From the Guidelines
Management of mineral bone disorder (MBR) in dialysis patients should prioritize a comprehensive approach targeting phosphate control, calcium balance, and parathyroid hormone (PTH) regulation, focusing on patients with overt hyperphosphatemia and avoiding inappropriate calcium loading, as recommended by the Kidney Disease: Improving Global Outcomes (KDIGO) 2017 clinical practice guideline update 1.
Key Components of MBR Management
- Phosphate control through dietary restriction (800-1000 mg/day) and phosphate binders such as calcium-based binders, sevelamer, or lanthanum carbonate.
- Calcium levels maintained between 8.4-10.2 mg/dL, with vitamin D analogs like calcitriol used for hypocalcemia.
- Treatment of secondary hyperparathyroidism with calcimimetics such as cinacalcet or etelcalcetide, considering the patient's dialysis status.
Monitoring and Assessment
- Regular monitoring with monthly measurements of calcium, phosphate, and quarterly PTH assessments.
- Annual bone mineral density scans to track bone health.
Considerations
- Treatment approaches should be based on serial assessments of biochemical variables (serum phosphate, calcium, and PTH) taken together, as therapeutic maneuvers aimed at improving one variable can have unintended effects on others 1.
- Current evidence does not support maintaining normal serum phosphate levels in patients not receiving dialysis, and there are safety concerns associated with aggressive phosphate-lowering therapy 1.
- Modest increases in PTH may represent an appropriate adaptive response to decreasing kidney function, and treatment should focus on patients with progressively increasing or persistently elevated PTH values above the upper limit of normal 1.
From the Research
MBR Management in Dialysis Patients
- MBR management in dialysis patients involves controlling hyperphosphatemia, secondary hyperparathyroidism, and other mineral bone disorders (CKD-MBD) 2.
- The pathophysiology of CKD-MBD focuses on abnormalities in serum levels of biomarkers such as FGF-23, klotho, phosphate, calcium, vitamin D, and PTH 2.
- Treatment strategies for CKD-MBD include control of hyperphosphatemia with dietary restriction, intestinal phosphate binders, and adequate dialysis, as well as the use of calcimimetic agents, vitamin D, and analogues 2.
Phosphate Binders
- Phosphate binders are used to reduce positive phosphate balance and lower serum phosphate levels in patients with CKD 3.
- Sevelamer, lanthanum, iron, and calcium-based phosphate binders have uncertain or inestimable effects on death, cardiovascular death, myocardial infarction, stroke, fracture, or coronary artery calcification in CKD patients not on dialysis 3.
- In patients with CKD G5D on dialysis, sevelamer may lower death and induce less hypercalcaemia compared to calcium-based binders 3.
Biomarkers and Inflammation Indexes
- Biomarkers such as serum alkaline phosphatase (ALP), C-reactive protein (CRP), and leukocyte count are associated with CKD-mineral and bone disorder (MBD) in patients with end-stage renal disease (ESRD) 4.
- Hypocalcemia, hyperphosphatemia, and increased levels of intact parathyroid hormone (iPTH) and CRP are common in ESRD patients 4.
Phosphate Balance and CKD-MBD
- Abnormal serum phosphate concentrations are an independent risk factor for cardiovascular morbidity and mortality, and overall mortality in CKD patients 5.
- Effective phosphate control is a logical therapeutic target for CKD-MBD treatment, and novel therapies such as tenapanor, a targeted sodium-hydrogen exchanger isoform 3 inhibitor, may be useful in reducing serum phosphate concentrations 5.