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Secondary Hyperparathyroidism

  • Secondary Hyperparathyroidism is a complication of end-stage chronic renal failure and is thus an aspect of uremia. Because elevated levels of Parathyroid Hormone (PTH) are a compensatory response to chronic renal failure thehHyperparathyroidism is considered "Secondary".
  • Overview
    • The pathophysiological sequence of Secondary Hyperparathyroidism is poorly-understood but is thought to be initiated by insufficient excretion of phosphate and Vitamin D synthesis by the failing kidney. These defects in turn collaborate to result in mild hypercalcemia that is compensated for by enhanced secretion of PTH.
  • Hyperphosphatemia
    • Recall that the kidneys regulate plasma phosphate levels through regulation of phosphate excretion. As GFR declines, phosphate intake rises above the capacity of renal phosphate excretion, resulting in hyperphosphatemia. The increased blood phosphate complexes free, ionic calcium, thus reducing the effective concentration of physiologically active calcium and thus causing mild hypocalcemia (see: Calcium and Phosphate Physiologic Forms).
  • Reduced Synthesis of Vitamin D
    • Recall that the kidneys is responsible for synthesis of physiologically active Vitamin D. Due to declining renal function, levels of Vitamin D are reduced, resulting in lowered levels of calcium absorption from the alimentary tract and thus contributing to the mild hypocalcemia (See: Vitamin D Physiology).
  • Hyperparathyroidism
    • The reduced levels of ionic calcium stimulate secretion of PTH (See: Parathyroid Hormone Physiology). High levels of PTH in turn result in enhanced resorption of bone, ultimately resulting in the pathology of "Renal Osteodystrophy" described below.
Morphology and Clinical Consequences
  • Long-term stimulation of the parathyroid gland typically results in symmetric hypertrophy of the four glands. Renal Osteodystrophy refers to pathological changes in bone that occur in the context of chronic renal failure due to secondary hyperparathyroidism. The morphology of renal osteodystrophy is similar, but slightly milder, than the "Osteitis Fibrosa Cystica" characteristic of primary hyperparathyroidism. Like primary hyperparathyroidism, bone pathology leads to increases in bone fractures.