INTRODUCTION:

Chronic kidney disease represents a sustained and progressive loss of renal structure and function that often culminates in end-stage renal disease (ESRD), where hemodialysis becomes essential to maintain life.¹ Although hemodialysis replaces key renal functions through diffusion and ultrafiltration, it cannot fully reconstitute the kidney’s finely tuned regulation of electrolytes, acid–base balance, and mineral metabolism.² As kidney function declines, derangements in potassium, calcium, and phosphorus emerge and intensify, interacting with disturbances in parathyroid hormone and vitamin D pathways. Even on maintenance dialysis, these imbalances are common and clinically consequential, shaping symptom burden, hospitalization risk, and long-term outcomes.^3,4,5

The global burden of CKD is rising, driven by aging populations and the expanding prevalence of diabetes and hypertension.¹Many individuals present late in the disease course, often with multiple comorbidities and limited physiologic reserve. In India and comparable settings, resource constraints, delayed nephrology referral, and the high cost and complexity of dialysis amplify the problem, translating into substantial morbidity, premature mortality, and significant financial strain on patients and health systems.⁶Beyond survival, quality of life is profoundly affected: pruritus, restless sleep, fatigue, muscle weakness, and bone pain are frequent, multifactorial, and often refractory to routine measures.^7,8,9

Electrolyte and mineral abnormalities sit at the center of this clinical picture. Hyperphosphatemia promotes secondary hyperparathyroidism and vascular calcification, increasing cardiovascular risk and contributing to calcific arteriolopathy.^4,10,11 Hyperkalemia poses an ever-present threat of arrhythmia and sudden cardiac death, modulated by dietary intake, residual renal function, medications, and inter-dialytic interval.^2,11 Hypocalcemia and the calcium–phosphorus product influence bone turnover and extra-skeletal calcification,^3,12while shifts during dialysis—driven by dialysate composition, treatment duration, and ultrafiltration targets, can provoke symptoms ranging from cramps and hypotension to post-dialysis fatigue and itching.¹³The pathophysiology is dynamic: inter-dialytic accumulation, intra-dialytic shifts, and post-dialytic rebound together create a moving target that challenges standard, one-size-fits-all protocols.^14,15

Despite advances in dialysis technology and protocols, clinically meaningful control of these biochemical disturbances remains uneven. Real-world practice must balance dietary counseling, binder adherence, dialysate customization, and medication management against patient tolerance, pill burden, and cost. Evidence gaps persist regarding the thresholds at which biochemical abnormalities precipitate symptoms such as pruritus, the relative contribution of phosphorus versus calcium–phosphorus product, and the best strategies to personalize dialysate potassium and calcium to minimize both arrhythmic risk and mineral bone disorder. Moreover, translating lab improvements into tangible symptom relief is not always straightforward, underscoring the need for pragmatic data rooted in routine care.

This study responds to those needs by characterizing the prevalence and pattern of electrolyte abnormalities in patients receiving maintenance hemodialysis, and examining their association with key clinical complications, especially pruritus and markers of mineral bone disorder. By linking biochemical profiles with symptoms and practical interventions, the work aims to identify leverage points for earlier and more precise action: tightening phosphate control, optimizing dialysate prescriptions, and reinforcing consistent dietary and binder strategies.

MATERIALS AND METHODS:

Study design and setting:

A prospective observational study was conducted at a tertiary care hospital in Kerala among adult patients with chronic kidney disease (CKD) stage V receiving maintenance hemodialysis (HD). Patients were evaluated at baseline and followed over at approximately three months. Dialysis was delivered via conventional bicarbonate hemodialysis using standard dialyzers, with session duration and frequency according to unit protocol and individualized clinical considerations. Dialysate composition (especially potassium and calcium concentrations) followed unit standards but could be modified based on clinical and biochemical needs.

Sample size:

The sample size was calculated using the formula: n = Z²Pq/ m².

Where ‘n’ is the sample size, p is the prevalence of CKD patients undergoing haemodialysis i.e., 5.5%, q = 100-p = 94.5%, z is the level of significance = 1.96, m is the allowable error i.e., 5.

The sample size was found to be 80.

Method of Selection:

Patients were selected based on inclusion and exclusion criteria.

Inclusion criteria:

· Patients of either gender ≥ 18 years of age.

· Patients undergoing maintenance haemodialysis (measured GFR≤ 30ml/min/1.73m2).

Exclusion criteria:

· Patients having any active malignancy.

Variables and Measurements:

The primary biochemical variables were serum phosphorus, potassium, and calcium. The calcium–phosphorus product was calculated to contextualize mineral load and potential calcific risk. Where available, adjunct measures (parathyroid hormone, alkaline phosphatase, and vitamin D levels) informed interpretation of CKD-MBD status but were not mandated for all participants. Baseline measurements were collected during routine pre-dialysis sampling on a mid-week session to avoid extremes associated with the long interdialytic interval. Follow-up sampling occurred after approximately three months under similar conditions.

Clinical variables included demographics (age, sex), CKD etiology (e.g., diabetes, hypertension, glomerulonephritis), comorbid conditions (notably cardiovascular disease and diabetes), dialysis vintage (time on HD), session frequency and duration, dialysate composition (potassium and calcium), and interdialytic weight gain as a proxy for volume status and dietary adherence. Medication data captured use of phosphate binders, potassium binders, vitamin D analogs, calcimimetics, diuretics (if residual kidney function), and other relevant agents.

Symptom assessment prioritized pruritus due to its burden and hypothesized link with phosphorus and the calcium–phosphorus product. Additional symptomatology pertinent to CKD-MBD (bone pain, fractures) and dialysis tolerability (cramps, hypotension) was recorded when present.

Data Collection Tools:

· Specially designed data collection form.

· 12-PSS questionnaire.¹⁶

Data Collection Methods:

During the study period, all eligible patients were enrolled, thus resulting in 91 patient population. Following informed consent, baseline data were abstracted from patient charts and dialysis records and supplemented by patient interviews. Biochemical tests were processed through the hospital laboratory according to standard protocols. Dialysis prescriptions were not altered for research purposes; however, treating teams could modify diet, dialysate, or medications as clinically indicated. These changes were recorded to contextualize observed biochemical shifts. At approximately three months, repeat assessments mirrored baseline collection. All collected information was carefully verified to ensure it met the predefined inclusion and exclusion criteria. Once validated, the data were entered into SPSS software and subsequently analyzed using its statistical tools.

Outcomes:

Primary outcomes were the prevalence of potassium, calcium and phosphate disturbances at baseline and follow-up, and the change in the overall proportion of patients with any electrolyte abnormality over the study period. Secondary outcomes included associations between electrolyte disturbances and pruritus presence/severity.

Statistical Analysis:

The collected data were analyzed and interpreted using SPSS and Microsoft Excel. Descriptive statistics, including frequencies and percentages of various parameters, were calculated using both software tools and presented through tables, charts, and pie diagram. Categorical variables were reported as counts and percentages. Associations between pruritus and biochemical parameters were explored using correlation tests and visual binning for categorical groupings (e.g., phosphorus above vs. below threshold). All statistical tests adhered to a 5% significance level, with SPSS employed for in-depth statistical computations.

RESULT:

Population Characteristics:

A total of 91 adults with stage V CKD on maintenance hemodialysis were included; 57(62.6%) were male and 34(37.4%) female. Mean age was 56.2±12.1 years and was comparable between sexes (male 55.8±11.9; female 56.8±12.5). 23.07% were aged under 50 years, 28.6% were 50–59 years, and 48.3% were ≥60 years. Diabetes mellitus and hypertension emerged as the leading comorbidity in 47.2% and 34.1%, often coexisting in the same patients; 80.2% had at least one comorbidity. Other notable comorbidities included nephrotic syndrome (20.8%), coronary artery disease (12%), and hypothyroidism (4.3%). Most patients dialyzed twice weekly (56%), while 41.7% underwent three sessions per week. The baseline characteristics are shown in table 1.

Table 1. Baseline characteristics of study population

Baseline characteristics	n = 91
Age, years (mean ± SD)	56.2 ± 12.1
Range	20 - 77
Age group, n(%)
<50 years	21 (23.07)
50 – 59 years	26 (28.6)
≥ 60 years	44 (48.3)
Gender, n (%)
Male	57 (62.6)
Female	34 (37.4)
No. of Comorbidities, n (%)
Single	73 (80.2)
≥ 2	18 (19.7)
Comorbidities, n (%)
Diabetes mellitus	43 (47.2)
Hypertension	31 (34.1)
Nephrotic syndrome	19 (20.8)
Coronary artery disease	11 (12.0)
Polycystic kidney disease	3 (3.2)
Dialysis Vintage, n (%)
< 2 years	35 (38.4)
≥ 2 years	56 (61.5)
Dialysis frequency, n (%)
Twice weekly	51 (56.0)
Thrice weekly	38 (41.7)
Four times weekly	2 (2.19)
Medications, n (%)
Calcitriol	91 (100)
Calcium acetate + calcitriol	33 (36.2)
Calcium acetate + sevelamer + calcitriol	34 (37.4)
Cinacalcet	1 (1.09)
Sodium acid phosphate	1 (1.09)
Electrolyte imbalances, n (%)
At least one	85 (93.4)

Biochemical Parameters:

Comparing the baseline and post values, the percentage of patients with no electrolyte imbalance tripled from 6.6 to 21.9. Hyperkalemia (>5.5mmol/L) fell from 36.3% to 17.6%(absolute change −18.7 percentage points). Hyperphosphatemia (>5.5mg/dL) decreased from 73.6% to 61.5% (−12.1 percentage points). Hypocalcemia (<8.5 mg/dL) decreased from 23.1% to 16.5% (−6.6 percentage points).

Table 2. Serum electrolyte profiles at baseline and after three months

Electrolyte	Level	Baseline, n (%)	Post, n (%)
Potassium	Low	1 (1.1)	0 (0)
	Normal	57 (62.6)	75 (82.4)
	High	33 (36.3)	16 (17.6)
Calcium	Low	27 (29.7)	24 (26.4)
	Normal	63 (69.2)	65 (71.4)
	High	1 (1.1)	2 (2.2)
Phosphorus	Low	1 (1.1)	1 (1.1)
	Normal	23 (25.3)	34 (37.4)
	High	67 (73.6)	56 (61.5)

Dialysis frequency and Biochemical stability:

Patients undergoing more frequent dialysis exhibited greater correction of electrolyte derangements. As illustrated in Table 3, those dialyzed four times per week achieved full normalization, while the twice-weekly group demonstrated substantial though incomplete improvement.

Table 3. Dialysis Frequency and Electrolyte Imbalance Correction

Dialysis Frequency	Baseline Imbalance (%)	Post Imbalance (%)
2/week	92.2	72.5
3/week	94.7	89.5
4/week	100	0

Clinical Manifestations:

Chronic Kidney Disease Associated Pruritus:

Pruritus affected 24.2% of patients, with varying intensity as assessed by the 12- point pruritus severity index.

Table 4. Severity of pruritus

Pruritus	n (%)
Nil	69 (75.8)
Mild	4 (4.4)
Moderate	14 (15.4)
Severe	4 (4.4)

Statistical analysis revealed a significant association between hyperphosphatemia and increased pruritus severity (p<0.05). Patients with higher phosphorus levels were more likely to report moderate-to-severe itching.

Table 5 displays this correlation, supporting the hypothesis that elevated phosphate levels may enhance deposition of calcium-phosphate complexes in the skin, provoking inflammation and sensory irritation.

In 62 patients with mild hyperphosphatemia, 74.1% had no symptoms of pruritus, 6.4% had mild pruritus and 19.3% had moderate pruritus. Out of the 3 patients with moderate hyperphosphatemia, 3.3% did not have pruritus and 6.6% had moderate pruritus. Of the 4 patients with severe hyperphosphatemia, 100% experienced severe pruritus.

Calcium-Phosphate product and Pruritus:

An elevated calcium–phosphate (Ca × P) product also showed a strong association with pruritus severity.

As illustrated in Table 6, patients with Ca × P > 80 mg²/dL² predominantly reported moderate-to-severe itching, while those with values below 50mg²/dL² had minimal symptoms.

Table 6. Correlation between calcium phosphate product and severity of pruritus

Ca × P (mg²/dL²)	Severity of Pruritus, n (%)				n= 91
Ca × P (mg²/dL²)	Nil	Mild	Moderate	Severe	n= 91
<50	48 (87.3)	5 (9.1)	2 (3.6)	0 (0)	55
50–80	18 (58.1)	6 (19.4)	5 (16.1)	2 (6.4)	31
>80	0 (0)	0 (0)	2 (40.0)	3 (60.0)	5

The Ca × P product was also linked to CKD-Mineral and Bone Disorder (CKD-MBD) risk.

As seen in Table 7, 5.4% of patients with Ca × P > 80 mg²/dL² demonstrated a high risk of developing CKD-MBD, while the majority with values below 50mg²/dL² had minimal risk.¹⁷

Muscle Cramps:

In the study population, 29.6% had reports of varying degrees of hypocalcaemia, with 15(16.4%) having mild, 8(8.7%) having moderate and 4(4.3%) having severe hypocalcaemia respectively. Muscle cramps were reported by 9/91(9.9%) patients. Table 8 displays the distribution of muscle cramps according to hypocalcaemia severity. None of the patients with no hypocalcaemia or with mild hypocalcaemia reported cramps. In the moderate hypocalcaemia group, 5 of 8 patients (62.5%) experienced muscle cramps, and all 4 patients (100%) with severe hypocalcaemia had cramps. The association between hypocalcaemia severity and muscle cramps was statistically significant (p<0.05).

Table 7. Association between hypocalcemia and muscle cramps

Hypocalcaemia	Muscle Cramps		n=91
Hypocalcaemia	Nil	Present	n=91
Nil (>8)	64	0	64
Mild (8-8.4)	15	0	15
Moderate (7.5-7.9)	3	5	8
Severe (≤7.4)	0	4	4
Total	82	9	91

DISCUSSION:

Our baseline assessment revealed a high prevalence of electrolyte disturbances, particularly hyperphosphatemia (73.6%) and hyperkalemia (36.3%), as detailed in Table 2. This aligns closely with the landmark work of Block et.al. and Monisha M, who established hyperphosphatemia as a nearly universal challenge in dialysis populations^4,18 and a key driver of mortality. The observed improvement after three months of management, while significant, was incomplete. The reduction of hyperphosphatemia to 61.5% and hyperkalemia to 17.6% underscores the tenacity of these imbalances. This persistent biochemical burden mirrors findings by Evenepoel et al.¹⁴, who emphasized that standard thrice-weekly hemodialysis is often insufficient for adequate phosphate clearance, necessitating aggressive adjunctive therapy with binders and dietary control. The partial correction seen in our study, especially in patients on a twice-weekly schedule (Table 3), reinforces the concept that dialysis frequency and adequacy are foundational to electrolyte management¹⁵.

An ancillary finding was the association between dialysis frequency and biochemical improvement. Patients on a more intensive schedule (four times weekly) achieved complete normalization of electrolytes, while those on a conventional twice-weekly schedule showed the least correction. The association between more frequent dialysis (four times weekly) and superior electrolyte correction (Table 3) offers a potential pathway for improvement, echoing the findings of the Frequent Hemodialysis Network trial¹⁵.

A key finding of this study is the strong association between disordered mineral metabolism and the distressing symptom of uremic pruritus. Table 5 clearly demonstrates a dose-response relationship: the prevalence and severity of pruritus escalated markedly with increasing severity of hyperphosphatemia. Notably, 100% of patients with severe hyperphosphatemia (>9 mg/dL) experienced severe pruritus. This correlation provides robust local evidence supporting the pathophysiological model proposed by Rayner et al.¹⁹, wherein calcium-phosphate micro-crystal deposition in the skin acts as a direct pruritogen. Furthermore, Table 6 strengthens this link by showing that an elevated calcium-phosphate product (Ca × P > 80mg²/dL²) was exclusively found in patients reporting moderate-to-severe itching. This aligns with the integrated risk marker concept from Goodman et al.¹¹, where the Ca × P product predicts not only vascular calcification risk but also, as our data suggests, patient-centric symptoms. Momose A et al²⁰in 2004 noted that an increased calcium phosphate product in CKD-MBD, can lead to increased calcium deposition, which in turn can affect the intensity and onset of pruritic symptoms.

Our findings thus validate and extend the observations from international registries like the DOPPS study⁷,confirming that in our setting, pruritus is not an isolated nuisance but a direct clinical manifestation of poor mineral control.

The clinical impact of electrolyte disturbance extended beyond pruritus to neuromuscular symptoms. Table 7 presented an association, where muscle cramps were absent in patients with normal or mild hypocalcemia but affected 62.5% of those with moderate and 100% of those with severe hypocalcemia. This severity-dependent relationship underscores the direct neuromuscular excitability caused by low ionized calcium levels during or after dialysis. This finding corroborates the clinical observations detailed by Bover et al. ^[17] on the systemic effects of calcium dysregulation in CKD-MBD, moving the focus beyond bone to include immediate quality-of-life parameters like cramp frequency.

CONCLUSION:

This study confirms the high prevalence of electrolyte imbalances, particularly hyperphosphatemia (73.6%) and hyperkalemia (36.3%), in stage V CKD patients on maintenance hemodialysis. After three months of dialysis and individualized management, the overall proportion of patients with any electrolyte abnormality decreased but remained substantial to 61.5% and 17.6% respectively. Critically, these biochemical disturbances are strongly linked to clinically significant symptoms: pruritus severity (24.2%) correlates directly with elevated serum phosphorus and calcium-phosphate and was assessed using the 12-Pruritus Severity Scale., while muscle cramps show a effect-response relationship with hypocalcemia. These findings underscore that pruritus and cramps are not merely incidental symptoms but direct manifestations of disordered mineral metabolism. A structured, multidimensional management strategy encompassing enhanced biochemical surveillance, individualized dialysis prescriptions, integrated pharmacotherapy, and symptom-driven intervention is therefore essential to improve both biochemical control and patient quality of life.

The study had limitations including it being single centred and conducted in a relatively short time frame. Biochemical indicatiors like sodium, magnesium, PTH were not included, which limited the study interpretation. Lack ECHO reports led to limitations in categorizing patients with valvular calcification. Future multi-center longitudinal studies with comprehensive biomarker profiling (including iPTH and FGF-23) are needed to validate these associations and assess long-term outcomes. Additionally, interventional trials evaluating personalized management protocols, alongside mixed-methods research exploring patient experience, are crucial to translate these insights into effective, patient-centered clinical practice. Addressing these gaps will be key to optimizing care and improving both survival and quality of life for the hemodialysis population.

CONFLICT OF INTEREST:

The authors have no conflicts of interest regarding this investigation.

ACKNOWLEDGMENTS:

The authors would like to sincerely thank Department of Nephrology, Lourdes hospital and St. Josephs College of Pharmacy for their kind support and encouragement.

ABBREVIATIONS:

1	CKD	Chronic Kidney Disease
2	CKD-MBD	Chronic Kidney Disease-Mineral and Bone Disorder
3	GFR	Glomerular Filtration Rate
4	ESRD	End Stage Renal Disease
5	HD	Hemodialysis
6	12-PSS	12 point Pruritus Severity Scale

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Received on 23.12.2025 Revised on 07.03.2026

Accepted on 30.04.2026 Published on 06.07.2026

Available online from July 20, 2026

Asian J. Pharm. Res. 2026; 16(3):251-256.

DOI: 10.52711/2231-5691.2026.00037

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Creative Commons License.

Hyperphosphatemia (mg/dl)	Severity of Pruritus, n (%)				n=91
Hyperphosphatemia (mg/dl)	Nil	Mild	Moderate	Severe	n=91
Nil (<4.5)	22 (100)	0 (0)	0 (0)	0 (0)	22
Mild (4.5-7.5)	46 (74.1)	4 (6.4)	12 (19.3)	0 (0)	62
Moderate (7.6-9)	1 (3.3)	0 (0)	2 (6.6)	0 (0)	3
Severe (>9)	0 (0)	0 (0)	0 (0)	4 (100)	4