Master Renal Osteodystrophy with Picmonic for Medicine

CKD results in decreased phosphate excretion and reduced calcitriol production. Hyperphosphatemia stimulates FGF-23 release, which inhibits 1α-hydroxylase in the kidney, decreasing calcitriol synthesis. Low calcitriol reduces intestinal calcium absorption, leading to hypocalcemia. Hypocalcemia and phosphate retention together drive secondary hyperparathyroidism.

Secondary hyperparathyroidism is a compensatory increase in parathyroid hormone (PTH) secretion in response to CKD-induced hypocalcemia and hyperphosphatemia. Chronic stimulation may progress to tertiary hyperparathyroidism, where parathyroid glands become autonomous, causing hypercalcemia and soft tissue calcifications.

Due to phosphate retention and decreased calcitriol, serum calcium is low, which triggers secondary hyperparathyroidism.

Hyperphosphatemia induces the release of fibroblast growth factor 23 from the bone. FGF-23 is an important mediator of phosphate homeostasis, which helps increase the excretion of phosphate via urine in hyperphosphatemia. It also reduces the production and function of active vitamin D, Calcitriol, which decreases calcium absorption, resulting in hypocalcemia.

CKD decreases conversion of vitamin D to active 1,25-dihydroxyvitamin D, reducing intestinal calcium absorption and contributing to secondary hyperparathyroidism.

This is the classic bone manifestation of secondary hyperparathyroidism in CKD. PTH increases osteoclast activity, causing subperiosteal bone resorption (especially in the phalanges), cortical thinning, and brown tumors (collections of fibrous tissue + hemosiderin from microhemorrhages). Patients present with bone pain and are at increased risk of fractures.

Renal osteodystrophy can lead to osteoporosis due to high bone turnover and impaired mineralization, characterized by trabecular thinning and increased fracture risk.

Decreased calcitriol causes impaired mineralization of bone matrix, leading to osteomalacia, which presents as diffuse bone pain and skeletal weakness.

Management of renal osteodystrophy in chronic kidney disease focuses on correcting mineral imbalances through a combination of strategies: controlling phosphate levels via dietary restriction (maintaining serum phosphate <5.5 mg/dL) and using phosphate binders (calcium-based such as calcium acetate or carbonate, or non-calcium agents like sevelamer and lanthanum); supplementing vitamin D with calcitriol or analogs (e.g., paricalcitol) to enhance calcium absorption; addressing secondary hyperparathyroidism with calcimimetics such as cinacalcet or, in refractory cases, parathyroidectomy; and providing additional supportive care, including sodium bicarbonate for metabolic acidosis and bisphosphonates when osteoporosis is severe.