Hypoparathyroidism and the Kidney

Munro Peacock

Research output: Contribution to journalArticle

Abstract

Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of PTH action, the renal mechanisms transporting calcium and phosphate reabsorption deregulate, resulting in hypocalcemia and hyperphosphatemia. Circulating calcium negatively regulates PTH secretion. Hypocalcemia causes neuromuscular disturbances ranging from epilepsy and tetany to mild paresthesia. Circulating phosphate concentration does not directly regulate PTH secretion. Hyperphosphatemia is subclinical, but chronically promotes ectopic mineralization disease. Vitamin D–thiazide treatment leads to ectopic mineralization and renal damage. PTH treatment has the potential for fewer side effects.

Original languageEnglish (US)
JournalEndocrinology and Metabolism Clinics of North America
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Hypoparathyroidism
Parathyroid Hormone
Hyperphosphatemia
Hypocalcemia
Kidney
Tetany
Paresthesia
Vitamins
Epilepsy
Phosphates
Calcium

Keywords

  • 1,25 dihydroxy vitamin D
  • Calcium homeostasis
  • Hypoparathyroidism
  • Kidney
  • Phosphate homeostasis
  • PTH
  • Tubular reabsorption calcium
  • Tubular reabsorption phosphate

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Hypoparathyroidism and the Kidney. / Peacock, Munro.

In: Endocrinology and Metabolism Clinics of North America, 01.01.2018.

Research output: Contribution to journalArticle

@article{39117d23aaaf4a41b4bda21e8db834ef,
title = "Hypoparathyroidism and the Kidney",
abstract = "Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of PTH action, the renal mechanisms transporting calcium and phosphate reabsorption deregulate, resulting in hypocalcemia and hyperphosphatemia. Circulating calcium negatively regulates PTH secretion. Hypocalcemia causes neuromuscular disturbances ranging from epilepsy and tetany to mild paresthesia. Circulating phosphate concentration does not directly regulate PTH secretion. Hyperphosphatemia is subclinical, but chronically promotes ectopic mineralization disease. Vitamin D–thiazide treatment leads to ectopic mineralization and renal damage. PTH treatment has the potential for fewer side effects.",
keywords = "1,25 dihydroxy vitamin D, Calcium homeostasis, Hypoparathyroidism, Kidney, Phosphate homeostasis, PTH, Tubular reabsorption calcium, Tubular reabsorption phosphate",
author = "Munro Peacock",
year = "2018",
month = "1",
day = "1",
doi = "10.1016/j.ecl.2018.07.009",
language = "English (US)",
journal = "Endocrinology and Metabolism Clinics of North America",
issn = "0889-8529",
publisher = "W.B. Saunders Ltd",

}

TY - JOUR

T1 - Hypoparathyroidism and the Kidney

AU - Peacock, Munro

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of PTH action, the renal mechanisms transporting calcium and phosphate reabsorption deregulate, resulting in hypocalcemia and hyperphosphatemia. Circulating calcium negatively regulates PTH secretion. Hypocalcemia causes neuromuscular disturbances ranging from epilepsy and tetany to mild paresthesia. Circulating phosphate concentration does not directly regulate PTH secretion. Hyperphosphatemia is subclinical, but chronically promotes ectopic mineralization disease. Vitamin D–thiazide treatment leads to ectopic mineralization and renal damage. PTH treatment has the potential for fewer side effects.

AB - Hypocalcemia and hyperphosphatemia are the pathognomonic biochemical features of hypoparathyroidism, and result directly from lack of parathyroid hormone (PTH) action on the kidney. In the absence of PTH action, the renal mechanisms transporting calcium and phosphate reabsorption deregulate, resulting in hypocalcemia and hyperphosphatemia. Circulating calcium negatively regulates PTH secretion. Hypocalcemia causes neuromuscular disturbances ranging from epilepsy and tetany to mild paresthesia. Circulating phosphate concentration does not directly regulate PTH secretion. Hyperphosphatemia is subclinical, but chronically promotes ectopic mineralization disease. Vitamin D–thiazide treatment leads to ectopic mineralization and renal damage. PTH treatment has the potential for fewer side effects.

KW - 1,25 dihydroxy vitamin D

KW - Calcium homeostasis

KW - Hypoparathyroidism

KW - Kidney

KW - Phosphate homeostasis

KW - PTH

KW - Tubular reabsorption calcium

KW - Tubular reabsorption phosphate

UR - http://www.scopus.com/inward/record.url?scp=85054559489&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85054559489&partnerID=8YFLogxK

U2 - 10.1016/j.ecl.2018.07.009

DO - 10.1016/j.ecl.2018.07.009

M3 - Article

C2 - 30390817

AN - SCOPUS:85054559489

JO - Endocrinology and Metabolism Clinics of North America

JF - Endocrinology and Metabolism Clinics of North America

SN - 0889-8529

ER -