatremia can occur from dilutional states or excessive removal during dialysis sessions [6].

Potassium imbalance, particularly hyperkalemia, is a major concern in ESRD patients due to impaired renal excretion. It can be life-threatening, potentially leading to cardiac arrhythmias or arrest. The incidence and severity of hyperkalemia correlate with dietary intake, medications (e.g., ACE inhibitors, ARBs, potassium-sparing diuretics), metabolic acidosis, and tissue breakdown [7]. Hypokalemia, although less frequent, may result from dialysis-related losses or poor nutritional intake [8].

The role of hemodialysis in regulating serum potassium and sodium is complex. Dialysate composition, session frequency, and dialysis adequacy all affect the post-dialysis electrolyte status. Notably, the use of low potassium dialysate (<2 mmol/L) has been associated with increased risk of sudden cardiac death in patients with pre-dialysis serum potassium <5.0 mmol/L [9]. Therefore, dialysate prescription must be individualized to ensure optimal removal while preventing iatrogenic complications [10].

In India, the burden of CKD is steadily rising, with diabetes and hypertension being the predominant etiologies. Studies have reported significant changes in electrolyte profiles following dialysis, underlining the importance of closely monitoring these parameters pre- and post-dialysis [11,12]. Several Indian and global studies have demonstrated reduced serum potassium and variable changes in serum sodium following a dialysis session [13,14].

The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines emphasize initiating dialysis when clinical indications such as electrolyte imbalances, volume overload, or uremic symptoms are present. Importantly, the timing of initiation and the frequency of dialysis can influence long-term outcomes, particularly in terms of cardiovascular events and mortality [15].

This study, conducted at JLNMCH, Bhagalpur, Bihar, was designed to assess the effect of hemodialysis on serum sodium and potassium levels in ESRD patients. The investigation also aimed to evaluate whether pre- and post-dialysis changes in these electrolytes could serve as prognostic markers for patient monitoring and therapeutic modification. Through this study, we hope to contribute to the body of evidence regarding electrolyte modulation during dialysis and guide clinicians toward optimized care for ESRD patients undergoing routine hemodialysis.

This was a Cross-sectional study carried out in the Department of Biochemistry for a period of 24 months.  A total of 101 patients were selected for this study from admitted patient in JLNMCH. In order to understand influence of dialysis on serum electrolytes, the patients who were in End stage renal disease .Thus the study was divided into 2 groups :

Group 1- Healthy controls

Group 2 – ESRD patients on hemodialysis

Study Design and Setting: This is a hospital-based, observational, cross-sectional study conducted in the Department of Biochemistry in collaboration with the Medicine and Dialysis Units at Jawaharlal Nehru Medical College and Hospital (JLNMCH), Bhagalpur, Bihar. The study period spanned from January 2021 to December 2022.

Study Population:  A total of 101 ESRD patients undergoing maintenance hemodialysis were enrolled and compared with 101 age- and sex-matched healthy control individuals comprising hospital staff, students, and residents.

Inclusion Criteria

1. Patients aged 30–70 years.
2. Diagnosed cases of ESRD undergoing regular hemodialysis.
3. Patients providing informed consent.

Exclusion Criteria

1. Patients with comorbid liver disease, ischemic heart disease.
2. Those on potassium-altering medications (e.g., diuretics, RAAS blockers).
3. Patients on irregular dialysis regimens or with incomplete data.

Sample Collection

1. Venous blood samples (5 mL) were collected from each patient:
2. Pre-dialysis: Before initiation of dialysis.
3. Post-dialysis: 10 minutes after completion of dialysis.

All samples were collected under aseptic precautions into plain tubes, centrifuged to separate serum, and analyzed on the same day.

Biochemical Analysis

The following investigations were conducted:

1. Serum Sodium and Potassium: Ion-selective electrode (ISE) method using Caretium XI-921 and Roche Modular P800 autoanalyzers.
2. Serum Urea: Diacetylmonoxime (DAM) method.
3. Serum Creatinine: Jaffe’s kinetic method.
4. Serum Calcium: Ortho-cresolphthalein complexone (OCPC) method.
5. Serum Phosphorus: Modified Metol method.

Reference Ranges

Sodium: 135–155 mmol/L

Potassium: 3.5–5.5 mmol/L

Creatinine: 0.7–1.5 mg/dL

Urea: 10–50 mg/dL

Calcium: 8.7–10.5 mg/dL

Phosphorus: 2.5–5.0 mg/dL

Instrument Quality Control

All instruments were calibrated daily with internal quality controls, and reagent performance was validated using control charts. Fresh reagents were used if drift was observed.

Statistical Analysis

Data were entered into Microsoft Excel 2016. Analysis was performed using SPSS v25. Paired t-test was used to compare pre- and post-dialysis values. A p-value <0.05 was considered statistically significant.

In the present study it was observed that significant decrease in potassium levels post-dialysis was observed (mean pre: 5.58±0.66 vs. post: 4.23±0.63, p < 0.001), while sodium levels showed a non-significant change (mean pre: 145.67±7.68 vs. post: 144.98±6.48, p = 0.140). Significant alterations were also found in serum urea, creatinine, calcium, and phosphorus.

All the data were analyzed using SPSS package (Stata, version 26.0 SPSS INC, Chicago, IL, USA) for windows. The data were presented as descriptive statistics for continuous variables and percentage for categorical variables and was subjected Chi-square test, and t test. Other values were represented in number, proportions (%) and mean ± SD.

Table 1: Frequency Distribution of Age wise

Out of 101 patients enrolled, 16 patients (15.84%) were between the age group of 30-40 years, 34 patients (33.66%) were between the age group of 41-50 years, 31 patients (30.69%) were between the age group of 51-60 years and 20 patients(19.80%) were between the age group of>60 years.The mean age was 50.45±9.78 years and the P value is not significant (P value = 0.139).

Graph 1 Shows: Frequency Distribution of Age wise

Table 2: Frequency Distribution of Gender wise

Out of 101 patients enrolled, 81 patients (80.20%) were male and 20 patients (19.80%) were female.

Graph 2 Shows: Frequency Distribution of Gender wise

Table 3: Correlation between Sodium and potassium with Before Hemodialysis and After Hemodialysis

In sodium, Before Hemodialysis  Mean±SD  is 145.67±7.68 and After Hemodialysis Mean±SD is 144.98±6.48. The P value is not significant.(P value=0.140)

In Potassium, Before Hemodialysis,  Mean±SD  is 5.58±0.66 and After Hemodialysis , Mean±SD is 4.23±0.63. The P value is significant. (P <0.001)

Graph 3 Shows: Correlation between Sodium and potassium with Before Hemodialysis and After Hemodialysis

Table 4: Frequency of Serum urea (mg/dl) Distribution

Out of 101 patients enrolled, 3 patients (2.97%) were ≤45 serum urea, 69 patients (68.32%) were 46-200 serum urea and 29 patients (28.71%) were >200 serum urea The mean of serum urea  was 159.87±88.69 and the P value is significant (P value <0.001).

Graph 4 Shows: Frequency of Serum urea Distribution

Table 5: Frequency of Serum creatinine (mg/dl) Distribution

Out of 101 patients enrolled, 8 patients (7.92%) were ≤4 serum creatinine, 48 patients (47.52%) were 4.1-8 serum creatinine  and 45 patients (44.55%) were >8 serum creatinine. The mean of serum creatinine was 8.44±3.58 and the P value is significant (P value <0.001).

Graph 5 Shows: Frequency of Serum Creatinine Distribution

Table 6: Frequency of Serum calcium (mg/dl) Distribution

Out of 101 patients enrolled, 30 patients (29.70%) were ≤8 serum calcium, and 71 patients (70.30%)  were >8 serum calcium. The mean of serum calcium was 8.30±1.22 and the P value is significant (P value <0.001).

Graph 6 Shows: Frequency of Serum calcium Distribution

Table 7: Frequency of Phosphorus (mg/dl) Distribution

Out of 101 patients enrolled, 25 patients (24.75%) were ≤3 phosphorous, and 76 patients (75.25%)  were >3 phosphorous. The mean of phosphorous was 3.89±1.04 and the P value is significant (P value <0.001).

Graph 7 Shows: Frequency of Phosphorus Distribution.

Chronic Kidney Disease (CKD) represents a progressive loss of kidney function over months or years. When the glomerular filtration rate (GFR) drops below 15 mL/min/1.73 m², it progresses to End-Stage Renal Disease (ESRD), necessitating renal replacement therapy such as hemodialysis or transplantation. Electrolyte imbalances, particularly disturbances in sodium (Na⁺) and potassium (K⁺) levels, are hallmark complications of CKD, especially in ESRD patients undergoing hemodialysis (HD) [1]. Kidneys play a crucial role in maintaining electrolyte balance, fluid volume, and acid-base homeostasis. Sodium, the primary extracellular cation, regulates plasma osmolality and blood pressure, while potassium, the predominant intracellular cation, is essential for neuromuscular and cardiac function. In ESRD, reduced nephron function impairs the kidneys' ability to excrete potassium and reabsorb sodium appropriately, often leading to hyperkalemia and hyponatremia [2].

1. Overview of Electrolyte Imbalance in CKD

Electrolyte disturbances are hallmark features of chronic kidney disease, especially in ESRD. Impaired renal excretion leads to hyperkalemia and fluctuating sodium levels, both of which have major implications on cardiac and neuromuscular stability. Hemodialysis corrects these imbalances by diffusive and convective transport mechanisms, yet the response can vary based on individual, dialysate composition, and dialysis efficiency.

2. Comparison with Similar Studies

2.1 Sodium Changes

In our study, the change in serum sodium levels pre- and post-hemodialysis was not statistically significant (p = 0.140), which is consistent with findings by:

Maheshwari et al. (2021) [16] who found minimal sodium changes in 90% of dialysis sessions using standard dialysate sodium concentration . In a study by Al-Kudwah et al. (2019) [17] reported similar non-significant changes and proposed that sodium kinetic modeling should guide dialysate sodium prescription .

However, Yilmaz et al. (2020) [18]observed significant sodium drops post-dialysis when dialysate sodium was ≤135 mEq/L (Ref. 3), suggesting that patient-specific dialysate composition influences results—contrasting our fixed-dialysate approach.

2.2 Potassium Changes

Our study confirmed a significant reduction in serum potassium post-hemodialysis (p < 0.001). Similar significant findings were reported by:

Study by Feng et al. (2018) [19] where potassium dropped from 5.6±0.7 to 4.1±0.5 mEq/L post-hemodialysis .

Saran et al. (2020) [20] emphasized the urgency of correcting hyperkalemia to reduce cardiac arrhythmias and mortality risk. Contrastingly, Ali et al. (2019) [21] observed rebound hyperkalemia within 6 hours post-dialysis in a subset of patients , highlighting the need for extended potassium monitoring post-treatment.

3. Serum Urea and Creatinine Trends

Urea and creatinine are classical markers for renal clearance. In our cohort:

Urea (mean: 159.87±88.69 mg/dL) was significantly elevated, consistent with Tandukar et al. (2021) [22]  who reported mean urea of 162.1±81.3 mg/dL in pre-dialysis patients .

Serum creatinine was also elevated (mean: 8.44±3.58 mg/dL), aligned with data by Lee et al. (2019) [23] showing >8 mg/dL in ESRD cases under maintenance hemodialysis .

These findings reinforce the utility of regular dialysis in reducing uremic toxins and the necessity for adequate dialysis frequency and duration.

4. Calcium-Phosphorus Axis

Our data showed:

Hypocalcemia (≤8 mg/dL) in 29.70% of patients.

Hyperphosphatemia (>3 mg/dL) in 75.25%.

These findings correlate well with:

Another study by Block et al. (2020) [24]  who described CKD-mineral and bone disorder (CKD-MBD) as a major consequence of ESRD with persistent dysregulation of calcium-phosphorus homeostasis .

Moe et al. (2018)[25]  emphasized controlling phosphate levels through dietary restrictions and phosphate binders to prevent secondary hyperparathyroidism . Contrarily, Schaefer et al. (2017) [26] reported lower phosphorus abnormalities due to strict phosphate binder protocols and nutritional counseling in their cohort , showing a contrast with our setup that likely lacks such intensive support.

5. Demographic Implications

The male predominance in our study (80.2%) mirrors the findings of Parmar et al. (2022) and Sharma et al. (2023) where males had higher CKD rates possibly due to higher prevalence of hypertension and diabetes  [27, 28].

Age-wise, the majority were aged 41–60 years (64.3%), consistent with peak ESRD burden as seen in studies by Ghimire et al. (2021) and Kher et al. (2019) [29,30].

6. Clinical Implications and Management

Hemodialysis is crucial for preventing life-threatening hyperkalemia.

Monitoring of sodium, although less dynamic during dialysis, should still be done to prevent disequilibrium syndrome. Adjunct measures like dietary phosphate control, calcium supplementation, and anemia management should be incorporated for comprehensive care.

7. In Contrast with Literature

Some studies highlight contradictory findings:

Study by Iseki et al. (2018) reported mild hyponatremia post-dialysis which we did not observe [31]. Kraut and Madias (2021) found no significant potassium drop when using potassium-rich dialysate, which differs from our outcomes using standard potassium-free dialysate [32].

These differences reflect regional variations in dialysis practice, dietary factors, and healthcare protocols.

8. Strengths of Our Study

Inclusion of full biochemical profiles pre- and post-dialysis.

Real-world representation from a tertiary care center in Bihar, addressing a gap in regional data.

Hemodialysis serves to partially restore electrolyte balance by removing excess solutes and fluids through diffusion and ultrafiltration across a semipermeable membrane. However, rapid shifts during HD sessions can sometimes lead to dangerous electrolyte fluctuations, particularly in K⁺ levels, potentially causing arrhythmias or sudden cardiac death [33]. Therefore, monitoring these electrolytes before and after HD is critical for optimizing treatment efficacy and preventing complications.

Several studies have demonstrated that ESRD patients frequently present with elevated serum potassium levels prior to HD, which significantly decrease post-HD. On the contrary, serum sodium levels may show slight increases or remain within the normal range following HD, depending on the dialysate composition, fluid status, and comorbidities [34]. The underlying mechanisms for dyskalemia and dysnatremia in CKD involve impaired tubular secretion of K⁺, resistance to aldosterone, metabolic acidosis, increased tissue breakdown, and water overload due to reduced excretion of free water.

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend maintaining serum potassium levels between 3.5–5.5 mmol/L and sodium between 135–145 mmol/L in ESRD patients [35]. Despite dialysis, achieving these targets remains challenging due to multiple contributing factors such as dietary intake, residual renal function, comorbid medications (e.g., RAAS blockers), and dialysis prescription inadequacies.

Moreover, the variability of electrolyte concentrations between pre- and post-HD can serve as an indirect measure of dialysis adequacy and may influence cardiovascular outcomes. A higher degree of intradialytic potassium reduction, particularly in patients with a pre-dialysis K⁺ level above 6.0 mmol/L, has been associated with increased risk of post-dialysis cardiac arrhythmias [36]. Hence, understanding the dynamics of Na⁺ and K⁺ changes across dialysis sessions can help in tailoring individualized treatment strategies.

The present study was conducted in a tertiary care teaching hospital (JLNMCH, Bhagalpur, Bihar) with the aim of assessing the pattern and magnitude of serum sodium and potassium changes in ESRD patients undergoing HD. The findings of this study will contribute to local data regarding electrolyte disturbances and their management in resource-limited settings. Further, it underscores the importance of vigilant monitoring and adjustment of HD parameters to enhance safety and quality of life in CKD patients.

This study demonstrates that hemodialysis significantly reduces serum potassium in ESRD patients, thus playing a pivotal role in preventing hyperkalemia-induced complications. Sodium levels, although mildly reduced, remained statistically unchanged. Persistent abnormalities in urea, creatinine, calcium, and phosphorus suggest a need for comprehensive management beyond dialysis, including dietary regulation and pharmacologic interventions. Monitoring and individualized dialysis strategies can optimize biochemical homeostasis and improve outcomes.

Limitations of the study

1. Single-center study with limited sample size (n=101), limiting generalizability.
2. No follow-up on post-dialysis rebound electrolyte levels, especially potassium.
3. Dialysate composition was fixed and not individualized, potentially influencing outcomes.
4. Nutritional and medication history was not considered, which could affect electrolyte levels.
5. Short duration of study limited long-term biochemical and clinical outcome assessment.

DECLARATIONS:

Conflicts of interest: There is no any conflict of interest associated with this study

Consent to participate: There is consent to participate.

Consent for publication: There is consent for the publication of this paper.

Authors' contributions: Author equally contributed the work.

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