From the Research
Patients typically start to develop bone mineral disease when their glomerular filtration rate (GFR) falls below 60 mL/min/1.73m², which corresponds to chronic kidney disease (CKD) stage 3, as this is the point where phosphate retention begins to occur, leading to disruptions in calcium and phosphate homeostasis 1, 2, 3, 4, 5.
Key Points to Consider
- The development of bone mineral disease in CKD patients is a complex process involving abnormalities in calcium, phosphorus, parathyroid hormone, and vitamin D metabolism, as well as bone turnover and mineralization 3.
- As GFR declines, especially below 30 mL/min/1.73m² (CKD stage 4), these abnormalities become more pronounced, leading to increased parathyroid hormone levels, decreased vitamin D activation, and progressive bone demineralization 2, 4.
- Management of CKD-mineral bone disorder (CKD-MBD) should begin with monitoring serum calcium, phosphate, parathyroid hormone, and vitamin D levels once GFR drops below 60 mL/min/1.73m², and may involve dietary phosphate restriction, phosphate binders, vitamin D supplementation, and calcimimetics like cinacalcet 1, 4.
- The goal of treatment is to prevent complications such as secondary hyperparathyroidism, renal osteodystrophy, and vascular calcification, which contribute significantly to morbidity and mortality in CKD patients 2, 3, 4, 5.
Treatment Strategies
- Dietary phosphate restriction (800-1000 mg/day) to reduce phosphate retention and slow the progression of CKD-MBD 4.
- Phosphate binders (such as calcium acetate, sevelamer, or lanthanum) to reduce phosphate absorption and decrease serum phosphate levels 1, 4.
- Vitamin D supplementation (calcitriol or vitamin D analogs) to maintain normal vitamin D levels and prevent secondary hyperparathyroidism 3, 4.
- Calcimimetics like cinacalcet to reduce parathyroid hormone levels and prevent vascular calcification 4.