Primary hyperparathyroidism and the kidney

Biochemical and clinical spectrum

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Primary hyperparathyroidism manifests biochemically as a disturbance in serum calcium homeostasis. The central organ setting serum calcium level is the kidney. It not only has the highest rate of active calcium transport, but the kidney also modulates serum calcium homeostasis by virtue of its endocrine role in 1,25-hydroxyvitamin D secretion. Receptors for PTH are widely expressed throughout the renal tubule and are involved in both calcium transport and endocrine function. Biochemical manifestations of primary hyperparathyroidism by the kidney include increased tubular reabsorption of calcium, decreased reabsorption of phosphate and bicarbonate, and hypercalciuria. A reduction in glomerular filtration may occur in some patients with primary hyperparathyroidism, which perturbs the diagnostic relationships among biochemical variables and induces further increases in PTH secretion. Parathyroidectomy rapidly restores the biochemical abnormalities to normal apart from chronic reduced glomerular filtration. Clinical manifestations are nephrolithiasis, which is common, and nephrocalcinosis, which is uncommon. Nephrocalcinosis may occur with or without nephrolithiasis. Risk factors for nephrolithiasis are oversaturation of urine with calcium phosphate and with calcium oxalate. Risk factors for nephrocalcinosis are not clearly defined. Parathyroidectomy greatly reduces the incidence of nephrolithiasis but has little effect on nephrocalcinosis.

Original languageEnglish
JournalJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
Volume17
Issue numberSUPPL. 2
StatePublished - Nov 1 2002

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Primary Hyperparathyroidism
Nephrocalcinosis
Nephrolithiasis
Calcium
Kidney
Parathyroidectomy
Homeostasis
Serum
Hypercalciuria
Calcium Oxalate
Active Biological Transport
Bicarbonates
Phosphates
Urine
Incidence

Keywords

  • 1,25-dihydroxyvitamin D
  • Calcium absorption
  • Calcium reabsorption
  • Hypercalcemia
  • Hypercalciuria
  • Hypophosphatemia
  • Nephrocalcinosis
  • Nephrolithiasis
  • Parathyroidectomy
  • Primary hyperparathyroidism
  • Serum calcium
  • Tubular reabsorption of calcium

ASJC Scopus subject areas

  • Surgery

Cite this

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abstract = "Primary hyperparathyroidism manifests biochemically as a disturbance in serum calcium homeostasis. The central organ setting serum calcium level is the kidney. It not only has the highest rate of active calcium transport, but the kidney also modulates serum calcium homeostasis by virtue of its endocrine role in 1,25-hydroxyvitamin D secretion. Receptors for PTH are widely expressed throughout the renal tubule and are involved in both calcium transport and endocrine function. Biochemical manifestations of primary hyperparathyroidism by the kidney include increased tubular reabsorption of calcium, decreased reabsorption of phosphate and bicarbonate, and hypercalciuria. A reduction in glomerular filtration may occur in some patients with primary hyperparathyroidism, which perturbs the diagnostic relationships among biochemical variables and induces further increases in PTH secretion. Parathyroidectomy rapidly restores the biochemical abnormalities to normal apart from chronic reduced glomerular filtration. Clinical manifestations are nephrolithiasis, which is common, and nephrocalcinosis, which is uncommon. Nephrocalcinosis may occur with or without nephrolithiasis. Risk factors for nephrolithiasis are oversaturation of urine with calcium phosphate and with calcium oxalate. Risk factors for nephrocalcinosis are not clearly defined. Parathyroidectomy greatly reduces the incidence of nephrolithiasis but has little effect on nephrocalcinosis.",
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