Chronic kidney disease mineral and bone disorders
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is the syndrome of disturbed calcium, phosphorus, PTH, vitamin D, and FGF-23 homeostasis, abnormal bone mineralization (renal osteodystrophy), and vascular calcification that develops as kidney function declines. Management centers on serial phosphorus/calcium/PTH monitoring, dietary phosphorus restriction plus phosphate binders (noncalcium-based preferred) to normalize phosphorus, avoiding hypercalcemia and unnecessary calcitriol before dialysis, and calcimimetics or activated vitamin D for uncontrolled secondary hyperparathyroidism on dialysis, reserving parathyroidectomy for tertiary disease.
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What this article covers
- Overview
A syndrome, not a single disease: chronic kidney disease-mineral and bone disorder (CKD-MBD) is the term for the linked triad of biochemical abnormalities (calcium, phosphorus, PTH, vitamin D…
- Epidemiology
Biochemical abnormalities track with CKD stage: FGF-23 rises first, detectable by stage G3a; PTH rises progressively as eGFR falls below 60 mL/min/1.73 m2; serum calcium and phosphorus typically…
- Risk factors
Advanced CKD stage (G3a-G5) and dialysis dependence, the dominant driver, since every biochemical and skeletal abnormality tracks with declining eGFR.
- Pathophysiology
PTH is the principal regulator of calcium and phosphorus, acting via three mechanisms: osteoclastic bone resorption, renal 1-alpha-hydroxylation of 25-hydroxyvitamin D to calcitriol, and renal tubular calcium reabsorption with phosphaturia.
- Clinical features
Most patients are asymptomatic until advanced disease, detected through routine calcium/phosphorus/PTH monitoring rather than symptoms.
- Differential diagnosis
Primary hyperparathyroidism: elevated calcium with elevated PTH and normal or near-normal kidney function, unlike the low-to-normal calcium of secondary CKD-MBD.
- Diagnosis
CKD-MBD is diagnosed by the combination of an eGFR consistent with CKD (typically stage G3a or beyond) together with the characteristic laboratory triad (abnormal calcium and/or phosphorus, elevated…
- Management
First, in CKD stages G3a to G5 not on dialysis, lower elevated phosphorus toward the normal range starting with dietary phosphorus restriction.
- Complications
Cardiovascular disease and mortality: elevated phosphorus, PTH, and FGF-23, plus vascular calcification, are independently linked to adverse cardiovascular events and death.
- Prognosis
Prognosis tracks with control of the phosphorus-PTH-FGF-23 axis and avoidance of vascular calcification, since these are independently associated with cardiovascular events and mortality.
- Prevention
Measure serum phosphorus, calcium, and intact PTH serially beginning at CKD stage G3a, with monitoring frequency increasing as eGFR falls, to detect the biochemical cascade before it becomes symptomatic.
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Related articles
- Chronic kidney disease
Chronic kidney disease is abnormal kidney structure or function present for more than 3 months, staged by the Kidney Disease: Improving Global Outcomes (KDIGO) system using estimated glomerular filtration rate and albuminuria, and managed with blood pressure control, renin-angiotensin blockade, an SGLT2 inhibitor, and correction of its metabolic complications.
- Secondary hyperparathyroidism
Secondary hyperparathyroidism is an appropriate, physiologic rise in parathyroid hormone driven by hypocalcemia or impaired vitamin D activation, most commonly from chronic kidney disease and less often from vitamin D deficiency or malabsorption. Management targets the underlying stimulus with dietary phosphorus restriction, phosphate binders, vitamin D repletion or active vitamin D analogs, and calcimimetics, reserving parathyroidectomy for disease refractory to medical therapy.
- Tertiary hyperparathyroidism
Tertiary hyperparathyroidism is autonomous parathyroid hormone hypersecretion that develops after long-standing, poorly controlled secondary hyperparathyroidism, most often in end-stage kidney disease, causing eucalcemia or hypercalcemia despite hyperplastic glands that no longer respond to normal feedback. Cinacalcet is first-line medical therapy, and subtotal or total parathyroidectomy with autotransplantation is reserved for disease refractory to medical management or a markedly elevated PTH.
- Hypocalcemia
Hypocalcemia is a low serum calcium concentration, most often from insufficient parathyroid hormone action (postsurgical or autoimmune hypoparathyroidism, hypomagnesemia, or PTH resistance) or from vitamin D deficiency and chronic kidney disease. Severe or symptomatic disease requires urgent intravenous calcium, while chronic disease is managed with oral calcium, vitamin D repletion, and calcitriol when PTH is absent or the kidney cannot activate vitamin D.
- Osteoporosis
Osteoporosis is low bone strength that raises fragility fracture risk, diagnosed by a hip or spine T-score of -2.5 or less or by a fragility fracture itself. First-line treatment is an oral bisphosphonate, alendronate or risedronate, alongside adequate calcium and vitamin D intake.
- Vitamin D deficiency rickets
Vitamin D deficiency rickets is defective mineralization of the growing cartilaginous growth plate from inadequate vitamin D, most often in a breastfed infant without supplementation, presenting with bowing of the legs, a rachitic rosary, and delayed motor development around 15 months of age. Diagnosis rests on a low 25-hydroxyvitamin D with elevated parathyroid hormone and characteristic metaphyseal cupping and fraying on long-bone radiographs, and first-line treatment is ergocalciferol 2,000 IU PO once daily for 6 weeks with calcium supplementation.