Chronic kidney disease (CKD) is one of the most important public health issues worldwide, with around 10–13% of the adult population suffering from the condition; it has significant morbidity, mortality, and healthcare cost implications. Loss of kidney function leads to several physiological abnormalities, such as disturbances in calcium, phosphate, vitamin D, and parathyroid hormone (PTH) metabolism, which are complex together and are known as chronic kidney disease–mineral and bone disorder (CKD-MBD). The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines define CKD-MBD as a systemic disease consisting of abnormalities of mineral metabolism, disturbances of bone metabolism and mineralization, and extra-skeletal calcification (especially vascular and soft tissue calcification) [1,2]. Patients with end-stage kidney disease (ESKD) who are on maintenance hemodialysis are especially susceptible to CKD-MBD, due to a high likelihood of severely impaired phosphate clearance, low renal production of 1,25(OH)2D, chronic hypocalcemia, and ongoing parathyroid stimulation. These abnormalities lead to secondary hyperparathyroidism, high-turnover bone disease, osteomalacia, adynamic bone disease, and progressive vascular calcification. Therefore, CKD-MBD significantly contributes to the risk of pathological fracture, bone pain, cardiovascular events, hospitalization, and death. Cardiovascular disease is the major cause of death in maintenance hemodialysis patients, and mineral metabolism disorders are important factors in its pathogenesis [3,4]. Hyperphosphatemia is one of the earliest and most clinically important biochemical abnormalities in advanced CKD. Persistent disturbances in calcium-phosphate homeostasis occur due to the effect of elevated serum phosphate on increasing the secretion of fibroblast growth factor-23 (FGF-23) and parathyroid hormone (PTH) and decreasing the production of calcitriol. At the same time, low vitamin D levels decrease calcium absorption from the intestine and worsen hypocalcemia and secondary hyperparathyroidism. If PTH is persistently high, it continues to cause bone loss, increasing bone turnover and causing bone fragility and decreased mineralization. High levels of calcium phosphate also lead to vascular smooth muscle calcification, causing arterial stiffness, left ventricular hypertrophy, ischemic heart disease, and cardiovascular mortality [5,6]. Maintenance HD patients have been reported to have CKD-MBD (60-90%) with significant regional variation in rates of this condition due to differences in dietary habits, dialysis adequacy, access to phosphate binders and vitamin D therapy, and routine biochemical monitoring. Low- and middle-income countries (LMICs) are likely to have more complex biochemical abnormalities at presentation because of delayed diagnosis, cost, and a lack of specialist nephrology services. Diabetes mellitus, hypertension, obesity, and aging are the precipitating factors in Pakistan, where the prevalence of chronic kidney disease is also growing. Despite this increasing burden, there is a lack of published local information on the prevalence and epidemiology of CKD-MBD [7,8]. Prompt detection and treatment of mineral metabolism disturbances is critical because dietary phosphate restriction, phosphate binders, vitamin D analogs, calcimimetics, and adequate dialysis can help to decrease complications and enhance patient outcomes. KDIGO recommends that patients on maintenance HD be monitored with regular tests of serum calcium, phosphate, intact parathyroid hormone (iPTH), and alkaline phosphatase levels, and that vitamin D be monitored as well [9]. So, it is important to be familiar with local epidemiology of CKD-MBD to help inform evidence-based management and help prevent disease progression and cardiovascular complications.

 

Study Objectives

To assess the prevalence of chronic kidney disease–mineral and bone disorder in maintenance hemodialysis patients and its association with demographics, dialysis duration, and biochemical parameters.

Study Design & Setting A cross-sectional study was conducted in the Department of Nephrology, Institute of Kidney Diseases, Hayatabad, Peshawar, Pakistan, from January 2025 to June 2025. Study Population Adult patients with end-stage kidney disease receiving maintenance hemodialysis at the nephrology unit were screened for eligibility. Eligible patients attending the maintenance hemodialysis unit during the study period were recruited using consecutive non-probability sampling after obtaining written informed consent until the required sample size was achieved. Participants All eligible patients attending the maintenance hemodialysis unit during the study period were screened consecutively for eligibility. Patients fulfilling the inclusion criteria and providing informed consent were enrolled until the required sample size was achieved. Sample Size Calculation The sample size was calculated using the WHO Sample Size Calculator based on the single population proportion formula (n = Z²P(1−P)/d²), assuming a prevalence of 50%, 95% confidence level, and 10% margin of error. The minimum required sample size was 96; therefore, 100 participants were enrolled. Inclusion Criteria • Adults aged ≥18 years. • Diagnosed with end-stage kidney disease. • Receiving maintenance hemodialysis for at least three months. • Undergoing hemodialysis two or three times weekly. • Provided written informed consent. Exclusion Criteria • Acute kidney injury. • Previous parathyroidectomy. • Active malignancy. • Pregnancy. • Inherited metabolic bone disease. • Incomplete biochemical investigations. • Refusal to participate. Data Collection Procedure After obtaining written informed consent, demographic and clinical information, including age, gender, duration of hemodialysis, body mass index, diabetes mellitus, and hypertension, was recorded using a structured data collection form. Venous blood samples were collected immediately before a scheduled hemodialysis session under aseptic conditions. Serum calcium, phosphate, alkaline phosphatase, intact parathyroid hormone, and 25-hydroxy vitamin D levels were analyzed using calibrated automated analyzers in the hospital laboratory following standard operating procedures and internal quality control measures. The principal investigator reviewed all laboratory results and clinical data to ensure completeness and accuracy before statistical analysis. Diagnostic and Management Strategy CKD-MBD was diagnosed according to the KDIGO 2017 Clinical Practice Guideline based on abnormalities in serum calcium, phosphate, intact parathyroid hormone, alkaline phosphatase, and 25-hydroxy vitamin D levels. Patients received routine clinical management according to institutional nephrology protocols; however, treatment outcomes were not evaluated because of the cross-sectional study design. Statistical Analysis Data were entered into SPSS version 27.0 after verification for completeness and accuracy. Normality of continuous variables was assessed using the Shapiro–Wilk test. Normally distributed variables were expressed as mean ± standard deviation, while categorical variables were presented as frequencies and percentages. An independent-samples t-test was used to compare continuous variables, whereas the Chi-square test was applied for categorical variables. A two-tailed p-value <0.05 was considered statistically significant.